Basic and Bedside Electrocardiography, 1st Edition (2009)

Chapter 23. Acute Coronary Syndrome: ST Elevation Myocardial Infarction

The Electrocardiogram (ECG) in Acute Coronary Syndrome

·         When a patient presents to the emergency department with chest discomfort or symptoms suspicious of acute myocardial infarction (MI), the standard of care requires that a full 12-lead ECG be obtained and interpreted within 10 minutes after the patient enters the medical facility. The ECG can provide the following useful information in patients with acute coronary syndrome:

o    The ECG is the only modality capable of making a diagnosis of ST elevation MI. It is the most important tool in defining the onset of the coronary event and the urgency for immediate revascularization. It serves as the only basis for deciding whether or not the patient is a candidate for thrombolytic therapy or primary angioplasty. It therefore remains central to the decision making process in managing patients with acute coronary syndrome.

o    It provides useful information on whether or not reperfusion therapy has been successful.

o    It can identify the culprit vessel, localize whether the lesion is proximal or distal, and therefore predicts the extent of jeopardized myocardium. Localizing the culprit vessel will also help in predicting potential complications that may inherently occur based on the geographic location of the MI.

Figure 23.1: Electrocardiogram Changes of Acute Coronary Syndrome. Complete occlusion of the vessel lumen by a thrombus causes ST elevation whereas partial occlusion of the vessel lumen will result in ST depression, T-wave inversion, or other less-specific ST and T-wave abnormalities.

o    It is the simplest and most useful tool in the diagnosis of right ventricular MI.

o    It is the most useful modality in identifying several complications of acute MI, including the various atrioventricular and intraventricular conduction abnormalities as well as the different bradycardias and tachycardias, which are frequent during hospitalization especially after the initial onset of symptoms.

·         In this era of modern and expensive technology, the ECG remains the most important and least expensive modality in evaluating and managing patients suspected of having acute symptoms from coronary artery disease. The ECG therefore remains the cornerstone in evaluating and managing patients with acute coronary syndrome and continues to provide very useful information that is not obtainable with other more expensive technologies.

Acute Coronary Syndrome

·         It is well recognized that acute coronary syndrome is caused by rupture of an atheromatous plaque, resulting in partial or total occlusion of the vessel lumen by a thrombus. Depending on how severely the coronary flow is compromised, varying degrees of myocardial ischemia will occur resulting in ST elevation MI, non-ST elevation MI, or unstable angina (Fig. 23.1).

Figure 23.2: Myocardial Ischemia with ST Elevation. ST elevation from an occlusive thrombus is persistent and generally does not resolve with coronary vasodilators, whereas ST elevation from coronary vasospasm is usually transient and responds to coronary vasodilators.

o    ST elevation MI: Acute ischemia associated with elevation of the ST segment indicates complete occlusion of the vessel lumen by a thrombus with complete cessation of coronary blood flow. When this occurs, myocardial necrosis with elevation of cardiac markers is always expected.

o    Non-ST elevation: When acute ischemia is associated with ST depression, T wave inversion or other less specific ST and T wave abnormalities, partial or incomplete occlusion of the vessel lumen by a thrombus has occurred. This type of ischemia may or may not be accompanied by cellular necrosis. When there is cellular necrosis, with increased cardiac markers in the circulation, non-ST elevation MI is present. When there is no evidence of myocardial necrosis, the clinical picture is unstable angina. The diagnosis of myocardial necrosis is based on the presence of increased cardiac troponins in the circulation. Regardless of symptoms or ECG findings, the diagnosis of acute MI is not possible unless these cardiac markers are elevated.

ST Segment Elevation

·         Acute coronary syndrome with elevation of the ST segment is almost always from complete occlusion of the vessel lumen by a thrombus resulting in complete cessation of coronary flow. It can also occur when there is coronary vasospasm (Fig. 23.2).

o    ST elevation from occlusive thrombus: ST elevation from an occlusive thrombus almost always results in cellular necrosis. Cardiac markers are expected to be always elevated. Unless the occluded vessel is immediately reperfused, pathologic Q waves will occur. ST elevation MI therefore is synonymous with a Q-wave MI.

o    ST elevation from coronary vasospasm: ST elevation from coronary vasospasm, also called Prinzmetal angina, is usually transient and can be reversed with coronary vasodilators such as nitroglycerin. Myocardial necrosis usually does not occur unless vasospasm becomes prolonged lasting more than 20 minutes.

·         The presence of ST segment elevation accompanied by symptoms of myocardial ischemia indicates that the whole thickness of the myocardium is ischemic. This type of ischemia is also called transmural ischemia.

·         Example of ST elevation due to coronary vasospasm is shown below (Figs. 23.3 and 23.4). The pattern of ST elevation is identical and cannot be differentiated from the ST elevation associated with an occlusive thrombus.

ECG Changes in ST Elevation MI

·         ST elevation from an occlusive thrombus: When a coronary artery is totally occluded by a thrombus, complete cessation of blood flow occurs. Unless adequate collaterals are present, all jeopardized myocardial cells supplied by the coronary artery will undergo irreversible necrosis, usually within 6 hours after the artery is occluded.

Figure 23.3: Coronary Vasospasm. ST elevation from coronary vasospasm is indistinguishable from ST elevation from an occlusive thrombus. ST elevation from coronary vasospasm, however, is usually transient and can be reversed by nitroglycerin, whereas ST elevation from an occlusive thrombus is usually persistent and unresponsive to coronary vasodilators.

Figure 23.4: Coronary Vasospasm. Electrocardiogram A and B are from the same patient. (A) ST elevation in multiple leads (arrows), which may be due to an occlusive thrombus or coronary vasospasm. (B) After nitroglycerin was given. The ST segment elevation has completely resolved within minutes consistent with coronary vasospasm. Coronary angiography showed smooth walled coronary arteries with no occlusive disease.

·         Necrotic changes in the myocardium are usually not microscopically evident during the first 6 hours after symptom onset. The cardiac troponins may not even be elevated in the circulation in some patients. The ECG, however, will usually show the most dramatic changes at this time. The ECG therefore is the most important modality in triaging patients with chest pain symptoms and is crucial to the diagnosis of ST elevation MI. It also serves as the main criteria in deciding whether or not thrombolytic agent or primary coronary angioplasty is needed.

Figure 23.5: ST Elevation Myocardial Infarction (MI). Giant or hyperacute T waves mark the area of ischemia (A-C) followed by ST elevation (B, C), diminution of the size of the R wave (D) or development of pathologic Q waves (E) and inversion of the T waves (D, E). The evolution of ST elevation MI from hyperacute T waves to the development of pathologic Q waves may be completed within 6 hours after symptom onset or may evolve more slowly for several days.

·         When a coronary artery is completely occluded, the following sequence of ECG changes usually occurs unless the occluded artery is immediately reperfused (Fig. 23.5):

o    Peaked or hyperacute T waves (Fig. 23.5A)

o    Elevation of the ST segments (Fig. 23.5B,C)

o    Changes in the QRS complex with development of pathologic Q waves or decrease in the size or amplitude of the R waves (Fig. 23.5D)

Figure 23.6: (A) Hyperacute T Waves. The initial electrocardiogram (ECG) of a patient presenting with acute onset of chest pain is shown. Tall, hyperacute T waves (arrows) are seen in V1 to V4 with elevation of the ST segments in V3-4. Note that the hyperacute T waves are confined to the distribution of the occluded vessel and are usually the first to occur before the ST segments become elevated. Subsequent ECGs are shown in (B-D). (B) ST elevation Myocardial Infarction (MI). This tracing was recorded 15 minutes after the initial ECG. In addition to the hyperacute T waves, ST elevation has developed in V1 to V4 (arrows).

o    Further changes in the ST segment and T waves (Fig. 23.5D,E)

·         Peaked or hyperacute T waves: One of the earliest ECG abnormalities to occur in ST elevation MI is the development of tall and peaked T waves overlying the area of ischemia (Fig. 23.6A). These hyperacute T waves usually precede or accompany the onset of ST segment elevation and are useful in identifying the culprit vessel and timing the onset of acute ischemia.

·         ST segment elevation: Hyperacute T waves are accompanied or immediately followed by ST segment elevation. ST segment elevation with symptoms of chest discomfort indicates an acute process. The leads with ST elevation are usually adjacent to each other and mark the area of injury and are helpful in identifying the culprit vessel. The extent of ST segment elevation is also helpful in predicting the severity of myocardial involvement.

Thrombolytic Therapy

·         ST elevation from acute coronary syndrome is a medical emergency requiring immediate reperfusion of the occluded artery with a thrombolytic agent or with primary percutaneous coronary intervention (PCI). The extent of myocardial necrosis can be minimized if reperfusion of the occluded artery is timely and successful.

·         Thrombolytic Therapy: According to American College of Cardiology (ACC)/American Heart Association (AHA) guidelines, thrombolytic therapy is indicated up to 12 hours after onset of symptoms. It may even be extended to 24 hours if the patient's symptoms persist or the chest pain is “stuttering” (waxing and waning) and the ST segments remain elevated at the time of entry. The thrombolytic agent should be infused within 30 minutes after the patient enters the medical facility on his own (door to needle time) or within 30 minutes after contact with emergency service personnel (medical contact to needle time).

o    The best results are obtained if the thrombolytic agent is given within 1 to 2 hours after symptom onset because thrombolytic therapy is time dependent and is more effective when given early.

o    The criteria for initiating a thrombolytic agent in a patient with symptoms of acute ischemia are ST segment elevation or new (or presumably new) onset left bundle branch block (LBBB).

§  St segment elevation:

Figure 23.6: (Continued) (C) ST Elevation MI. The above ECG was recorded approximately 1.5 hours from the initial ECG (see A). The ST segments continued to evolve even after thrombolytic therapy. ST elevation has become more pronounced in V2 to V6 and slight elevation of the ST segments is noted in II, III, and aVF. Hyperacute T waves are still present in V2 to V5 (arrows). (D) ST Elevation MI. ECG recorded 13 days later. QS complexes or decreased amplitude of the r waves are seen in V1 to V5. The ST segments are isoelectric and the T waves are inverted from V1-6 and leads I, II, and aVL.

§  ST elevation >1 mm in any two or more adjacent precordial or limb leads.

§  ST elevation is measured at the J point. The J point is the junction between the terminal portion of the QRS complex and beginning of the ST segment. The preceding T-P segment serves as baseline for measuring the ST elevation. The PR interval is used if the T-P segment is too short or is obscured by a U wave or a P wave of sinus tachycardia.

§  New-onset LBBB: The presence of LBBB will mask the ECG changes of acute MI. If the LBBB is new or presumably new and accompanied by symptoms of acute myocardial ischemia, thrombolytic therapy is indicated.

·         Thrombolytic therapy is not indicated (and may be contraindicated) in patients with acute ischemia associated with ST depression or T wave inversion even if the cardiac markers (troponins) are elevated.

·         The ECG is the most important modality not only in selecting patients for thrombolytic therapy but also in monitoring successful response to therapy. One of the earliest signs of successful reperfusion during thrombolytic therapy is relief of chest pain and resolution of the initial ST segment elevation by at least 50% within 60 to 90 minutes after initiation of therapy (Fig. 23.7). If ST segment resolution does not occur within 90 minutes after initiating thrombolytic therapy, rescue PCI should be considered.

·         Other signs of successful reperfusion include T wave inversion occurring during the first hours of reperfusion therapy and the presence of accelerated idioventricular rhythm.

Primary Angioplasty

·         Primary PCI: Primary PCI requires immediate cardiac catheterization and is the preferred method for revascularizing patients with ST elevation MI (Fig. 23.8). The ACC/AHA guidelines recommend that primary PCI should be performed within 90 minutes after first medical contact with emergency personnel (door to balloon or medical contact to balloon) time. Unlike thrombolysis, it is more effective in reestablishing coronary blood flow regardless of the duration of symptoms. It is the preferred method in patients who are unstable, are hemodynamically decompensated, when symptoms exceed 3 hours in duration or the diagnosis of ST elevation MI is in doubt.

Figure 23.7: ST Elevation Myocardial Infarction. Electrocardiogram (ECG) A was recorded before thrombolytic therapy. ST segment elevation is present in II, III, aVF, and V4-6 (arrows)with ST depression in V1-2. (B) Taken 1 hour after thrombolytic therapy. ST elevation in the inferolateral leads have resolved and inverted T waves are now present in lead III, both are signs of successful reperfusion.

Figure 23.8: ST Elevation Myocardial Infarction. Electrocardiogram (ECG) A shows ST elevation in V2-6, I and aVL (arrows). Coronary angiography showed completely occluded proximal left anterior descending coronary artery. ECG B was recorded 4 hours after successful percutaneous coronary intervention. The ST segment elevation has normalized without developing pathologic Q waves, a sign of successful reperfusion.

 

Figure 23.9: ST Elevation. ST elevation MI may show different patterns in different leads and may appear convex or coved (A, B), horizontal or plateau (C, D), oblique (E), or concave (F) with a dart and dome configuration. Arrows point to the J points, which are all elevated.

ST Elevation MI

·         ST elevation MI generally indicates the presence of a large infarct. The extent of the infarct is proportional to the number of leads with ST segment elevation. ST elevation MI is associated with a lower ejection fraction, higher incidence of heart failure, and a higher immediate and in-hospital mortality when compared with non-ST elevation MI or unstable angina.

·         ST elevation MI may present with several ECG patterns (Fig. 23.9). Although the characteristic example of ST elevation MI is an ST segment that is coved or convex upward (Fig. 23.9A,B), the ST elevation may be horizontal or plateau (Fig. 23.9C,D), or it may be oblique, resembling a ski-slope (Fig. 23.9E) or concave (Fig. 23.9F).

·         Tombstone pattern: “Tombstoning” is a type of ST elevation MI where the ST segment is about the same level as the height of the R wave and top of the T wave (Figs. 23.4A and23.6C). The QRS complex, ST segment, and T wave therefore blends together to form a large monophasic complex similar to the shape of a transmembrane action potential (Fig. 23.9C,D). Although this pattern of ST elevation has been shown to indicate a grave prognosis when compared with other patterns of ST segment elevation, it is consistent with the observation that the extent of muscle damage is proportional to the magnitude of ST elevation. Tombstoning is more commonly associated with acute anterior MI. Involvement of the left anterior descending coronary artery is usually proximal and is more severe and extensive than when other patterns of ST elevation are present.

·         Reciprocal ST depression: One of the features of ST elevation MI that distinguishes it from other causes of ST elevation is the presence of reciprocal ST depression. Reciprocal ST depression is the flip side image recorded directly opposite the lead with ST elevation.

o    For example, if ST elevation occurs in lead III (+120°), a flip side image will be recorded directly opposite lead III at -60° (Fig. 23.10).

o    Because there is no standard limb lead representing -60°, aVL (-30°), which is closest to -60° and almost directly opposite lead III, will show reciprocal ST depression (Figs. 23.11 and 23.12).

o    Similarly, if ST elevation is present in aVL, reciprocal ST depression will occur in lead III because lead III is the closest lead directly opposite aVL.

·         ST segment elevation always points to the area of injury. It is the primary abnormality even if reciprocal ST depression is more pronounced than the ST elevation.

Localizing the Infarct

·         The coronary arteries: Although variation in coronary anatomy commonly occurs, three epicardial coronary arteries are generally present. Each artery supplies specific regional areas in the heart. These areas are topographically represented by the following groups of leads:

Figure 23.10: Reciprocal ST Depression. When ST elevation from myocardial ischemia is recorded in any lead, a flip side image is recorded directly opposite the lead. In the above example, ST elevation is recorded in lead III (+120°), reciprocal ST depression is also recorded at -60°. Because there is no frontal lead representing -60°, lead aVL, which is adjacent to -60°, will exhibit the most pronounced reciprocal change (see Figs. 23.11 and 23.12).

Figure 23.11: Reciprocal ST Depression. ST elevation in lead III is associated with reciprocal ST depression directly opposite lead III. Because lead aVL is the closest lead opposite lead III, aVL will show the most pronounced reciprocal ST depression among the standard electrocardiogram (ECG) leads. The standard limb lead ECG is shown in Figure 23.12.

o    Left anterior descending (LAD) coronary artery: The LAD supplies the anterior, anteroseptal or anterolateral wall of the left ventricle (LV) (leads V1-V6, I, and aVL).

o    Right coronary artery (RCA): The RCA supplies the inferior wall (leads II, III, and aVF), often posterolateral wall of the LV (special leads V7, V8, V9). The RCA is the only artery that supplies the right ventricular free wall (special leads V3R to V6R).

o    Left circumflex (LCx) coronary artery: The LCx supplies the anterolateral (leads I, aVL, V5, and V6) and posterolateral (special leads V7, V8, V9) walls of the LV. In 10% to 15% of patients, it supplies the inferior wall of the LV (leads II, III, and aVF).

·         The following groups of leads represent certain areas of the heart:

o    V1-2: ventricular septum.

o    V2-4: anterior wall of the LV. V2 overlaps the septum and anterior wall and is both a septal and anterior lead.

o    V1-V3: anteroseptal wall of the LV.

o    V4-V6, I, and aVL: anterolateral wall of the LV.

o    V4-V6: lateral wall of the LV. V4 overlaps the anterior and lateral walls of the LV and is both an anterior and lateral lead.

o    V7-V9: (special leads) posterolateral wall of the LV.

o    V3R to V6R: (special right-sided precordial leads) right ventricle.

o    I and aVL: basal anterolateral or high lateral wall of the LV.

o    II, III, and aVF: inferior or diaphragmatic wall of the LV.

·         Not all the areas of the heart are represented by the 12-lead ECG. The areas not represented include the right ventricle and posterolateral wall of the LV. Special leads V3R to V6Rand V7 to V9 are needed to record these areas, respectively. ST elevation involving the posterolateral wall of the LV is suspected when there is ST depression in leads V1 to V3.

·         ST segment elevation points to the area of injury and is helpful in identifying the infarct related artery. Acute MI presenting as ST depression is frequently associated with multivessel coronary disease and is less specific in localizing the culprit vessel.

Myocardial Distribution of the Three Main Coronary Arteries

·         The myocardial distribution of the three coronary arteries is shown in Figure 23.13.

Left Anterior Descending Coronary Artery

·         Anatomy: The left main coronary artery divides into two large branches: the LAD and the LCx coronary arteries. The LAD courses toward the apex through the anterior interventricular groove and supplies the anterior wall of the LV. The artery may continue to the inferoapical wall by wrapping around the apex of the LV (Fig. 23.14).

o    First branch: The first branch of the LAD is the first diagonal artery. This branch runs parallel to the LCx coronary artery and supplies the basal anterolateral wall of the LV. If the first diagonal is a large branch, complete occlusion of this artery causes ST elevation in leads I and aVL with reciprocal ST depression in III and aVF. These ECG changes may be indistinguishable from that due to occlusion of a small LCx coronary artery.

o    Second branch: The second branch of the LAD is the first septal branch. This artery may be the first instead of the second branch. The artery penetrates the ventricular septum perpendicularly and supplies the basal septum including the proximal conduction system. Involvement of the first septal perforator will cause ST elevation in V1. It may also involve the conduction system causing new onset right bundle branch block.

·         Anterior MI: Depending on the location of the coronary lesion and whether the LAD is large or small, complete occlusion of the LAD will cause extensive anterior MI with varying degrees of ST elevation in V1 to V6 as well as leads I and aVL.

o    Before the first branch: If the LAD is occluded proximally at the ostium or before the first branch (first diagonal), ST elevation will occur in V1 to V4 (or up to V6) and leads I and aVL from extensive anterior MI. The ST elevation in leads I and AVL represent involvement of the first diagonal branch and is usually accompanied by reciprocal ST depression in III and aVF (Figs. 23.15 and 23.16).

o    Between the first and second branches: If the lesion is distal to the first diagonal (but proximal to the first septal branch), ST elevation will include V1 to V4 but not leads I and aVL consistent with acute anteroseptal MI. ST elevation in V1 indicates involvement of the first septal branch (Fig. 23.17).

o    After the second branch: If the lesion is distal to the first diagonal and first septal branches, ST elevation will involve V2-V4 but not V1 or I and aVL consistent with anterior often called apical MI.

o    Occlusion of the first diagonal branch: If a large first diagonal branch is the only artery occluded, and the LAD is spared, ST elevation is confined to leads I and aVL consistent with high lateral MI, which involves the base of the LV (Fig. 23.18).

Figure 23.12: Reciprocal ST Depression. ST elevation is present in leads II, III, and aVF and is most marked in lead III (arrows). Reciprocal ST depression is most pronounced in aVL (double arrows) because aVL is almost directly opposite lead III (see Fig. 23.11).

Figure 23.13: Myocardial Distribution of the Coronary Arteries. The diagrams summarize the myocardial distribution of the three coronary arteries. The diagram in the upper left represents the frontal view of the heart. The left ventricle is transected by three lines labeled 1, 2, and 3. Line 1 is at the level of the mitral valve which corresponds to the base of the left ventricle. The short axis view is shown on the upper right diagram. Line 2 corresponds to the midventricle and the short axis is shown at the lower left. Line 3corresponds to the apex of the left ventricle and the short axis is shown at the lower right. Ao, Aorta; LA, left atrium; LV, left ventricle; LAD, left anterior descending; LCx, left circumflex; LV, left ventricle; MV, mitral valve; PA, pulmonary artery; PDA, posterior descending artery; PM, papillary muscle; RA, right atrium; RCA, right coronary artery; V1 to V6, the precordial electrodes superimposed on the heart.

 

Figure 23.14: Diagrammatic Representation of the LAD and its Branches. The left main coronary artery divides into two main branches: the LAD and LCx coronary arteries. The LAD courses through the anterior interventricular groove. It gives diagonal branches laterally and septal branches directly perpendicular to the interventricular septum. LA, left atrium; LAD, left anterior descending artery; LCx, left circumflex; LV, left ventricle; RA, right atrium; RV, right ventricle.

Figure 23.15: Extensive Anterior Myocardial Infarction (MI). ST elevation is present in leads V1-6, I, and aVL. Cardiac catheterization showed complete occlusion of the proximal left anterior descending (LAD) artery. Note that the ST elevation in I and aVL is due to involvement of the first diagonal branch, which is usually the first branch of the LAD. ST depression in II, III, and aVF is a reciprocal change due to ST elevation in I and aVL.

Figure 23.16: Extensive Anterior Myocardial Infarction. ST elevation is present in V1-6, I, and aVL. Coronary angiography showed complete occlusion of the proximal LAD. This electrocardiogram is similar to that in Figure 23.15.

 

Figure 23.17: Left Anterior Descending (LAD) Artery Occlusion Distal to the First Diagonal Branch. The electrocardiogram shows acute anteroseptal myocardial infarction with ST segment elevation confined to V1 to V4. This is due to occlusion of the LAD distal to the first diagonal branch (no ST elevation in I and aVL) but proximal to the first septal branch (ST elevation is present in V1).

LAD Coronary Artery

·         Two ECGs showing anterior MI from occlusion of the LAD. The first ECG in Figure 23.16 shows ST elevation in I and aVL from occlusion of the LAD before the first diagonal branch. The second ECG in Figure 23.17 shows anterior MI without ST elevation in I and aVL because of occlusion of the LAD after the first diagonal branch.

·         Figure 23.18 shows occlusion confined to the first diagonal branch of the LAD, resulting in high lateral wall MI. ST elevation is present in leads I and aVL only. The ST segment depression in leads III and aVF are reciprocal changes due to the elevated ST segments in I and aVL.

·         If the LAD is a long artery, it may wrap around the apex and continues to the inferoapical wall of the LV. Occlusion of a wrap around LAD may cause ST elevation and eventually Q waves not only in the anterior wall but also inferiorly in II, III, and aVF (Fig. 23.19).

Figure 23.18: Acute High Lateral Myocardial Infarction from Isolated Lesion Involving the First Diagonal Branch of the Left Anterior Descending (LAD) Artery. ST segment elevation is confined to leads I and aVL. Coronary angiography showed complete occlusion of the first diagonal branch of the LAD. The LAD itself is patent. Occlusion of the first diagonal branch of the LAD causes ST elevation in I and aVL with reciprocal ST depression in III and aVF.

LCx Artery

·         Anatomy: The LCx coronary artery circles the left atrioventricular (AV) groove laterally between the left atrium and LV and gives branches that supply the anterolateral and posterolateral walls of the LV (Fig. 23.20). The artery may be small and may terminate very early. In 10% to 15% of cases, the LCx continues posteriorly toward the crux of the heart and down the posterior interventricular groove as the posterior descending coronary artery. When this occurs, the LCx is the dominant artery and supplies not only the inferior wall of the LV but also gives rise to the artery to the AV node. Occlusion of the LCx artery will cause:

Figure 23.19: Anterior and Inferior Myocardial Infarction. QS complexes with ST elevation is noted in V1 to V5 (anterior wall) and also in leads II, III, and aVF (inferior wall) due to an occluded left anterior descending artery that wraps around the apex of the left ventricle extending to the inferoapical left ventricular wall. The right coronary artery is small but patent.

o    Anterolateral MI:When the LCx coronary artery is occluded proximally, ST elevation will occur in leads I, aVL, V5, and V6. The MI is confined to the area bounded by the two papillary muscles posterolaterally from the base to the proximal two thirds of the LV (Fig. 23.21). The ST elevation may occur only in leads I and aVL and may be difficult to differentiate from an occluded first diagonal branch of the LAD (Figs. 23.18 and 23.22).

o    Posterolateral MI: The posterolateral wall of the LV is not directly represented by any standard ECG lead. When posterolateral MI occurs, reciprocal ST depression is noted in V1-V3. V5, and V6 may show ST elevation (Fig. 23.23).

Figure 23.20: Left Circumflex (LCx) Coronary Artery. The diagram represents the LCx artery and its main branches. In 10% to 15% of patients, the LCx artery is the dominant artery by continuing as the posterior descending artery (dotted lines) and supplying the artery to the AV node. LV, left ventricle; MA, mitral annulus; RV, right ventricle; TA, tricuspid annulus.

·         The myocardial distribution of the LCx coronary artery is shown in Fig. 23.21. Acute MI from occlusion of the LCx coronary artery is shown in the ECG in Figure 23.22.

·         Posterolateral MI: Occlusion of the LCx artery can cause posterior, straight posterior, or posterolateral MI. Because there are no leads representing the posterolateral wall of the LV, a posterolateral MI is suspected in the 12-lead ECG when there is ST depression in V1 to V3. These leads are directly opposite the posterolateral wall and will show reciprocal ST depression when a posterior MI is present. Posterior MI can be confirmed by placing extra electrodes in V7, V8, and V9 (V7 is located at the left posterior axillary line, V8 at the tip of the left scapula, and V9 at the left of the spinal column in the same horizontal plane as V4-6). These special leads will show Q waves with ST elevation if a posterolateral MI is present. Prominent R waves may or may not be present in the anterior precordial leads (Fig. 23.23).

·         Although ST depression is not an indication for thrombolytic therapy, ST depression in V1 to V3 may be due to posterior MI, which represents a true ST elevation MI. Before thrombolytic therapy is given, leads V7-9 should be recorded to verify that the ST depression in V1-3 is due to posterior MI and not from subendocardial injury involving the anterior wall of the LV.

·         ST elevation confined to leads I and aVL usually indicate lateral MI due to involvement of the LCx coronary artery (Fig. 23.24). ST elevation in leads I, aVL, V5, and V6 is often accompanied by ST elevation in V7 to V9 and reciprocal ST depression in V1 to V3 from posterolateral MI. ST elevation in V6 is usually accompanied by ST elevation in V7 to V9because these leads are adjacent to V6 (Figs. 23.25 and 23.26).

·         Figure 23.26 shows the importance of recording special leads V7 to V9 when a posterolateral MI is suspected.

The standard 12-lead ECG shows ST depression in V1 to V3 and ST elevation in V5 and V6. Special leads V7 to V9 recorded posteriorly shows Q waves with ST segment elevation similar to V6. These changes are consistent with a transmural posterolateral MI. The coronary angiogram confirmed the presence of a completely occluded LCx artery.

Figure 23.21: Myocardial Distribution of the Left Circumflex (LCx) Coronary Artery. The LCx coronary artery supplies the territory represented by the purple checkered lines. These include the proximal two thirds (base and midportion) of the lateral wall of the left ventricle. In 10% to 15% of patients, the LCx is the dominant artery and continues inferiorly to the apex of the left ventricle as the posterior descending coronary artery (A) long axis view. (C) Short axis view of the apex. Ao, aorta; LA, left atrium; LAD; left anterior descending coronary artery; LCx, left circumflex; LV, left ventricle; PM, papillary muscle; RV, right ventricle.

Figure 23.22: High Lateral Myocardial Infarction (MI). Q waves with elevation of the ST segments are confined to leads I and aVL. The ST depression in III and aVF is reciprocal to the ST elevation in I and aVL. This represents high lateral MI resulting from occlusion of the left circumflex coronary artery. This electrocardiogram finding can also occur when there is occlusion of the first diagonal branch of the left anterior descending coronary artery (see Fig. 23.18).

Figure 23.23: Acute Posterolateral Myocardial Infarction (MI). There is marked depression of the ST segments in V1 to V3 with tall R waves in V1-2. The amplitude of the R waves in V5-6 is diminished and the ST segments are elevated. This represents an acute posterolateral MI from an occluded left circumflex coronary artery. The ST depression and tall R waves in V1-V3 are reciprocal changes due to the posterior MI. Anterior subendocardial injury and straight posterior MI can be differentiated by recording V7-9, which will show ST elevation if posterior MI is present. This distinction is important because ST elevation MI involving the posterior wall of the left ventricle may require thrombolysis, whereas anterior wall subendocardial injury does not.

 

Figure 23.24: Acute High Lateral Myocardial Infarction. ST segment elevation is noted in I and aVL with reciprocal ST depression in III and aVF from occlusion of the left circumflex coronary artery. The ST depression in II, III, and aVF is reciprocal to the ST elevation in I and aVL.

·         Inferior MI: Acute inferior MI is due to occlusion of the RCA in 85% to 90% of patients but it can occur in 10% to 15% of patients when the LCx is the dominant artery. In acute inferior MI, the ST segments are elevated in II, III, aVF. If the LCx is the culprit vessel, the ST elevation in lead II is greater than or equal to the ST elevation in lead III (Fig. 23.27).

·         If the LCx is small and nondominant, occlusion of the artery may not show any ECG changes (Fig. 23.28). Thus, a normal ECG does not exclude acute MI especially when the LCx is the culprit vessel because most of the area supplied by the LCx is not represented in the standard 12-lead ECG.

Figure 23.25: Acute Posterolateral Myocardial Infarction (MI). ST depression is present in V1-V4. These changes can represent subendocardial injury involving the anterior wall or ST elevation MI involving the posterior wall of the left ventricle. The presence of ST elevation in V6, I, and aVL favors acute posterolateral MI rather than anterior wall injury. This can be confirmed by recording V7-9, which will show ST elevation if posterior MI is present.

Right Coronary Artery

·         Anatomy: The RCA courses around the medial AV groove between the right atrium and right ventricle and supplies acute marginal branches to the right ventricle. In 85% to 90% of cases, it is the dominant artery in that it gives rise to the artery to the AV node before continuing posteriorly toward the apex of the LV as the posterior descending artery, which supplies the inferior wall of the LV. The artery often continues posterolaterally beyond the crux to the opposite (lateral or left) AV groove and sends posterolateral branches to the LV (Fig. 23.29).

·         Total occlusion of the RCA will cause the following ECG changes:

o    Inferior MI: ST elevation in leads II, III, and aVF with reciprocal ST depression in I and aVL (Fig. 23.30).

o    Inferolateral MI: ST elevation in leads II, III, aVF, V5, and V6. ST elevation in V5-V6 suggests that the lateral wall of the LV is also involved (Figs. 23.31 and 23.32).

Figure 23.26: Posterolateral Myocardial Infarction (MI) and Special Leads V7-9. Electrocardiogram (ECG) A is a 12-lead ECG of a 58-year-old male presenting with chest pain. There is ST elevation in leads I, V5, and V6, and ST depression in V1-3. (B) The same as ECG A and shows only the precordial leads together with V7 to V9. ST elevation is present in V6 as well as V7, V8, and V9 consistent with acute posterolateral MI. These examples show the importance of recording special leads V7 to V9 in confirming the diagnosis of posterolateral MI. ECG courtesy of Kittane Vishnupriya, MD.

o    Inferoposterior MI: ST elevation in leads II, III, and aVF with ST depression in V1 to V3. Reciprocal ST depression in V1-V3 indicates the presence of a posterolateral MI (Figs. 23.33 and 23.34). Tall R waves may develop in V1 or V2, although this usually occurs much later several hours after the acute episode. Special leads V7-9 will record ST elevation and tall hyperacute T waves during the acute episode.

Figure 23.27: Acute Inferior Myocardial Infarction (MI) from Occlusion of the Left Circumflex Coronary Artery. Note that the ST elevation in lead II is more prominent than lead III. Additionally, the ST segment is isoelectric in aVL and minimally elevated in lead I. ST depression is present in V1 to V3 with ST elevation in V6 from posterolateral MI.

·         ST depression in V1-V3 may be due to ST elevation MI involving the posterolateral wall (Figs. 23.33A and 23.34). It may also be due to subendocardial injury involving the anterior wall of the LV. To differentiate one from the other, leads V7 to V9 should be recorded. If posterolateral ST elevation MI is present, V7 to V9 will record ST segment elevation. If there is subendocardial injury involving the anterior wall, the ST segments will not be elevated in V7 to V9.

Figure 23.28: Acute Myocardial Infarction with Normal Electrocardiogram (ECG). The ECG is from a 56-year-old male who presented with acute persistent chest pains. Serial ECGs were all normal although the cardiac markers were elevated. The coronary angiogram showed completely occluded left circumplex corona artery (LCx). Among the three coronary arteries, LCx coronary disease is the most difficult to diagnose electrocardiographically.

Acute Inferior MI

·         Inferior MI: In 85% to 90% of patients with acute inferior MI, the culprit vessel is the RCA and in the remaining 10% to 15%, the LCx coronary artery. Inferior MI can also occur when a long LAD that goes around the apex of the LV is occluded resulting in anterior MI that extends to the inferoapical wall (Fig. 23.19).

·         RCA and inferior MI: The following ECG findings indicate that the RCA is the culprit vessel when inferior MI is present.

o    Right ventricular MI (RVMI): The presence of RVMI always indicates RCA involvement. RVMI is possible only when the proximal RCA is occluded. It is diagnosed by the presence of ST elevation ≥1 mm in any of the right sided precordial leads V3R to V6R, with lead V4R the most sensitive (Fig. 23.35). If right-sided precordial leads were not recorded, V1 should be examined for ST segment elevation. Occlusion of the LCx will not result in RVMI because the LCx circles the lateral AV groove and does not supply branches to the right ventricle (diagram in Fig. 23.20).

Figure 23.29: Diagrammatic Representation of a Dominant Right Coronary Artery (RCA). The RCA continues posteriorly as the posterior descending artery and often goes beyond the crux to supply posterolateral branches to the left ventricle (dotted lines). LV, left ventricle; MA, mitral annulus; RV, right ventricle; TA, tricuspid annulus.

o    ST elevation in lead III > II: When the RCA is totally occluded, the highest ST elevation will be recorded in lead III (Fig. 23.36). This is based on the anatomical location of the RCA, which circles the right AV groove, and is closer to lead III than lead II in the frontal plane. This is in contrast to the LCx coronary artery, which is closer to lead II than lead III because it circles the left or lateral AV groove.

o    Reciprocal ST depression in aVL > lead I: Because lead III has the highest ST elevation when the RCA is occluded, the most pronounced ST depression will be recorded opposite lead III at -60°. Because aVL (at -30°) is adjacent to -60°, aVL will record the deepest reciprocal ST depression if the RCA is the culprit vessel.

·         LCx and inferior MI: If a dominant LCx is the cause of the inferior MI, ST elevation in lead III is not taller than lead II and the ST segments are isoelectric (or may be elevated) in aVL and lead I as shown in Figure 23.27. ST elevation in leads II, III, and aVF with ST depression in V2 and V3 also favors a LCx lesion since the LCx supplies posterolateral branches to the LV, which is diametrically opposite V2 and V3. However, if the LCx is small and the RCA is the dominant artery, the RCA may continue beyond the crux to the left AV groove to supply posterolateral branches to the LV.

Figure 23.30: Acute Inferior Myocardial Infarction (MI). ST segment elevation is present in II, III, and aVF with reciprocal ST depression in I and aVL consistent with acute inferior MI. This is due to occlusion of the right coronary artery.

Figure 23.31: Acute Inferolateral Myocardial Infarction. The ST segments are elevated in leads II, III, and aVF with reciprocal ST depression in aVL. ST segments are elevated in V5 and V6 with ST segment depression in V1 and V2. Coronary angiography showed complete occlusion of the proximal right coronary artery.

Figure 23.32: Acute Inferolateral Myocardial Infarction. ST elevation is noted in II, III, aVF, and V4 to V6 with reciprocal ST depression in I and aVL. The findings are similar to those in Figure 23.31.

Figure 23.33: Posterolateral Myocardial Infarction (MI). Posterolateral MI is a true ST segment elevation MI. This is suspected when there is ST segment depression in V1-3 (A). The ST depression in V1-3 is a reciprocal pattern due to ST elevation in the posterolateral wall similar to the reciprocal pattern seen in aVL when there is ST elevation in lead III (B). Posterolateral MI can be verified by recording special leads V7-9, which will confirm the presence of ST elevation in this area.

 

Figure 23.34: Acute Inferoposterior Myocardial Infarction (MI). ST segments are elevated in II, III, and aVF with reciprocal ST depression in leads I and aVL consistent with an acute inferior MI. There is also ST depression in V1 to V4 and ST elevation in V6 from posterolateral MI. The P waves (arrows) are completely dissociated from the QRS complexes because of AV block.

Figure 23.35: Right-Sided Precordial Leads. The right-sided precordial leads are labeled V3R to V6R (open circles). The leads are obtained by repositioning the standard precordial electrodes V3-6 (dark circles) to the right side of the chest. Leads V1 and V2 remain in their original location.

Figure 23.36: Acute Inferior Myocardial Infarction (MI). The 12-lead electrocardiogram shows ST segment elevation in II, III, and aVF with reciprocal ST depression in I and aVL from acute inferior MI. There is also reciprocal ST depression in V2 and V3 from involvement of the posterior wall of the left ventricle. Note that the ST elevation in lead III is higher than the ST elevation in lead II and ST depression in aVL is deeper than the ST depression in I, suggesting that the culprit vessel is the right coronary artery. The right-sided precordial leads are shown.

 

Figure 23.37: Acute Inferior MI with Right Ventricular Myocardial Infarction (RVMI). The diagnosis of RVMI is based on the presence of ≥1 mm ST elevation in any of the right sided precordial leads V3R to V6R (arrows). The electrocardiogram shows at least 1 mm of ST elevation in V4R, V5R, and V6R consistent with RVMI. It is not necessary to switch V1 and V2, as was done above when recording right-sided precordial leads. The presence of RVMI suggests that the culprit vessel is the proximal right coronary artery.

Right Ventricular Myocardial Infarction

·         RVMI: RVMI is a common complication of acute inferior MI. If the initial ECG confirms the diagnosis of acute inferior MI, right-sided precordial leads should be recorded immediately (Fig. 23.37). This is a Class I indication according to the 2004 ACC/AHA guidelines on ST elevation MI. If right-sided precordial leads are not immediately recorded, ST elevation in the right precordial leads may disappear within 10 hours after symptom onset in approximately half of patients with RVMI.

·         Right sided precordial leads are recorded by repositioning the precordial leads V3, V4, V5, and V6 to the right side of the chest in the same standard location as that on the left (Fig. 23.35). Right-sided precordial leads are not routinely recorded if there is no evidence of acute inferior MI.

Figure 23.38: Right Ventricular Myocardial Infarction (RVMI). The diagnosis of RVMI should always be suspected in the standard 12-lead electrocardiogram when acute inferior MI is present. ST elevation in lead III greater than lead II and presence of ST elevation in V1 indicate RVMI as shown above. If the ST elevation in V1 extends to V2 or V3, it may resemble acute anterior MI.

·         Any ST elevation ≥1 mm in any of the right sided precordial leads V3R to V6R is consistent with RVMI. These leads, especially V4R, are the most sensitive and most specific for the diagnosis of RVMI.

·         RVMI is possible only when the proximal RCA is occluded. It does not occur when the distal RCA or LCx coronary artery is involved. This is important prognostically because occlusion of the proximal RCA usually implies the presence of a larger infarct and is associated with a high incidence of AV nodal block when compared to occlusion of a nondominant LCx or distal RCA.

·         RVMI: Very often, right-sided precordial leads are not recorded at the time of entry. These leads are special leads and are not routine in a regular 12-lead ECG.

Even if they were recorded, they may be recorded much later and not within the limited time window in which RVMI can be diagnosed. RVMI can be suspected if the initial standard 12-lead ECG will show the following changes:

Figure 23.39: (A) Myocardial Distribution of the Right Coronary Artery (RCA). The red stippled areas represent myocardial distribution of the RCA. These include the right ventricular free wall, lower one-third of the posterolateral wall (A, B), inferior half of the ventricular septum (B) and the posterior portion of the LV apex (C). Note that the posteromedial PM (B) is supplied only by the RCA, whereas the anterolateral PM is supplied by two arteries, the LAD and LCx. Ao, aorta; LA, left atrium; LAD, left anterior descending; LCx, left circumflex; LV, left ventricle; PM, papillary muscle; RV, right ventricle. (D) Electrocardiogram (ECG) of RCA Involvement. Twelve-lead ECG showing a proximally occluded RCA. There is inferior myocardial infarction (MI) with ST elevation in lead III taller than lead II and ST depression in aVL more pronounced than lead I. Even when right sided precordial leads are not recorded, the presence of right ventricular MI can be diagnosed by the ST elevation in V1.

o    ST elevation in lead III is greater than lead II: This suggests that the RCA (and not the LCx), is the cause of the inferior MI (Figs. 23.30, 23.38, and 23.39B).

o    ST elevation is present in V1 (Figs. 23.30 and 23.38): Although V1 is not a very sensitive lead for the diagnosis of RVMI when compared with V4R, V1 is also a right-sided precordial lead. Thus, ST elevation in V1 during acute inferior MI may be the only indication that an RVMI is present if right-sided precordial leads were not recorded in the ECG. The ST elevation may extend to V3 resembling anterior MI (Fig. 23.38).

·         Conversely, RVMI is not possible if the LCx coronary artery is the culprit vessel. If the LCx artery is the culprit vessel, ST elevation in III is not greater than lead II. ST depression is not present in aVL and ST elevation may be present in lead I (Fig. 23.27).

·         The myocardial distribution of the RCA is summarized in Figures 23.39A-C. The RCA is the dominant artery when it is the origin of the posterior descending coronary artery. This occurs in 85% to 90% of all patients. It supplies the whole inferior wall from base to apex and is the only artery that supplies the right ventricular free wall (Fig. 23.39A).

·         Figures 23.39D shows the ECG of a patient with occluded proximal RCA. The presence of RVMI can be recognized even when the right-sided precordial leads are not recorded.

Complications of Acute MI

·         The ECG can provide very useful information not only in correctly identifying the culprit coronary artery but also in predicting possible complications based on the geographic location of the acute MI. Table 23.1 identifies the location of the MI based on the leads with ST elevation, identifies the infarct related artery, and the possible complications associated with the MI.

 

 TABLE 23.1 ST Elevation, MI Location, and Possible Complications

 

 Leads with ST Elevation

Location of the MI

Infarct-Related Artery

Possible Complications

 II, III, aVF

Inferior wall of the left ventricle

RCA in 85% to 90%

LCx in 10% to 15%

RCA = VT/VF, RVMI, bradyarrhythmias including sinus bradycardia, hypotension and AV block, LV dysfunction, postero-medial papillary muscle dysfunction, or rupture

Dominant LCx: VT/VF, LV dysfunction, AV block but no RVMI or papillary muscle dysfunction

 I and aVL

High lateral

LCx or first diagonal branch of LAD

VT/VF, LV dysfunction

 V1-V4

Anteroseptal

LAD

VT-VF, extensive LV dysfunction, RBBB ± fascicular block, cardiogenic shock

 V5-V6 + I, aVL

Lateral

LCx

VT/VF, LV dysfunction

 ST depression in V1-V3 ±  tall R waves

Posterior or straight posterior

LCx , RCA also possible

VT/VF, LV dysfunction

 II, III, aVF + V3R, V4R, or  V5R

RVMI

Proximal RCA

VT/VF, AV block, bradycardia, hypotension, atrial infarction

 AV, atrioventricular; LAD, left anterior descending; LCx, left circumflex; LV, left ventricular; PM, papillary muscle; RBBB, right bundle  branch block; RCA, right coronary artery; RVMI, right ventricular MI; VT/VF, ventricular tachycardia/ventricular fibrillation.

           

 

·  Ventricular tachycardia (VT) or ventricular fibrillation (VF): Most deaths from acute MI occur suddenly usually during the first hour after onset of symptoms due to VF (Fig. 23.40). More than half of these deaths occur even before the patient is able to reach a medical facility.

Figure 23.40: Ventricular Fibrillation. This rhythm strip was obtained from a 54-year-old male with ST elevation myocardial infarction. His initial electrocardiogram is shown in Figure 23.18. He developed ventricular fibrillation while he was being monitored in the emergency department. His timely arrival to the hospital allowed him to be resuscitated successfully. The coronary angiogram showed total occlusion of the first diagonal branch of the left anterior descending artery, which was successfully stented. He left the hospital without neurologic sequelae and only minimal myocardial damage.

o    Sustained VT or VF within the first 48 hours: In-hospital mortality is increased among patients with acute MI who develop VT/VF. Survivors of VT/VF occurring within 48 hours after onset of acute MI have the same long-term prognosis compared with a similar group of patients without VT/VF. In these patients, VT/VF is due to electrical instability associated with acute myocardial injury, which may resolve after the acute injury has subsided.

Figure 23.41: Accelerated Idioventricular Rhythm. The 12-lead electrocardiogram (ECG) in A shows normal sinus rhythm and acute inferior MI. (B) The same patient a few minutes after ECG A was recorded, showing accelerated idioventricular rhythm.

o    Sustained VT or VF after 48 hours: Survivors of cardiac arrest due to VT/VF occurring after 48 hours of acute MI continue to be at risk for VT/VF. Unless the arrhythmia has been shown to be due to electrolyte abnormalities or due to recurrent acute ischemia, which are reversible, these patients are at high risk for developing recurrence of VT/VF and will benefit from implantation of an automatic defibrillator even without electrophysiologic testing.

·         One of the most important factors that determine the prognosis of patients with acute MI is the extent of myocardial damage. The presence of severe myocardial damage and a low left ventricular ejection fraction predisposes to ventricular arrhythmias, which may cause sudden death.

·         Other ventricular arrhythmias: Some arrhythmias may be related to reperfusion after successful thrombolysis and should be recognized. The most frequent ECG finding associated with successful reperfusion is accelerated idioventricular rhythm (AIVR).

·         AIVR: AIVR is a ventricular rhythm with a rate of 60 to 110 beats per minute (bpm). AIVR commonly occurs as a reperfusion arrhythmia and is more commonly seen after thrombolysis rather than with primary PCI. It occurs with about equal frequency in patients with acute inferior (Fig. 23.41) and anterior MI (Fig. 23.42). The arrhythmia is generally benign and does not require any therapy.

·         AIVR may be difficult to recognize and may be mistaken for ventricular tachycardia or new onset bundle branch block (Fig. 23.42). In AIVR, the QRS complexes are not preceded by P waves or there is complete AV dissociation. This may result in decreased cardiac output because atrial contraction no longer contributes to left ventricular filling.

·         Acute inferior MI and AV block: When acute inferior MI causes AV block, the AV block is at the level of the AV node (Figs. 23.43 and 23.44).

Acute MI and Right Bundle Branch Block (RBBB)

·         Among 26,003 patients with acute MI studied in GUSTO-1 (Global Utilization of Streptokinase and tPA for Occluded Coronary Arteries), 289 patients (1.1%) had RBBB. Most of these patients with RBBB had anterior MI. In 133 patients, only RBBB was present. In 145 patients, left anterior fascicular block was also present. Only 11 patients had RBBB with left posterior fascicular block.

Figure 23.42: Accelerated Idioventricular Rhythm. Electrocardiogram (ECG) A shows normal sinus rhythm with acute anteroseptal MI. ECG B shows a sudden change in the configuration of the QRS complexes with tall R waves in V1 and a rightward shift in the axis of the QRS complex in the frontal plane due to accelerated idioventricular rhythm. This ECG can be mistaken for new-onset right bundle branch block with left posterior fascicular block.

Figure 23.43: Acute Inferior Myocardial Infarction (MI) and Complete Atrioventricular (AV) Block. The P waves (arrows) and QRS complexes are completely dissociated consistent with complete AV block. When complete AV block occurs in the setting of an acute inferior MI, the AV block is at the level of the AV node. The AV block is usually reversible and permanent pacing is usually not indicated.

 

Figure 23.44: Acute Inferolateral Myocardial Infarction with 2:1 Atrioventricular (AV) Block. The electrocardiogram shows 2:1 AV block. The arrows identify the second P wave that is not conducted.

·         Changes in the ST segment and T wave when there is (RBBB): The diagnosis of acute MI is not difficult when there is RBBB. Changes in the Q waves, ST segment, and T waves continue to be useful.

o    RBBB without MI: In RBBB without MI, the ST segments and T waves are normally discordant (opposite in direction) in relation to the terminal portion of the QRS complex. Thus, in V1, the T waves are normally inverted and the ST segments are depressed because terminal R′ waves are present when there is RBBB. In V6, the T waves are upright and the ST segments are elevated since terminal S waves are present (Figs. 23.45A and 23.46).

o    RBBB with acute MI: When ST elevation MI is complicated by RBBB, the ST segments become concordant (same direction) in relation to the terminal portion of the QRS complex. Thus, in anterior MI, the ST segments are elevated in V1 and often in V2 because terminal R′ waves are normally present in these leads. Similar concordant changes may be noted in leads II, III, and aVF when there is inferior MI (Figs. 23.47 and 23.48B).

Figure 23.45: ST-T Changes in Right Bundle Branch Block (RBBB). (A) In uncomplicated RBBB, the ST segment and T wave are normally discordant (opposite in direction) to the terminal portion of the QRS complex. (B)When ST elevation myocardial infarction occurs, the ST segment (and T wave) becomes concordant (same direction) in relation to the terminal portion of the QRS complex.

·         Two examples of RBBB are shown in Figure 23.46, in which the RBBB is uncomplicated without evidence of MI. Note the presence of normally discordant ST segments and T waves. The second patient has inferior MI complicated by RBBB (Fig. 23.47). Note the presence of concordant ST elevation in leads III, aVF, and V1, and concordant ST depression in leads I, aVL, and V2.

·         Q wave changes: RBBB does not interfere with the diagnosis of acute ST elevation MI. Changes in the Q waves or QRS complexes remain useful and can be used for diagnosis. This is unlike LBBB, where the QRS complexes are significantly altered by the conduction abnormality making diagnosis of ST elevation MI by ECG extremely difficult.

Figure 23.46: Right Bundle Branch Block (RBBB) without Myocardial Infarction. In uncomplicated RBBB without ST elevation MI, the ST segments and T waves are normally discordant. Thus, the ST segments and T waves are inverted in V1 because the QRS complex ends with a terminal R′ wave. In leads I and II, the ST segments are normally elevated and T waves are upright because the QRS complex ends with an S wave. These ST-T abnormalities are secondary to the presence of RBBB.

Anterior MI and AV Block

·         Acute anterior MI can result in varying degrees of AV block. The AV block is usually preceded by intraventricular conduction defect, more commonly RBBB with or without fascicular block. The AV block is usually infranodal, at the level of the bundle of His or at the level of the bundle branches or fascicles. These patients usually have extensive myocardial damage and significantly higher mortality than those without AV block. Implantation of permanent pacemakers in these patients may prevent bradycardia, but may not alter the overall prognosis since there is extensive myocardial damage, which can result in malignant ventricular arrhythmias (Figs. 23.49 and 23.50).

Figure 23.47: Right Bundle Branch Block (RBBB) with ST Elevation Myocardial Infarction (MI). When RBBB with ST elevation MI is present, the ST segments and T waves become concordant. Thus, the ST segments (and T waves) are elevated in leads III, aVF, and in V1 because the QRS complex ends with an R wave and the ST segments are depressed in leads I, aVL, and V2 because the QRS complex ends with an S wave.

·         Figures 23.49A,B and 23.50A,B are from the same patient. There is acute anterior MI complicated by RBBB. The patient went on to develop complete AV dissociation (Fig. 23.50A) and subsequently sustained VT (Fig. 23.50B). Patients with acute anterior MI complicated by intraventricular conduction defect usually have extensive myocardial damage and are prone to develop VT/VF. The patient received a permanent pacemaker and an automatic defibrillator.

Figure 23.48: (A) Acute Anteroseptal Myocardial Infarction (MI). ST elevation is present in V1-5 consistent with occlusion of the left anterior descending artery proximal to the first septal perforator. The anterior MI was subsequently complicated by RBBB as shown by the electrocardiogram (ECG) in B. (B) Acute MI with RBBB and Left Anterior Fascicular Block. This ECG was obtained 14 hours later from the same patient in (A). The QRS complexes are wider and a qR pattern has developed in V1 to V4. There is also left axis deviation. These changes are consistent with acute anterior MI, RBBB, and left anterior fascicular block. Note that the diagnosis of acute ST elevation MI is possible even in the presence of RBBB.

Figure 23.49: Right Bundle Branch Block (RBBB) and Acute Myocardial Infarction (MI). Electrocardiogram (ECG) A and B are from the same patient. (A) Baseline ECG showing left anterior fascicular block. (B) ECG taken a few weeks later showing acute anteroseptal MI complicated by RBBB. The diagnosis of acute MI is based on the presence of pathologic Q waves in V1 to V5 and concordant ST elevation in V1 to V3. There is also first-degree atrioventricular block and left anterior fascicular block, which in the presence of RBBB may suggest trifascicular block.

 

Figure 23.50: Acute Myocardial Infarction and Atrioventricular (AV) Block. Electrocardiograms A and B are from the same patient asFigure 23.49. (A) Complete AV dissociation (the P waves are marked by the arrows). (B) Ventricular tachycardia occurring 5 days later. The patient was successfully resuscitated and was discharged with a permanent pacemaker and automatic implantable defibrillator.

Acute MI and LBBB

·         LBBB: When LBBB complicates acute MI, the ECG changes of ST elevation MI may not be recognized because it is concealed by the conduction abnormality. This makes diagnosis of acute MI extremely difficult using the ECG. Among 26,003 patients studied in GUSTO-1, 131 patients (0.5%) developed LBBB. Acute MI in patients with LBBB can be recognized by the following ECG findings (Figs. 23.51,23.52,23.53,23.54,23.55):

Figure 23.51: Acute Myocardial Infarction (MI) and Left Bundle Branch Block (LBBB). When there is complete LBBB, the presence of concordant ST segment deviation ≥1 mm(A, B) and discordant ST elevation ≥5 mm (A) are consistent with acute MI when accompanied by symptoms of acute ischemia.

o    Concordant ST segment: In uncomplicated LBBB (LBBB without MI), the ST segments are normally discordant (Fig. 23.51A,B). Thus, the ST segments are depressed in leads with tall R waves and are elevated in leads with deep S waves. When LBBB is complicated by acute MI, the ST segments become concordant (same direction as the QRS complexes) and measure ≥1 mm. Thus, ST segment depression ≥1 mm in leads with deep S waves (V1, V2, or V3; Fig. 23.51A) or ST elevation ≥1 mm in leads with tall R waves (V5, V6, and often in II, III, and aVF; Fig. 23.51B) are consistent with acute ST elevation MI.

Figure 23.52: Acute Anteroseptal Myocardial Infarction (MI). The initial electrocardiogram (ECG) (A) shows acute anteroseptal MI. ECG (B) taken a few hours later show left bundle branch block with concordant ST elevation ≥1 mm in lead aVL (arrow).

o    Discordant ST segment: Acute MI can also be diagnosed if the ST segments are abnormally discordant (opposite direction to the QRS complexes) and measure ≥5 mm. Thus, ST elevation ≥5 mm in any lead with deep S waves such as V1 to V3 is consistent with acute MI when accompanied by symptoms of acute ischemia (Fig. 23.51A).

·         The two ECGs (Figs. 23.54 and 23.55) show discordant ST segments. In Figure 23.54, discordant ST segment elevation of more than 5 mm is present in V2 and V3. These ECG changes are associated with symptoms of acute ischemia. In Figure 23.55, there is concordant ST segment depression in V4, which is accepted as a criterion for acute MI. In addition, there is also discordant ST segment depression of 5 mm in V5. Presently, discordant ST depression ≥5 mm is not included in the literature as a criterion for acute MI in the presence of LBBB.

Figure 23.53: Acute Myocardial Infarction (MI) and Left Bundle Branch Block (LBBB). LBBB is present with wide QRS complexes measuring >0.12 seconds. Concordant ST segment elevation >1 mm is present in leads with tall R waves including V5, V6, and leads II, III, and aVF (arrows) consistent with acute ST elevation MI.

Common Mistakes in ST Elevation MI

·         Other causes of ST elevation: There are several other causes of ST elevation other than acute MI. These entities should be recognized especially when thrombolytic agents are being considered as therapy for the acute MI.

Figure 23.54: Acute Myocardial Infarction (MI) and Left Bundle Branch Block (LBBB). LBBB is present with discordant ST segment elevation >5 mm in V2 and in V3 (arrows), which in the presence of symptoms chest pain indicate acute MI.

o    Normal elevation of the ST segment at the transition zone

o    Early repolarization

o    LBBB

o    Left ventricular hypertrophy (LVH)

o    Acute pericarditis

o    Left ventricular aneurysm

o    Electrolyte abnormalities: hyperkalemia and hypercalcemia

o    Wolff-Parkinson-White (WPW) syndrome

o    Osborn wave of hypothermia

o    Brugada ECG

o    Others: Pacemaker rhythm, ectopic ventricular complexes, Takotsubo cardiomyopathy, tumors or trauma involving the ventricles.

·         ST elevation at the transition zone: Elevation of the ST segment is common in normal individuals at the precordial transition zones V2, V3, or V4. The transition zone is at the mid-precordial leads, where the R wave becomes equal to the S wave as the precordial electrodes move up from V1 to V6. The ST segments in these transition leads have upsloping configuration and are usually not isoelectric. The elevation of the ST segment is a normal and expected finding and should not be considered a variant of normal (Fig. 23.56).

Figure 23.55: Discordant Pattern. This patient ruled in for acute myocardial infarction (MI) with markedly elevated troponins. The electrocardiogram shows left bundle branch block (LBBB) with concordant ST segment depression >1 mm in V4. There is also discordant ST segment depression ≥5 mm in V5 (arrows). Discordant ST depression is presently not included as a criterion for acute MI when there is LBBB.

·         Early Repolarization: J point elevation with ST elevation from early repolarization is common in normal individuals. The ST elevation is usually seen in the precordial leads and can be mistaken for transmural myocardial injury. The following are the characteristic features of early repolarization:

o    ST elevation is commonly seen in leads V2 to V6 and also in leads II, III, and aVF. The ST elevation is concave upward (Fig. 23.57).

o    Early repolarization is not accompanied by reciprocal depression of the ST segment.

o    A prominent notch is usually inscribed at the terminal portion of the QRS complex in leads with ST elevation (Fig. 23.57).

o    The ST elevation usually becomes isoelectric or less pronounced during tachycardia and becomes more accentuated during bradycardia (Figs. 23.58 and 23.59).

o    The T waves in V6 are usually tall when compared with the height of the ST segment. Thus, the ratio between the height of ST segment and that of the T wave is usually ≤25 % in V6. This ratio is helpful when pericarditis is being considered. Elevation of the ST segments in pericarditis is usually prominent. Thus, when the ratio between the height of the ST segment compared with that of the height of the T wave is >25% in V6, pericarditis is the more likely diagnosis.

Figure 23.56: Normal ST Elevation at the Transition Zone. Elevation of the ST segment is common in normal individuals at the transition zone which is usually in V2, V3, or V4 (arrows). This is a normal finding often described as “high take-off” of the ST segment. Very often, the T waves are also peaked and taller than the R wave at the transition zone. This is also a normal finding.

Figure 23.57: Early Repolarization. ST segment elevation is noted in V3 to V6 (arrows), which can be mistaken for acute myocardial injury. There is no reciprocal ST depression in any lead and a prominent notch is present at the end of the R wave in V4. Note that the height of the ST segment in V6 measures 1.0 mm and the height of the T wave measures 6 mm (ST elevation/T wave ratio <25%). A ratio ≤25% suggests early repolarization. If pericarditis is being considered, the ratio is >25% because the height of the T waves is generally lower in pericarditis.

Figure 23.58: Early Repolarization during Holter Monitoring. Three rhythm strips with different heart rates are shown above in the same patient undergoing Holter monitoring. Note that there is more pronounced ST segment elevation because of early repolarization when the heart rate is slower than when the heart rate is faster. Arrows point to the ST segment elevation. HR, heart rate.

 

Figure 23.59: Early Repolarization Before and During Maximal Exercise. (A) A 12-lead baseline electrocardiogram from a 56-year-old male. The baseline heart rate was 84 beats per minute. ST segments were elevated in II, III, aVF, and V2 to V6. (B) The same patient during maximal exercise. Heart rate was 146 beats per minute. The ST segments have become isoelectric.

o    In early repolarization, the ST segment elevation is more prominent when the heart rate is slower as shown in Figures 23.58 and 23.59.

o    Hyperkalemia: Hyperkalemia can cause elevation of the ST segment in the ECG (see Chapter 25, Electrolyte Abnormalities). The ST segment elevation can be mistaken for acute ST elevation MI (Fig. 23.60). When ST segment elevation of this magnitude occur during hyperkalemia, the serum potassium level is usually >8 mEq/L.

o    LBBB: In LBBB, the ST segments and T waves are normally discordant with the QRS complex. Thus, ST segment elevation and upright T waves are recorded in leads with deep S waves such as V1 to V3 and ST depression with inverted T waves recorded in leads with tall R waves such as V5 or V6 (Fig. 23.61).

Figure 23.60: ST Elevation from Hyperkalemia. The electrocardiogram can be mistaken for acute myocardial infarction (MI) resulting from the marked ST-T changes resembling acute ST elevation MI. Note the presence of peaked T waves in virtually all leads.

o    LVH:When LVH is present, the ST segment and T wave become discordant. ST depression and T wave inversion are recorded in leads with tall R waves; ST elevation and upright T waves are recorded in leads with deep S waves. Thus, ST elevation is usually present in V1 to V3 because deep S waves are normally expected in these leads when there is LVH (Fig. 23.62).

o    Brugada ECG: The Brugada ECG is an electrocardiographic abnormality confined to leads V1 and V3. There is RBBB configuration with rSR′ pattern in V1 or V2. The J point and ST segment are elevated measuring ≥1 mm, with a coved or upward convexity terminating into an inverted T wave (Fig. 23.63).

Figure 23.61: ST Elevation from Left Bundle Branch Block (LBBB). In LBBB, ST elevation (arrows) is usually seen in leads with deep S waves such as V1 to V3.

o    Brugada ECG: The Brugada ECG associated with symptoms of VT/VF is called the Brugada syndrome. The Brugada syndrome is not associated with structural heart disease or prolonged QTc, but is a genetic disease that can cause sudden cardiac death. The abnormality is the result of a defect in the sodium channel of myocytes in the epicardium of the right ventricle and is inherited as an autosomal dominant pattern. The ST elevation in V1 and in V2 may be saddle shaped or triangular instead of coved in configuration and the ECG abnormality may wax and wane (Fig. 23.64A,B). The significance as well as prognosis of asymptomatic patients with the Brugada ECG is unknown since not all patients with the Brugada ECG will develop ventricular arrhythmias or syncope (see Chapter 21, Ventricular Arrhythmias).

o    Hypothermia: Hypothermia is characterized by J point elevation. The J point marks the end of the QRS complex and beginning of the ST segment. A markedly elevated J point is also known as J wave or Osborn wave. The J wave is shaped like a letter “h.” The magnitude of the J point elevation follows the severity of the hypothermia (Fig. 23.65A) and disappears when the temperature is restored to normal (Fig. 23.65B).

o    Acute pericarditis: Acute pericarditis or inflammation of the pericardium is associated with diffuse ST segment elevation (Fig. 23.66A). The ST elevation usually involves almost all leads. Reciprocal ST depression is confined to leads V1 and aVR. Depression of the P-R segment is often present. Unlike ST elevation MI, the ST elevation in acute pericarditis does not evolve into q waves. The ST elevation usually persists for a week followed by T wave inversion. It may take another week or more before the inverted T waves revert to normal.

Figure 23.62: ST Elevation from Left Ventricular Hypertrophy (LVH). Elevation of the ST segment in LVH is frequently seen in V2 and V3, as shown by the arrows.

o    Left ventricular aneurysm: ST segment elevation that does not resolve after acute transmural MI usually suggests the presence of a left ventricular aneurysm. The ST segment elevation is present in leads with Q waves. The T waves are usually inverted. Almost all aneurysms are located at the anteroapical wall of the LV and, much less commonly, the base of the inferior wall. The elevation of the ST segment is usually permanent (Fig. 23.67). In this era of reperfusion therapy, the presence of a left ventricular aneurysm should be suspected in patients with ST elevation MI when pathologic Q waves occur and the ST elevation does not resolved within a few days.

o    Pacemaker-induced ventricular complexes: ST elevation is also seen in pacemaker captured ventricular complexes (Fig. 23.68) and ectopic ventricular rhythms. The ST elevation is secondary to the abnormal activation of the ventricles.

o    Takotsubo cardiomyopathy: Takotsubo cardiomyopathy (CMP), also called left ventricular apical ballooning syndrome, is increasingly becoming more recognized as a clinical entity characterized by substernal chest pain accompanied by ECG changes identical to the ECG of acute coronary syndrome. These includes ST elevation, ST depression, T wave inversion and development of pathologic Q waves. The most common presentation is ST elevation involving the anterior precordial leads. These ECG changes are accompanied by mild troponin elevation. Unlike acute coronary syndrome, which results from thrombotic occlusion of the coronary artery, Takotsubo CMP is associated with normal coronary arteries. There is ballooning of the anteroapical left ventricular wall and compensatory hyperkinesis of the basal segments. This angiographic appearance resemble an octopus trap (takotsubo) and is usually reversible. Although originally described in Japan it is increasingly recognized in Europe and the United States, mostly in post-menopausal women who have experienced physical or emotional distress. The cause of the CMP is uncertain although it is probably related to excessive sympathetic stimulation, microcirculatory dysfunction, or myocardial stunning resulting from severe multivessel coronary spasm.

Figure 23.63: Brugada Electrocardiogram (ECG) with Convex ST Segment. The Brugada ECG has a right bundle branch block pattern in V1 to V3 with J point elevation, coved ST segment, and inverted T waves (arrows). Courtesy of Athol Morgan, MD.

Figure 23.64: Brugada Electrocardiogram (ECG) with Concave ST Segment. The ST elevation in V1 and V2 (A) is concave (saddle back), which is another type of ST elevation in the Brugada ECG.

 

Figure 23.65: Hypothermia. The initial electrocardiogram (ECG) shows Osborn waves (arrows) representing elevation of the J point due to hypothermia. There is also sinus bradycardia with a rate of 50 beats per minute. ECG B was taken 4 hours after the initial ECG. The Osborn waves have disappeared.

Figure 23.66: Acute Pericarditis. The initial electrocardiogram (ECG) (A) on admission shows diffuse ST elevation in almost all leads consistent with acute pericarditis. The ST-T ratio in V6 is >25% (arrow). ECG (B) was obtained 4 to 5 weeks later showing ST depression, T inversion but no pathologic Q waves.

 

Figure 23.67: Left Ventricular Aneurysm. ST segment elevation persists more than 5 years after acute ST elevation myocardial infarction from left ventricular aneurysm. Note that the ST segment elevation is confined to leads with pathologic Q waves V1 to V4 (arrows). The ST segments have an upward convexity and the T waves are inverted. Echocardiogram and nuclear perfusion scans confirmed the presence of an anteroapical left ventricular aneurysm.

Q Waves

·         Q waves: Q waves associated with acute ST elevation MI generally indicate transmural myocardial necrosis, which is a more advanced stage of myocardial involvement. Q waves, which mark the area of transmural necrosis, signify permanent myocardial damage. Although Q waves are the usual sequelae of ST elevation MI, not all patients with ST elevation MI will develop Q waves. Additionally, some patients with non-ST elevation MI may develop Q waves. Thus, ST elevation MI is a more concise terminology instead of Q-wave MI.

·         The development of Q waves during ST elevation MI may take a few hours to several days, depending on collateral flow. When collaterals are absent or are inadequate, Q waves may develop very early, within a few hours after symptom onset and may be present when the initial ECG is recorded (Fig. 23.69). Similar to ST elevation, pathologic Q wave serves as a useful marker in identifying the infarct related coronary artery, even after the ST-T abnormalities have resolved. Pathologic Q waves may be recorded unexpectedly in a routine ECG and may be the only marker that a previous MI had occurred.

Figure 23.68: ST Elevation from Pacemaker-Induced Ventricular Rhythm. Lead II rhythm strip showing ST elevation during pacemaker captured ventricular complexes (arrows) but not in normally conducted complexes. The ST segment elevation is secondary to abnormal activation of the ventricles.

·         The presence of Q waves during ST elevation MI is not a contraindication to thrombolytic therapy. Progression of ST elevation MI to a Q wave MI may be prevented if reperfusion is timely and successful.

·         Normal Q waves: Q waves may be normal or abnormal. Normal Q waves represent activation of the ventricular septum in a left to right direction (see Chapter 6. Depolarization and Repolarization). These Q waves are often called septal Q waves. Septal Q waves are normally recorded in leads located at the left side of the ventricular septum including V5, V6, and leads I and aVL. The size of the normal Q wave is variable and depends on the thickness of the ventricular septum. In normal individuals, the Q waves are usually narrow measuring <0.03 seconds in duration and are <25% of the height of the R wave. Q waves in lead III do not represent septal Q waves. Thus, the Q waves in lead III may be wide and deep but are not necessarily pathologic even when it exceeds 0.03 seconds in duration.

·         Abnormal Q waves: The differential diagnosis of abnormal Q waves is limited to a few conditions.


These include transmural MI, idiopathic hypertrophic subaortic cardiomyopathy, LVH, abnormal activation of the ventricles from WPW syndrome, LBBB and fascicular blocks, myocardial scarring from cardiomyopathy, infiltrative disease involving the myocardium, or when the rhythm is ectopic or pacemaker induced.

Figure 23.69: Acute Anteroseptal Myocardial Infarction (MI). Initial electrocardiogram of a patient with chest pain showing deep Q waves in V1 to V3 with marked ST elevation across the precordium consistent with acute extensive anterior MI. Note the early appearance of QS complexes in V1 to V3, suggesting the presence of transmural myocardial necrosis involving the anteroseptal wall. Coronary angiography showed complete occlusion of the left anterior descending coronary artery after the first diagonal branch.

Pathologic Q Waves

·         Pathologic Q waves from transmural myocardial necrosis: Pathologic Q waves from transmural necrosis are easy to identify during the acute episode when they are accompanied by ST elevation and T-wave abnormalities. However, when the MI is remote and the ST-T abnormalities have resolved, Q waves from transmural necrosis may be difficult to differentiate from normal septal Q waves. The following are the features of pathologic Q waves due to transmural myocardial necrosis or clinically established MI according to a joint European Society of Cardiology and American College of Cardiology committee proposal.

o    In leads I, II, aVL, aVF, V4, V5, or V6: a pathologic Q wave should measure ≥0.03 seconds in duration. The abnormal Q wave must be present in any two contiguous leads and should be ≥1 mm deep.

o    In V1, V2, and V3: any Q wave is pathologic regardless of size or duration.

o    QRS confounders such as LBBB, LVH, and WPW syndrome should not be present.

·         Similar to ST segment elevation, pathologic Q waves are specific in localizing the area of the transmural MI. Some Q waves, however, are not permanent. Contraction of the scar tissue may occur during the healing process and may cause the Q waves to become narrower and may even disappear.

·         Inferior MI: The diagnosis of inferior MI is based on the following:

o    Q in II and aVF are ≥0.03 seconds in duration and are ≥1 mm deep.

o    Q in Lead III ≥0.04 seconds in duration or the Q waves have an amplitude of 5 mm or ≥25% of the height of the R wave plus a Q wave in aVF that is ≥0.03 seconds in duration and ≥1 mm deep.

o    A QS complex in lead III alone, no matter how deep or wide, is not enough to make a diagnosis of inferior MI.

·         Anterior MI: The diagnosis of anterior MI is based on the following:

o    Q waves in V1: Although the 2000 European Society of Cardiology (ESC)/ACC proposal on the redefinition of MI mentions that any size Q wave is abnormal in V1, V2, or V3, the more recent 2007 ESC/American College of Cardiology Foundation (ACCF)/AHA/World Health Federation (WHF) consensus document on the universal definition of MI considers a QS complex in V1 as a normal finding. Q waves in V1 and in V2 have also been shown to be normal in some patients with chronic pulmonary disease because the diaphragm is displaced downward. It may also be a normal finding when the electrodes are inadvertently misplaced at a higher location at the second instead of the fourth intercostal space.

Figure 23.70: Pathologic Q waves due to Idiopathic Hypertrophic Subaortic Stenosis (IHSS). Pathologic Q waves are noted in V2-6, as well as in leads I and aVL from idiopathic hypertrophic cardiomyopathy. The Q waves in IHSS represent normal activation of an unusually thick septum, which is often two to three times thicker than a normal septum. These Q waves can be mistaken for anterolateral myocardial infarction.

o    Q waves in V1 To V3: When Q waves are present in V1 to V3, they are pathologic regardless of size or duration since normal septal q waves are not normally recorded in all three leads. Other causes of q waves such as LVH, fascicular block, LBBB, and WPW ECG should be absent.

o    Poor R wave progression: The size of the R wave does not increase from V1 to V4. This may be due to anterior MI, although this finding is less specific for anterior MI because this may be caused by several other conditions that can cause clockwise rotation (see Chapter 4, The Electrical Axis and Cardiac Rotation).

·         Posterior or inferobasal MI: Posterior MI will show tall R waves in V1 or V2. The tall R waves are reciprocal changes due to the presence of deep Q waves over the posterior wall. If special leads V7 to V9 are recorded, QS complexes will be present. Other causes of tall R waves in V1 and V2 are further discussed in Chapter 4, The Electrical Axis and Cardiac Rotation.

·         Lateral MI: Q waves ≥0.03 seconds in I and aVL or in V5 and V6 or in all four leads are pathologic and consistent with lateral MI.

Figure 23.71: Pathologic Q waves from Preexcitation. Deep Q waves are seen in V1, V2, V3, and leads III and aVF from preexcitation (Wolff-Parkinson-White electrocardiogram). These Q waves represent delta waves directed posteriorly and inferiorly can be mistaken for anteroseptal or inferior myocardial infarction.

Other Causes of Pathologic Q Waves

·         Pathologic Q waves resulting from idiopathic hypertrophic subaortic stenosis (IHSS): When there is excessive thickening of the ventricular septum such as IHSS, the septal Q waves become exaggerated and can be mistaken for Q waves of MI (Fig. 23.70).

·         Pathologic Q waves from preexcitation: The presence of preexcitation (WPW ECG) can also cause abnormal Q waves that can be mistaken for MI (Fig. 23.71).

·         Pathologic Q waves from LBBB: Activation of the LV is abnormal when there is LBBB. In LBBB, deep QS complexes in V1,2,3 and often in leads II, III, and aVF are not necessarily pathologic (Fig. 23.72). However, any size Q wave in V5 and V6 is pathologic when there is LBBB because the ventricular septum is activated from right to left and Q waves should not be present in these leads. In LBBB, Q waves in V5,6 indicate a septal infarct (Fig. 23.73).

·         Pathologic Q waves resulting from ectopic ventricular rhythms: Accelerated idioventricular rhythm, ventricular tachycardia, or ventricular pacemaker rhythm may cause Q waves from abnormal activation of the ventricles.

Figure 23.72: Q Waves in Left Bundle Branch Block (LBBB). QS complexes are present in leads III, aVF, and V1 to V3 (arrows), which can be mistaken for myocardial infarction. These QS complexes are not pathologic and do not indicate a Q wave infarct when LBBB is present.

Acute Coronary Syndrome

ECG Findings ECG Findings of ST Elevation Myocardial Infarciton

·         The ECG of acute coronary syndrome can be divided into two types:

o    ST segment elevation

o    Non-ST segment elevation

§  ST segment depression

§  T-wave inversion

§  Other less specific ST and T wave abnormalities

·         ECG changes of ST elevation myocardial infarction:

o    ST segment elevation of ≥1 mm in two or more adjacent leads

o    New or presumed new-onset LBBB

o    Development of pathologic Q waves

ST Elevation versus Non-ST Elevation

·         Acute coronary syndrome is usually the result of rupture of an atherosclerotic plaque resulting in obstruction of the vessel lumen by a thrombus. Depending on the severity of coronary obstruction, thrombotic occlusion of the vessel lumen may cause varying degrees of myocardial ischemia, which can be divided into those with and those without ST elevation. These two ECG abnormalities have distinctive pathologies and have different prognostic and therapeutic significance.

Figure 23.73: Left Bundle Branch Block (LBBB) and Septal Q Waves. When there is LBBB, septal Q waves should not be present in V5 or V6 or in leads I or aVL. When Q waves are present in these leads (arrows), no matter how small or microscopic, these Q waves are pathologic and indicate a septal myocardial infarction.

o    ST segment elevation: Acute coronary syndrome with ST elevation in the ECG indicates that one of the three epicardial coronary arteries is totally occluded with TIMI 0 flow (Thrombolysis in Myocardial Infarction grade flow indicating no antegrade flow beyond the point of occlusion). Thrombotic occlusion of the vessel lumen with ST segment elevation almost always results in cellular necrosis with elevation of the cardiac troponins in the circulation. If myocardial perfusion is not restored in a timely manner, changes in the QRS complex with development of Q waves or decreased amplitude of the R waves will occur. Acute coronary syndrome from coronary vasospasm can also cause ST elevation although coronary vasospasm is usually transient and responds to coronary vasodilators such as nitroglycerin.

o    Non-ST segment elevation: When the vessel lumen is partially occluded by a thrombus, myocardial ischemia may or may not occur depending on the severity of coronary artery obstruction, presence of collateral flow and myocardial demand for oxygen. Even if the vessel lumen is partially occluded if myocardial oxygen demand does not exceed its blood supply, myocardial ischemia may not develop. If myocardial ischemia occurs, it may or may not result in myocardial necrosis.

§  Non-ST elevation MI: Partial occlusion of the vessel lumen accompanied by cellular necrosis indicates non-ST elevation MI. The most important marker of cellular necrosis is increased cardiac troponins in the circulation. The diagnosis of non-ST elevation MI is not established unless these cardiac markers are elevated. The ECG will show ST segment depression, T wave inversion, or less-specific ST and T wave abnormalities. Occasionally, the ECG may not show any significant abnormalities.

§  Unstable angina: In unstable angina, the ECG changes are identical to that of non-ST elevation MI, although the cardiac troponins are not elevated in the circulation.

·         Acute MI: With the advent of troponins as a marker of myocardial necrosis, acute MI was redefined in 2000 by a consensus document of the ESC/ACC and again in 2007 by the ESC/ACCF/AHA/WHF, as myocardial necrosis in a clinical setting consistent with myocardial ischemia.

o    Myocardial necrosis: Myocardial necrosis is based on the rise and/or fall of cardiac troponins.

o    Myocardial ischemia: Evidence of myocardial ischemia is based on any of the following:

§  Clinical symptoms of ischemia

§  ECG changes indicative of new ischemia, which includes any of the following:

§  New ST-T changes

§  New LBBB

§  Development of pathologic Q waves

§  Imaging abnormalities

§  New loss of viable myocardium

§  New regional wall motion abnormality

·         Thus, increased in cardiac troponins in the circulation is the most important marker of myocardial necrosis. The diagnosis of acute MI is not possible unless the troponins are elevated. If sudden cardiac death occur before blood samples for troponins could be obtained or before troponins become elevated, acute MI is diagnosed by the associated symptoms and ECG changes of myocardial ischemia.

Clinical Implications

·         ST segment elevation from acute coronary syndrome indicates complete obstruction of the vessel lumen. Therapy requires that coronary blood flow be restored immediately. T-wave inversion and ST segment depression indicate less severe form of myocardial ischemia from a combination of diminished coronary blood flow and increased myocardial oxygen demand. Immediate therapy for T-wave inversion and ST segment depression is directed toward stabilizing the thrombus and lowering myocardial demand for oxygen.

·         ST segment elevation: Thrombotic occlusion of the vessel lumen with persistent elevation of the ST segment is always associated with troponin elevation. Unless adequate collaterals are present or unless the occluded coronary artery is immediately reperfused, virtually all myocardial cells supplied by the totally occluded artery become irreversibly damaged within 6 hours after symptom onset. No significant pathologic abnormalities in the myocardium may be detected microscopically, if the patient dies suddenly within this period. The ECG, however, is very useful in identifying the presence of acute transmural ischemia and in timing the various stages of the infarct.

o    Hyperacute T waves: Hyperacute T waves are usually the earliest ECG abnormality to occur in ST elevation MI. The presence of peaked and tall T waves overlying the area of ischemia often occur very early during the initial onset of symptoms and is often helpful in timing the onset of an acute ischemic process. The hyperacute T waves may be due to local hyperkalemia or presence of an electrical gradient between normal and injured myocardial cells during electrical systole.

o    ST Elevation: When ST elevation is present, it is usually the most striking abnormality in the ECG during the acute phase of myocardial ischemia. The magnitude of ST elevation is measured at the J point. ST elevation is usually confined to leads geographically representing the territory supplied by the occluded artery. Thus, the presence of ST elevation is helpful in identifying the infarct related artery. The greater the number of leads with ST elevation and the more pronounced the ST elevation, the more severe the myocardial ischemia and the more extensive the myocardial damage. Myocardial ischemia, which is reversible, may be severe and relentless and transition to necrosis, which is irreversible, may be completed within 6 to 24 hours after onset of symptoms. This transition is highly variable and often unpredictable because of collateral flow and remodeling within the thrombus. For example, if the thrombus undergoes spontaneous lysis and rethrombosis, the symptoms and ECG findings may wax and wane and the above sequence of evolution may take several days or even weeks before the infarct is finally completed.

o    Q waves: ST elevation MI generally results in the development of pathologic Q waves or diminution in the size of the R waves. Q waves are pathologic when they measure ≥0.03 seconds in duration and are at least ≥1 mm deep in leads I, II, AVF, aVL, and V4 to V6. Any size Q wave is pathologic when present in V2 and also in V3. The presence of pathologic q waves indicates transmural necrosis, which is usually permanent. Although ST elevation MI is synonymous with Q wave MI, Q waves may not always occur especially if the occluded coronary artery is revascularized in a timely fashion. Additionally, approximately 25% of patients with non-ST elevation MI may develop Q waves; thus, non-ST elevation MI rather than Q wave MI is the preferred terminology.

Identifying the Infarct-Related Artery

·         ST segment elevation or pathologic Q waves in the ECG is useful in identifying the location of the infarct-related artery.

·         When ST elevation or Q waves are localized in the anterior precordial leads V1 to V4 (or to V6), acute anterior MI is present. This identifies the LAD artery as the culprit vessel. The ESC/ACC task force on the redefinition of acute MI requires that ST elevation in V1 to V3 should be present in at least two leads and should measure ≥2 mm in contrast to other leads which requires only 1 mm of ST elevation.

·         When ST elevation or pathologic Q waves occur in leads II, III, and aVF, acute inferior MI from occlusion of the posterior descending coronary artery is present. The RCA is the culprit vessel in 85% to 90% of patients with acute inferior MI and the LCx coronary artery in the remaining 10% to 15%. Inferior MI may also occur when there is anterior MI because the LAD may circle the apex of the LV and extend inferoapically. This is not a true inferior MI because the posterior descending coronary artery is not involved. This is merely an extension of the anterior MI.

·         When ST elevation or pathologic Q waves are confined to leads I and aVL or leads V5 and V6, acute lateral MI is present and identifies the LCx coronary artery as the culprit vessel. This is often associated with ST depression in V2 and in V3.

·         The posterolateral wall of the LV is not represented in the standard 12-lead ECG. Acute posterolateral MI with ST segment elevation in V7, V8, and V9 may not be recognized because these leads are not routinely recorded. It is usually suspected when there is ST elevation in V6 and ST depression in V2 and V3. Tall R waves may also be present in V1and V2, which are reciprocal changes due to the presence of deep Q waves posterolaterally. This usually identifies the LCx as the culprit lesion, although, occasionally, it may be due to a dominant RCA.

LAD Coronary Artery

·         Area supplied: The LAD is a large artery that supplies the whole anterior wall of the LV. It is the main blood supply to the intraventricular conduction system including the bundle of His, bundle branches, and distal fascicular system.

·         Anatomy: The LAD courses through the anterior interventricular groove and supplies the ventricular septum and anterior wall of the LV.

o    The length of the LAD can be short (terminates before the apex), medium (terminates at the apex), or large (wraps around the apex and continues to the inferior wall of the LV).

o    The first branch of the LAD is the first diagonal (D1), which courses laterally between the LAD and left circumflex coronary artery. Usually one to three diagonal branches are given off by the LAD. D1 is often the largest diagonal branch and supplies the base of the anterolateral wall of the LV.

o    The second branch is the first septal branch (S1). S1 may be the first instead of the second branch. About three to five septal branches arise at right angles from the LAD and directly insert perpendicularly into the myocardium and supply the anterior two thirds of the ventricular septum. S1 supplies the basal anteroseptal region of the LV and is the main blood supply of the distal His bundle and proximal left and right bundle branches.

·         Occlusion of the proximal LAD: The following is a summary of the ECG findings when complete occlusion involves the proximal LAD:

o    Occlusion of the LAD before the first branch (D1 or S1):

§  ST elevation in V1 to V4 (anteroseptal) and leads I and aVL (basal lateral or high lateral wall). Because the first septal branch or S1 supplies the base of the ventricular septum, ST elevation will occur in V1.

§  ST elevation in aVL. Because the first diagonal branch or D1 supplies the base of the lateral wall, ST elevation will occur in aVL.

§  Reciprocal ST depression is present in III and aVF (from ST elevation in aVL, which is diametrically opposite lead III)

§  If ST elevation is confined to V1 to V3, reciprocal ST depression may be present in V5 or V6.

§  Complete RBBB may occur.

§  If the LAD is large and extends to the left ventricular apex and contiguous inferior wall, ST elevation may occur in leads II, III, and aVF (acute inferior MI), in addition to the ST elevation in the precordial leads.

§  ST elevation may be present in aVR.

o    Occlusion of the LAD distal to the first diagonal and first septal branches:

§  Occlusion of the LAD distal to D1 and S1 results in a less extensive infarct compared with a more proximal lesion and will cause ST elevation only in V2 to V4.

§  ST elevation will not occur in V1 nor lead aVL or lead I because the first septal and first diagonal branches are spared. Because ST elevation is not present in lead aVL, reciprocal ST depression will not occur in lead III.

·         Common Complications Associated with Acute Anterior MI:

o    Tachyarrhythmias: Ventricular fibrillation is the most common cause of death usually within the first few hours after symptom onset. Although ventricular tachycardia and fibrillation can occur in any patient with acute MI, acute anterior myocardial infarction is more commonly associated with tachyarrhythmias including sinus tachycardia, ventricular tachycardia, and ventricular fibrillation in contrast to inferior MI, which is usually associated with bradyarrhythmias such as sinus bradycardia and varying degrees of AV block.

o    Intraventricular conduction defects: Occlusion of the LAD proximal to the first septal branch can jeopardize the conduction system and can cause transient or permanent conduction abnormalities.

§  RBBB with or without fascicular block: This is usually from the involvement of the first septal branch of the LAD. Diagnosis of acute MI in the presence or RBBB is not difficult because activation of the LV is not altered.

§  LBBB: LBBB is less frequently seen as a complication of MI compared with RBBB. Although LAD disease is commonly expected to cause LBBB, LBBB complicating acute MI are usually non-anterior in location with the lesion more commonly associated with the right rather than left coronary artery as shown in the subset analysis of patients with acute MI in the GUSTO-1 databases. The diagnosis of acute MI in the presence of LBBB is difficult because the LV is activated abnormally from the right bundle branch. This was previously discussed in Chapter 10, Intraventricular Conduction Defect: Bundle Branch Block.

o    Complete AV block:When complete AV block occurs in the setting of acute anterior MI, the AV block is infranodal because the LAD supplies most of the distal intraventricular conduction system. The AV block is often preceded by RBBB with or without fascicular block. Prognosis remains poor even with temporary or permanent pacing because occlusion of the LAD complicated by RBBB is usually an extensive MI. Atropine does not reverse the AV block because the conduction abnormality is infranodal, at the His-Purkinje level. The indication for the implantation of permanent pacemakers in patients with intraventricular conduction defect and AV block associated with acute MI is discussed under treatment.

o    LV dysfunction and pump failure: Acute anterior MI is associated with a higher incidence of heart failure and cardiogenic shock. Cardiogenic shock usually occurs when at least 40% of the left ventricular myocardium is involved. Heart failure and cardiogenic shock are more common with acute anterior MI because acute anterior MI is generally a large infarct.

o    Late ventricular arrhythmias and sudden death: Patients with extensive myocardial damage and severe left ventricular dysfunction who survive their MI are at high risk for ventricular arrhythmias and sudden death. These complications are more frequently seen in patients with anterior MI.

LCx Artery

·         Anatomy and area supplied: The LCx coronary artery circles around the left or lateral AV groove and sends three or more obtuse marginal branches to the lateral wall of the LV. It continues posteriorly as the posterior AV artery sending three or more posterolateral branches to the LV. In 10% to 15% of patients, the LCx artery continues as the posterior descending coronary artery, which supplies the inferior wall of the LV. When this occurs, the pattern of coronary distribution is described as left dominant.

·         Occlusion of the LCx: The following is a summary of the ECG changes when the LCx coronary artery is occluded:

o    Acute lateral MI with ST elevation (or pathologic Q waves) in I and aVL or V5 and V6 with or without ST depression in V1 to V3.

o    Acute inferior MI with ST elevation or pathologic Q waves in II, III, and aVF if the LCx artery is the dominant artery.

o    No significant ECG changes. When acute MI is diagnosed clinically without significant ECG changes, the culprit vessel is usually the LCx coronary artery.

o    Unless there is unusual variation in coronary anatomy, occlusion of the LCx coronary artery does not result in right ventricular infarction.

o    Straight posterior MI or acute posterolateral MI with prominent q waves and ST elevation in special leads V7, V8, and V9. Tall R waves may be present in V1 and V2 with reciprocal ST depression from V1 to V3.

§  If the MI involves the basal posterior wall of the LV or is directly posterior or posterolateral, the ECG will show reciprocal ST depression in V1 to V3 because these leads are diametrically opposite the posterior or posterolateral wall. Unfortunately, ST depression in V1 to V3 can be mistaken for ischemia involving the anterior wall of the LV rather than a transmural posterior MI. This dilemma can be resolved by recording extra leads V7, V8, and V9, which overlie the posterolateral wall of the LV. Leads V7 to V9 will show ST elevation if an acute transmural posterolateral MI is present but not when there is anterior wall ischemia and injury. ST elevation of 0.5 mm is significant because of the wider distance between these leads in relation to the heart. ST elevation in V7 to V9 makes the patient a candidate for thrombolytic therapy.

§  Tall R waves in V1 to V2 may also occur although these changes usually develop several hours later.

·         Common Complications Associated with Acute Lateral or Posterolateral MI:

o    Tachyarrhythmias: Ventricular tachycardia and ventricular fibrillation can occur similar to any acute MI during the first few hours after onset of symptoms.

o    Left ventricular dysfunction: This can occur as a complication if the artery is large and supplies a significant portion of the myocardium.

o    AV block: AV can occur at the level of the AV node only if the LCx coronary artery is dominant and there is associated inferior MI.

Right Coronary Artery

·         Anatomy and area supplied: The right coronary artery (RCA) courses around the right or medial AV groove and gives acute marginal branches to the right ventricle. The RCA is the dominant artery in 85% to 90% of cases by continuing posteriorly to the crux of the heart and giving rise to a branch that supplies the AV node and the posterior descending artery, which supplies the inferior wall of the LV. The RCA often continues beyond the crux toward the left AV groove as the right posterior AV artery, which gives posterolateral branches to the LV.

·         Occlusion of the RCA:

o    Occlusion of the RCA will cause acute inferior MI with ST elevation in II, III, and aVF.

o    ST elevation in V5 and V6 may occur because of posterolateral involvement of the LV.

o    Reciprocal ST depression in V1 to V3 with inferior MI suggests the presence of a posterolateral MI. This can be verified by recording extra precordial leads V7, V8, and V9which will show ST elevation consistent with a transmural posterolateral MI (see LCx Coronary Artery Occlusion).

·         Acute inferior MI is usually due to occlusion of the RCA, except in some patients where the LCx is the dominant artery. Occlusion of the proximal RCA can cause right ventricular infarction, which does not occur if the LCx coronary artery is the culprit vessel. Inferior MI complicated by right ventricular infarction is a large infarct with a high mortality of 25% to 30% compared with inferior MI without RV infarction, which has a mortality of approximately 6%.

·         Acute inferior MI from occlusion of the RCA can be differentiated from acute inferior MI due to occlusion of the LCx coronary artery by the following ECG findings:

o    If ST elevation in lead III > lead II, the RCA is the culprit vessel. This is based on the anatomical location of the RCA, which circles the right AV groove and is closer to lead III than lead II whereas the LCx circles the left AV groove and is closer to lead II than lead III. Thus, if ST elevation in lead III > lead II, the proximal or mid RCA is the culprit vessel, whereas if ST elevation in lead II > lead III or ST elevation in III is not greater than II, the LCx artery is the culprit vessel.

o    ST depression in lead aVL > lead I, RCA is the culprit lesion. This is corollary to the observation mentioned previously, that lead III has a higher ST elevation when the RCA is the culprit vessel. Because lead III is diametrically opposite aVL, reciprocal ST depression will be more pronounced in aVL than in lead I.

o    RV infarction can occur only if the proximal or mid RCA is occluded (but not the LCx or distal RCA). The presence of RV infarct is best diagnosed by recording right sided precordial leads.

·         Complications of Acute Inferior MI:

o    VT and VF: This is similar to the complications of any acute MI.

o    Bradyarrhythmias and AV block: Sinus bradycardia and other sinus disturbances are very common findings in acute inferior MI and are more common when the RCA is involved. The RCA carries vagal afferent fibers, which can cause sinus bradycardia due to reflex stimulation rather than due to direct suppression of sinus node function. Varying degrees of AV block (first, second, and third degree) can occur with acute inferior MI. The AV block is at the level of the AV node because the RCA supplies the AV node in 85% to 90% of patients and by the LCx in the remaining 10% to 15%. AV block at the level of the AV node has a better prognosis than AV block occurring in the distal conduction system. AV block occurring during the first few hours of a myocardial infarct is usually due to a vagal mechanism and has a better prognosis compared to AV block occurring late post-MI.

o    Intraventricular conduction defect: Intraventricular conduction defect (IVCD), either RBBB or LBBB, may occur as a complication of acute MI. IVCD complicating acute MI is usually associated with an extensive MI and mortality is much higher when compared with patients who do not develop IVCD. These patients have higher incidence of asystole, AV block, VF, both primary and late, as well as cardiogenic shock. The IVCD may be transient or persistent. When the IVCD is transient, the prognosis seems to be similar to patients who never developed the conduction abnormality. Acute (new-onset) LBBB or a previously existent (old) LBBB may conceal the ECG changes of acute MI, whereas the ECG diagnosis of acute MI can be recognized even when RBBB is present.

o    Atrial ischemia or infarction: Atrial branches to the right atrium are usually supplied by the RCA which can result in atrial ischemia or infarction when there is occlusion of the proximal RCA. The acute onset of atrial fibrillation may be the only clue that atrial infarction had occurred. Atrial infarction can also be diagnosed when depression of the P-Q segment is present in the setting of acute inferior MI.

o    Papillary muscle rupture: Most papillary muscle rupture involves the posteromedial papillary muscle because it has a single blood supply originating from the RCA. The anterolateral papillary muscle is less prone to rupture because it has dual blood supply from the LAD and LCx coronary arteries. Papillary muscle rupture is rare but is incompatible with life because of acute severe mitral regurgitation.

o    RVMI: RVMI can occur only with acute inferior infarction due to occlusion of the proximal or probably mid-RCA. It does not occur when the lesion involves the distal RCA or LCx coronary artery.

§  When acute inferior MI is diagnosed, RVMI should always be routinely excluded by recording right-sided precordial leads. The right-sided precordial leads should be recorded immediately, because the ECG changes in half of patients with RVMI may resolve within 10 hours after the onset of symptoms. Right-sided precordial leads are the most sensitive, most specific, and the least expensive procedure in the diagnosis of RVMI. ST elevation of ≥1 mm in any of the right-sided precordial leads is diagnostic of RVMI with lead V4R the most sensitive. Changes in the QRS complex is not a criteria for the diagnosis of RVMI because the right ventricle does not contribute significantly in the generation of the QRS complex.

§  If right-sided precordial leads were not recorded or were recorded late during the course of the MI, the diagnosis of RVMI may be missed. Using the standard 12-lead ECG, RVMI is suspected when ST elevation in lead III is greater than lead II (suggesting proximal RCA occlusion) and ST elevation is present in V1.

§  RVMI often presents with a special hemodynamic subset of patients with acute MI who can develop the clinical triad of hypotension, jugular neck vein distension, and clear lungs. This subset of patients can be mistaken for cardiogenic shock. The presence of Kussmaul sign characterized by distension of the neck veins during inspiration is diagnostic of RVMI when acute inferior MI is present. Approximately one third to one half of patients with acute inferior MI have RVMI but only 10% to 15% of patients with RVMI will manifest the hemodynamic abnormality. The hemodynamic picture of RVMI usually disappears after a few weeks, suggesting that the RVMI is due to myocardial stunning rather than necrosis. The thinwalled right ventricle has a lower oxygen demand and may partially receive its blood supply from the blood within the right ventricular cavity, thus limiting the extent of myocardial necrosis.

Treatment

·         The ECG remains the most useful test in planning the initial strategies in the therapy of a patient with acute coronary syndrome. If a patient presents to a medical facility with symptoms of acute ischemia, the ACC/AHA guidelines recommend that the ECG should be obtained and interpreted within 10 minutes after patient entry. If ST elevation is present in the initial ECG and patient is having symptoms due to myocardial ischemia, 0.4 mg of sublingual nitroglycerin should be given immediately, if not previously given, and repeated every 5 minutes for three doses. This is a Class I indication according to the ACC/AHA guidelines on ST elevation MI. Nitroglycerin is helpful in excluding vasospasm as the cause of the ST segment elevation. If the ST elevation persists after three successive doses, immediate reperfusion of the occluded artery with a thrombolytic agent or with primary PCI should be considered without waiting for the results of cardiac troponins. Although acute coronary syndrome with ST segment elevation is almost always associated with increased troponins in the circulation, the troponins may not be elevated in some patients presenting to the hospital within 6 hours after symptom onset.

·         Thrombolytic therapy: Thrombolytic therapy or primary PCI should be considered if the chest pain is at least 20 minutes in duration.

o    The following are the ECG criteria for immediate thrombolytic therapy or PCI:

§  ST elevation >1 mm is present in any two adjacent leads.

§  New or presumably new-onset LBBB associated with symptoms of ischemia.

§  ST segment depression even in the presence of cellular necrosis (elevated cardiac troponins) is not an indication for thrombolytic therapy. The only exception is ST segment depression in V1 to V3, which may represent a straight posterior or posterolateral infarct. A posterior infarct is a transmural infarct and can be verified by the presence of ST elevation in leads V7 to V9.

o    Virtually all myocardial cells supplied by the infarct related artery become necrotic within 6 hours after symptom onset, unless collateral flow is adequate. Thus, if thrombolytic therapy is elected, it should be given within 30 minutes after patient entry to the emergency department (door to needle time) or first contact with emergency personnel (medical contact to needle time). Thrombolytic therapy is most effective when given within 2 hours after symptom onset. With further delay, the benefits of any type of reperfusion therapy decline.

o    The therapeutic window for thrombolytic therapy is up to 12 hours after symptom onset. This may be extended to 24 hours for some patients who continue to have stuttering symptoms of chest pain with persistent ST elevation.

o    Absolute contraindications to thrombolytic therapy according to the 2004 ACC/AHA guidelines include: any prior intracranial hemorrhage, known structural cerebrovascular lesion such as arteriovenous malformation, known malignant intracranial neoplasm either primary or metastatic, ischemic stroke within 3 months, suspected aortic dissection, active bleeding or bleeding diathesis other than menses, and significant closed head or facial trauma within 3 months.

o    Relative contraindications include history of chronic severe, poorly controlled hypertension, severe uncontrolled hypertension on presentation (systolic blood pressure >180 mm Hg or diastolic blood pressure >110 mm Hg), history of prior ischemic stroke >3 months, dementia or known intracranial pathology that is not included under absolute contraindications, traumatic or prolonged cardiac resuscitation >10 minutes, major surgery <3 weeks, recent (within 2 to 4 weeks) internal bleeding, noncompressible vascular punctures, pregnancy, active peptic ulcer, current use of anticoagulants (the higher the International Normalized Ratio, the higher the risk of bleeding), and prior exposure (>5 days) to streptokinase/anistreplase or prior allergic reaction to these agents.

o    Intracerebral hemorrhage is a major complication and is expected to occur in approximately 1% of patients receiving thrombolytic therapy. It is fatal in up to two thirds of patients with this complication. Patients older than 65 years, a low body weight of <70 kg, and alteplase (as opposed to streptokinase) as the thrombolytic agent, are associated with higher incidence of intracerebral hemorrhage.

o    There are five thrombolytic agents approved for intravenous use: (1) tissue plasminogen activator or tPa (alteplase), (2) recombinant tissue plasminogen activator or rtPa (reteplase), (3) tenecteplase, (4) streptokinase, and (5) anistreplase. Alteplase, reteplase, and tenecteplase are plasminogen activators. These are selective agents that specifically convert plasminogen to plasmin and are given concomitantly with intravenous heparin infusion. Streptokinase and anistreplase do not require heparin infusion because these nonselective thrombolytic agents can cause depletion of the coagulation factors and produce massive amounts of fibrin degradation products, which have anticoagulant properties. If patient is a high risk for systemic emboli such as the presence of a large infarct, atrial fibrillation, left ventricular thrombus, or previous embolus, Activated partial thromboplastin time should be checked 4 hours after these nonselective thrombolytic agents have been given and heparin started when activated partial thromboplastin time is <2 times control (or <70 seconds).

·         Additional medical therapy for ST elevation MI include:

o    Aspirin: The initial dose of aspirin is 162 to 325 mg orally. This should be given immediately even before the patient arrives to a medical facility. Plain aspirin (not enteric coated), should be chewed. Maintenance dose of 75 to 162 mg daily is continued indefinitely thereafter.

§  If the patient is allergic to aspirin, clopidogrel should be given as a substitute.

§  In patients undergoing coronary bypass surgery, aspirin should be started within 48 hours after surgery to reduce closure of the saphenous vein grafts.

§  Patients who have PCI with stents placed should initially receive the higher dose of aspirin at 162 to 325 mg daily for one month for bare metal stent, 3 months for sirolimus and 6 months for paclitaxel eluting stent and continued at a dose of 75 to 162 mg daily indefinitely.

o    Clopidogrel: Similar to aspirin, clopidogrel is considered standard therapy and is a Class I recommendation in patients with acute coronary syndrome including patients with ST elevation MI with or without reperfusion therapy according to the 2007 focused update of the ACC/AHA 2004 guidelines for ST elevation MI. The maintenance dose is 75 mg orally daily for a minimum of 14 days and reasonably up to a year. The loading dose is 300 mg orally, although in elderly patients >75 years especially those given fibrinolytics, the loading dose needs further study.

§  In patients undergoing coronary bypass surgery, clopidogrel should be discontinued at least 5 days and preferably for 7 days unless the need for surgery outweighs the risk of bleeding.

o    Unfractionated heparin: When unfractionated heparin is given concomitantly with a selective thrombolytic agent such as tPA, rtPA, or tenecteplase, the recommended dose is 60 U/kg given as an IV bolus. The initial dose should not exceed 4,000 U. This is followed by a maintenance dose of 12 U/kg/hour not to exceed 1,000 U/hour for patients weighing more than 70 kg. Activated partial thromboplastin time should be maintained to 50 to 70 seconds or 1.5 to 2 times baseline. Heparin is usually given for 48 hours, but may be given longer if there is atrial fibrillation, left ventricular thrombi, pulmonary embolism, or congestive heart failure. Platelets should be monitored daily. When given to patients not on thrombolytic therapy, the dose is 60 to 70 U/kg bolus followed by maintenance infusion of 12 to 15 U/kg/hour. According to the ACC/AHA 2007 revised guidelines on unstable angina and non-ST elevation MI, patients who did not receive thrombolytic therapy may receive other types of heparin other than unfractionated heparin for the whole duration of hospitalization or for a total of 8 days. This includes low-molecular-weight heparin (enoxaparin) and fondaparinux.

§  Enoxaparin: An initial 30 mg IV bolus is followed by a subcutaneous injection of 1 mg/kg every 12 hours. For patients older than 75 years of age, the initial bolus is omitted and the subcutaneous dose is 0.75 mg/kg every 12 hours. The dose should be adjusted if the serum creatinine is ≥2.5 mg/dL in men and ≥2.0 mg/dL in women.

§  Fondaparinux: The initial dose is 2.5 mg IV followed by subcutaneous doses of 2.5 mg once daily up to the duration of hospitalization or a maximum of 8 days provided that the creatinine is <3.0 mg/dL.

o    Nitroglycerin: Nitroglycerin is initially given sublingually unless the patient is hypotensive with a blood pressure <90 mm Hg or heart rate is <50 bpm or there is suspected RVMI. Intravenous nitroglycerin is given when there are symptoms of ongoing ischemia or congestive heart failure or for uncontrolled hypertension.

o    Oxygen: Oxygen supplementation is given to improve arterial saturation.

o    Morphine sulfate: Morphine sulfate is the analgesic of choice with a Class I recommendation for pain relief for ST elevation MI but only a Class IIa recommendation for non-ST elevation MI. The dose is 2 to 4 mg IV and repeated in increments of 2 to 8 mg at 5- to 15-minute intervals.

o    Beta blockers: Beta blockers should be given orally in the first 24 hours unless the patient has contraindications to beta blocker therapy such as PR interval >0.24 seconds, second-degree AV block or higher, signs of heart failure, or low cardiac output and bronchospastic pulmonary disease. This is given a Class I recommendation in the ACC/AHA guidelines. Beta blockers have been shown to decrease the incidence of ventricular arrhythmias after acute MI. Beta blockers may be administered IV if hypertension is present. This carries a Class IIa recommendation.

o    Antagonists of the renin-angiotensin system: The use of angiotensin-converting enzyme inhibitors is a Class I recommendation in patients with ST elevation MI. It should be given orally (not IV) and continued indefinitely in patients with ST elevation MI with left ventricular ejection fraction ≤40% and patients with hypertension, diabetes, or chronic renal disease in the absence of contraindications to angiotensin-converting enzyme inhibitor therapy. Angiotensin receptor blockers, specifically valsartan or candesartan, may be given if the patient cannot tolerate angiotensin-converting enzyme inhibitors. The routine use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers is reasonable in patients with acute ST elevation MI without any of the above indications. This carries a Class IIa recommendation.

o    Aldosterone antagonist: Aldosterone antagonists (eplerenone in post-MI patients and spironolactone in patients with chronic heart failure), have been shown to reduce mortality. The 2007 focused update of the ACC/AHA 2004 guidelines on ST elevation MI gives a Class I recommendation for the use of aldosterone blockers to patients with ejection fraction of ≤40% and have either diabetes or heart failure unless there is renal dysfunction (serum creatinine ≥2.5 mg/dL in men and ≥2.0 mg/dL in women and potassium ≥5.0 mEq/L).

o    Cholesterol-lowering agents: Statins or if contraindicated, other lipid-lowering agents, should be given to lower low-density lipoprotein cholesterol to <100 mg/dL in all patients and further lowering to <70 mg/dL is reasonable in some patients.

o    IIB/IIIA inhibitors: Other antiplatelet agents such as IIB/IIIA inhibitors (abciximab, eptifibatide, and tirofiban) are not indicated in the treatment of ST elevation MI unless the patient is being readied for primary PCI. The use of standard dose IIB/IIIA inhibitor (abciximab) in combination with half-dose thrombolytic agent (reteplase) has not been shown to improve mortality in the short term (30 days) or long term (1 year) compared with the use of the thrombolytic agent alone.

·         Primary PCI: Primary PCI is the most effective reperfusion method and has now become the standard therapy for reperfusing ST elevation MI in centers that are capable of doing the procedure in a timely fashion. The success rate of being able to reperfuse the occluded artery with primary PCI is >90%, whereas the 90-minute patency rate with thrombolytic therapy is approximately 65% to 75%. Unfortunately, PCI can be performed only in centers with interventional cardiac catheterization laboratories, and in some states, only when backup cardiac surgery is available. The most recent 2007 focused update of the ACC/AHA guidelines on ST elevation MI reemphasizes the previous recommendation that reperfusion of the occluded artery should be started as early as possible since the greatest benefit of any type of reperfusion therapy depends on the shortest time in which complete reperfusion is achieved. Therefore, the delay in performing PCI should be considered when deciding whether thrombolytic therapy or primary PCI is the best modality of reperfusion. Thus, if the patient is admitted to a hospital that is capable of doing PCI, the procedure should be performed within 90 minutes after first medical contact. If the patient is admitted to a facility that is not capable of doing PCI and it is not possible to perform PCI within 90 minutes with interhospital transfer, thrombolytic therapy should be given unless contraindicated, within 30 minutes of hospital presentation. Transfer to another hospital with PCI capabilities should be considered when:

o    Thrombolytic therapy is contraindicated.

o    PCI can be performed within 90 minutes (door to balloon time) of first medical contact.

o    Thrombolytic therapy had been tried but failed to reperfuse the occluded artery (rescue PCI).

o    PCI is also the therapy of choice when the patient is hemodynamically unstable especially when there is cardiogenic shock or pump failure, onset of symptoms is more than 3 hours or the diagnosis of ST elevation MI is in doubt.

·         Facilitated PCI: This involves the administration of heparin in high doses, IIb/IIIa antagonists, fibrinolytic agents in less than full doses or a combination of the agents discussed previously before PCI is attempted. Full dose thrombolytic therapy followed by immediate PCI may be harmful and is not recommended (Class III recommendation according to the 2007 focused update ACC/AHA 2004 guidelines for the management of patients with ST elevation MI). These antithrombotic agents are given to improve patency of the occluded coronary artery. Facilitated PCI is performed if primary PCI is not available within 90 minutes after first medical contact. This is usually performed when the patient is initially admitted to a hospital without PCI capabilities and interhospital transfer is being planned to a facility that is capable of doing PCI.

·         Cardiac pacemakers and acute MI:

o    In patients with acute MI complicated by AV block, implantation of permanent pacemakers depends on the location of the AV block (which should be infranodal), rather than the presence or absence of symptoms. Most patients with infranodal block have wide QRS complexes. However, when AV block is persistent and is associated with symptoms, the AV block may or may not be infranodal before a permanent pacemaker is implanted.

o    Whenever a patient who has survived an acute MI becomes a candidate for permanent pacemaker, two other conditions should be answered. These include the need for biventricular pacing because most of these patients will have an intraventricular conduction defect and the need for implantable cardioverter defibrillator (ICD) because most of these patients have left ventricular dysfunction.

o    Indications of implantation of permanent pacemaker after acute MI: The following are indications for insertion of a permanent pacemaker following acute ST elevation MI according to the ACC/AHA/Heart Rhythm Society (HRS) 2008 guidelines for device-based therapy of cardiac rhythm abnormalities and the ACC/AHA 2004 guidelines for the management of ST elevation MI.

§  Class I recommendation:

§  Persistent second-degree AV block in the His-Purkinje system with bilateral bundle-branch block or third-degree AV block within or below the His-Purkinje system.

§  Transient advanced second- or third-degree AV block at the infranodal level and associated bundle branch block. An electrophysiologic study may be necessary if the site of the block is uncertain.

§  Persistent and symptomatic second- or third-degree AV block.

§  Class IIb recommendation:

§  Persistent second- or third-degree AV block at the level of the AV node.

§  Class III recommendation: permanent pacing is not recommended in the following conditions:

§  Transient AV block without intraventricular conduction defect.

§  Transient AV block in the presence of isolated left anterior fascicular block.

§  Acquired left anterior fascicular block in the absence of AV block.

§  Persistent first-degree AV block in the presence of bundle branch block, old or indeterminate.

·         Ventricular and supraventricular tachycardia: The treatment of ventricular and supraventricular tachycardia following acute MI is similar to the general management of these arrhythmias in patients without ischemic heart disease.

·         Implantation of ICD after acute MI: In patients with acute MI, the following are indications for implantation of ICD according to the ACC/AHA 2004 guidelines for the management of ST elevation MI:

o    Class I recommendation:

§  Patients with VF or hemodynamically significant VT more than 2 days after acute MI not from reversible ischemia or from reinfarction.

§  Left ventricular ejection fraction of 31% to 40% at least 1 month after acute MI even in the absence of spontaneous VT/VF or have inducible VT/VF on electrophysiological testing.

o    Class IIa recommendation:

§  Left ventricular dysfunction (ejection fraction ≤30%) at least 1 month after acute MI and 3 months after coronary artery revascularization.

o    Class IIb recommendation:

§  Left ventricular dysfunction (ejection fraction 31% to 40%) at least 1 month after acute ST elevation MI without additional evidence of electrical instability such as nonsustained VT.

§  Left ventricular dysfunction (ejection fraction 31% to 40%) at least 1 month after acute ST elevation MI and additional evidence of electrical instability such as nonsustained VT but do not have inducible VF or susfained VT on electrophysiologi testing.

o    Class III recommendation: ICD is not indicated when ejection fraction is >40% at least 1 month after acute ST elevation MI.

·         RVMI: Left ventricular preload may be diminished from right ventricular failure and volume is needed to optimize diastolic filling and cardiac output. Treatment of RVMI therefore usually requires adequate hydration with IV fluids.

o    The use of nitroglycerin may further reduce preload and potentiate the hemodynamic abnormalities associated with RVMI and should be used cautiously when acute inferior MI is present. It is contraindicated if systolic blood pressure is <90 mm Hg or heart rate is <50 bpm.

o    Acute inferior MI complicated by RVMI involves not only the right ventricle but may be associated with significant left ventricular dysfunction. If left ventricular output is low and LV filling pressure is high (high pulmonary wedge pressure), inotropic support with dopamine or dobutamine should be considered.

o    Complete AV block may occur as a complication of RVMI because the artery to the AV node is usually compromised when there is occlusion of the proximal or mid-RCA. If the AV block is associated with a low ventricular rate of <50 bpm or patient is hemodynamically unstable with low output, atropine is the drug of choice. The dose is 0.5 to 1.0 mg IV repeated every 3 to 5 minutes until a total dose of 3 mg (0.04 mg/kg) is given within a period of 3 hours. This dose can result in complete vagal blockade and need not be exceeded. Doses of <0.5 mg should be discouraged because it may slow instead of increase heart rate by stimulation of the vagal nuclei centrally resulting in parasympathomimetic response. If AV block does not respond to atropine, temporary dual chamber pacing to preserve AV synchrony may be needed to optimize left ventricular output because ventricular performance is dependent on atrial contribution to left ventricular filling.

Prognosis

·         Acute MI continues to be the leading cause of death and disability in spite of the advances in the diagnosis and therapy of coronary disease. About half of all deaths from acute MI will occur during the initial hours after the onset of symptoms with most deaths from ventricular fibrillation. Most deaths occur before the patients are able to reach a medical facility. Of those who survive and are able to seek medical care, prognosis is dependent on the extent and severity of myocardial damage.

·         ST elevation MI is more extensive than non-ST elevation MI resulting in a lower ejection fraction, higher incidence of heart failure, ventricular arrhythmias, and higher immediate and in-hospital mortality of up to 10% compared with non-ST elevation MI, which has a lower incidence of the above complications and a lower in-hospital mortality of 1% to 3%.

Suggested Readings

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Antman EM, Hand M, Armstrong PW, et al. 2007 Focused update of the ACC/AHA 2004 guidelines for the management of patients with ST elevation myocardial infarction. J Am Coll Cardiol. 2008;51:210-247.

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