The Normal P Wave
· Normal sinus rhythm: The sinus node is the origin of the normal impulse. The normal sinus P wave has the following features.
o Frontal plane:
§ Axis: The axis of the normal P wave is approximately 45° to 60°. Thus, the P wave is upright in lead II. This is the most important lead in recognizing that the rhythm is normal sinus. If the P wave is not upright in lead II, the P wave is probably ectopic (not of sinus node origin).
§ Contour: The normal P wave is smooth and well rounded and should not be peaked or notched.
§ Amplitude: The normal P wave is >2.5 mm in height.
§ Duration: The normal P wave is >2.5 mm wide or >100 milliseconds in duration.
o Horizontal plane:
§ Sinus P waves are normally upright in V3 to V6. In V1 and often in V2, the contour of the normal P wave may be upright, inverted or biphasic. Biphasic means that the initial portion of the P wave is upright and the terminal portion is inverted (Fig. 7.1). The inverted portion should measure <1 mm in duration and <1 min in depth.
Figure 7.1: The Normal P Wave. The sinus P wave is well rounded and smooth and is upright in leads I, II, and aVF measuring ≤2.5 mm in height and ≤2.5 mm in width. In V1, a normal P wave can be upright, biphasic, or inverted.
Right Atrial Enlargement
· Right atrial enlargement: The following changes occur when there is right atrial enlargement.
o Frontal plane:
§ Axis: The axis of the P wave is shifted to the right of +60°. Thus, the P waves are tall in leads II, III, and aVF. The P waves in lead III are usually taller than in lead I (P3 > P1).
§ Contour: The contour of the P wave is peaked and pointed. These changes are often described as “P-pulmonale” because right atrial enlargement is frequently caused by pulmonary disease.
§ Amplitude: The height or amplitude of the P wave increases to >2.5 mm. These P wave changes are best seen in leads II, III, and aVF (Fig. 7.2).
§ Duration: The total duration of the P wave is not prolonged unless the left atrium is also enlarged. Because the right atrium is activated earlier than the left atrium, any delay in the propagation of the impulse from enlargement of the right atrium will coincide with the activation of the left atrium.
Figure 7.2: Right Atrial Enlargement. In right atrial enlargement, the P waves are peaked and tall with an amplitude >2.5 mm in leads II, III, or aVF. Changes in V1 are less obvious, although the upward deflection is often peaked. The duration of the P wave is not widened.
Figure 7.3: Right Atrial Enlargement. In the frontal plane, the right atrium enlarges downward and to the right causing a shift in the P wave axis to the right (from arrow 1 to arrow 2). In the horizontal plane, the enlargement of the right atrium is slightly anterior, which may cause slight peaking of the P waves in lead V1. The shaded portion indicates the changes that occur when the right atrium enlarges. S, superior; I, inferior; R, right; L, left; A, anterior; P, posterior; RA, right atrium; LA, left atrium.
o Horizontal plane: In V1, there may not be any significant P wave changes. The P wave remains normally upright, biphasic, or inverted. The initial upright portion may be slightly peaked or pointed or it might be slightly taller than normal.
· When there is right atrial enlargement, the right atrium enlarges downward and to the right, thus the axis of the P wave is shifted vertically to the right of +60° (Fig. 7.3). This causes the P wave in lead III to be taller than the P wave in lead I.
Figure 7.4: Right Atrial Enlargement. Twelve-lead electrocardiogram showing right atrial enlargement. Tall and peaked P waves, also called “P-pulmonale,” are seen in leads II, III, and aVF (arrows). Note that the P waves are taller in lead III than in lead I. Leads II, III, aVF, and V1 are magnified to show the abnormal P wave contour. The patient has chronic obstructive pulmonary disease.
Electrocardiogram of Right Atrial Enlargement
· The P waves are tall and peaked measuring >2.5 mm in leads II, III, or aVF (Fig. 7.4).
· The duration of the P wave is not increased unless the left atrium is also enlarged.
· Normal sinus P waves: The sinus node is located at the right upper border of the right atrium near the entrance of the superior vena cava. The sinus impulse has to spread from right atrium to left atrium downward in a right-to-left direction. The initial portion of the P wave represents right atrial activation and the terminal portion, left atrial activation. In the frontal plane, the normal P wave axis is approximately +45° to +60° and is upright in leads I, II, and aVF. The tallest P wave is usually recorded in lead II and the amplitude of the normal P wave is ≤2.5 blocks. In V1, the normal sinus P wave can be upright, biphasic, or inverted. The normal cutoff for the total duration varies among different authors. The World Health Organization/International Society and Federation of Cardiology Task Force define the normal duration as ≤110 milliseconds, which is not easy to measure in the electrocardiogram (ECG). A width of ≤2.5 small blocks (≤100 milliseconds) will be used as the normal P wave duration in this text.
· Right atrial enlargement: The right atrium enlarges downward and to the right causing the direction of the sinus impulse to slightly shift to the right of +60°. This causes the P waves to be taller and more peaked in leads II, III, and aVF. Thus the P wave in lead III is usually taller than the P wave in lead I (P3 > P1). In V1 and V2, the initial portion of the P wave may increase in amplitude, although the terminal portion representing left atrial activation is not affected. Because the right atrium is activated earlier than the left atrium, any delay in activation of the atria due to enlargement of the right atrium will coincide with activation of the left atrium. Thus, the duration of the P wave is not prolonged.
· Enlargement of the right or left atrium occurring independently is rare. It is usually associated with disease of the valvular structures or the ventricles. The most common cause of right atrial enlargement without left atrial enlargement in the adult population is pulmonary disease. Thus, the tall, narrow, and peaked P wave of right atrial enlargement is often described as “P-pulmonale.” Right atrial enlargement can be due to tricuspid or pulmonary valve disease, pulmonary hypertension, acute pulmonary embolism, and right ventricular failure or hypertrophy from varied causes.
· Enlargement of either atria predisposes to atrial arrhythmias, especially atrial flutter or atrial fibrillation. It is uncommon for atrial flutter or fibrillation to become sustained and self-perpetuating unless the atria are enlarged or diseased.
· When the lungs are hyperinflated because of emphysema, the diaphragm is pushed downward. The right atrium may also be displaced downward. When this occurs, the P wave in V1 may become totally inverted because the diaphragm and the heart are pushed vertically downward while the standard location of the V1 electrode remains unchanged at the 4th intercostal space to the right of the sternum. The inverted P wave may be mistaken for an enlarged left atrium.
· Right atrial enlargement is due to volume or pressure overload within the right atria. This causes the right atrial size to increase. Right atrial enlargement is recognized at bedside by the presence of distended neck veins. When the patient is semirecumbent at an angle of 45°, and the neck veins are distended above the clavicle, the pressure in the right atrium is elevated.
Figure 7.5: Left Atrial Enlargement. The duration of the P wave is prolonged measuring >2.5 mm in leads I, II, or aVF, with a bifid or M-shaped configuration. This type of P wave is called “P-mitrale.” In lead V1, the P wave may be totally inverted or it may be biphasic. The inverted portion is broad and deep measuring ≥1 mm wide and ≥1 mm deep.
Treatment and Prognosis
· The treatment and prognosis of right atrial enlargement will depend on the etiology of the right atrial enlargement.
Left Atrial Enlargement
· Left atrial enlargement: The ECG changes of left atrial enlargement are best reflected in the terminal half of the P wave because the right atrium is activated earlier than the left atrium. The ECG features of left atrial enlargement are summarized in Figure 7.5.
o Frontal plane:
§ Axis: The axis of the P wave is shifted to the left, thus the P waves are taller in lead I than in lead III (P1 > P3).
§ Contour: The contour of the P wave is bifid or “M” shaped. The first hump represents activation of the right atrium and the second hump represents activation of the left atrium. These two humps are separated by at least one small block and are best seen in leads I, II, aVF, V5, and V6. This type of P wave is often called “P-mitrale,” indicating that at some time in the past, mitral stenosis is the most common cause of left atrial enlargement.
§ Amplitude: The height or amplitude of the P wave is not significantly increased.
§ Duration: The duration or width of the P wave is increased and should measure >2.5 mm (>100 milliseconds).
o Horizontal plane:
§ In lead V1, the P wave is biphasic or inverted. The inverted portion measures ≥1 mm in depth and ≥1 mm (0.04 seconds) in duration.
The left atrium enlarges to the left and posteriorly shifting the P wave axis to the left of +45°. The P wave abnormalities are best seen in leads I, II, aVF and V1 (Figs. 7.6 and 7.7).
· Bi-atrial enlargement:When both atria are enlarged, the criteria for right atrial and left atrial enlargement are both present because the atria are activated separately (Fig. 7.8).
o Frontal plane: In the frontal plane, the P waves are tall measuring >2.5 mm because of right atrial enlargement. At the same time, the P waves are broad, notched, or M-shaped measuring >2.5 mm wide from left atrial enlargement. These changes are best seen in leads I, II, and aVF (Fig. 7.9).
Figure 7.6: Left Atrial Enlargement. The left atrium enlarges to the left and posteriorly. Because activation of the atria is sequential, starting from right atrium to left atrium, the duration of the P wave is prolonged. The P waves are not only wide but are notched in leads I, II, and aVF. The terminal portion is inverted in lead V1. S, superior; I, inferior; R, right; L, left; A, anterior; P, posterior; RA, right atrium; LA, left atrium.
o Horizontal plane: In the horizontal plane, the P wave in V1 is biphasic or inverted. The initial positive portion is usually peaked due to right atrial enlargement and the terminal negative portion is ≥1 mm wide and ≥1 mm deep from left atrial enlargement.
Figure 7.7: Left Atrial Enlargement. The P waves are wide in leads I, II, III, and aVF as well as several other leads. The configuration of the P wave is M-shaped (P-mitrale). The P wave is negative in V1. The negative deflection measures at least 1 × 1 (1 mm wide and 1 mm deep).
Figure 7.8: Bi-atrial Enlargement. Bi-atrial enlargement is characterized by tall and broad P waves measuring >2.5 mm in height and >2.5 mm in duration. In V1, the P wave is biphasic or inverted. The initial portion may be peaked due to right atrial enlargement. The inverted portion is broad and deep measuring ≥1 mm wide and ≥1 mm deep because of left atrial enlargement.
· Intra-atrial block: According to an ad hoc working group organized by the World Health Organization and International Society and Federation in Cardiology, the P wave duration should not exceed 0.11 seconds in the adult. The normal cutoff for the P wave duration, however, varies among authors. Increased duration of the P wave implies that there is intra-atrial block that may be due to left atrial enlargement but can also be caused by scarring or fibrosis of the atria.
Figure 7.9: Electrocardiogram of Bi-atrial Enlargement. The P waves are peaked and wide. In leads II and aVF, the P waves are >2.5 mm tall and >2.5 mm wide (>100 milliseconds in duration). In V1, the P waves are terminally negative and are 1 mm wide and 1 mm deep.
· Left atrial enlargement: In left atrial enlargement, the P wave duration is always prolonged because of intra-atrial block or prolonged atrial conduction. Increased left atrial pressure or volume is not always present. Thus, left atrial abnormality may be a better terminology to describe the P wave changes associated with left atrial enlargement.
· A 12-lead ECG is shown in Figure 7.10. The P waves are notched with an M-shape configuration in lead II. The P wave measures >2.5 mm wide with both peaks separated by one small block. The configuration of the P wave is consistent with “P-mitrale.” The P wave in V1 is not deep or wide. Although there is intra-atrial block, not all the P wave changes satisfy the criteria for left atrial enlargement.
Figure 7.10: Intra-atrial Block. Any sinus P wave that is prolonged, measuring >2.5 blocks is intra-atrial block. This could be due to left atrial enlargement, but could also be due to other causes. Leads II and V1 are enlarged so that the P waves are better visualized.
Left Atrial Enlargement
ECG of Left Atrial Enlargement
· The duration of the P wave is increased in leads I, II, or aVF. The P waves are often notched with M shape pattern measuring >2.5 mm in width or >100 milliseconds in duration.
· Terminally inverted P waves in V1 measuring ≥1 mm in depth and ≥1 mm in duration.
· When there is left atrial enlargement, the initial portion of the P wave representing right atrial activation is not altered. The terminal portion representing left atrial activation becomes longer, resulting in a broader P wave. Thus, the total duration of the P wave is prolonged. The general direction of the P wave is slightly altered becoming more horizontal at 20° to 40°. Thus, the P wave in lead I is taller than the P wave in lead III (P1 > P3). The P wave abnormalities are best seen in lead II and often in leads I and aVF and precordial leads V5and V6. The P wave is frequently bifid with two separate humps, at least 0.04 seconds apart. The first hump represents right atrial activation and the second hump represents activation of the enlarged left atrium. Because mitral valve disease is a common cause of left atrial enlargement, the notched and M-shaped P wave of left atrial enlargement is described as “P-mitrale.”
· Because the left atrium is oriented to the left and posterior to that of the right atrium, an enlarged left atrium will cause the terminal forces of the P wave to be directed to the left and posteriorly. In V1, the terminal portion, which represents left atrial activation, will be oriented more posteriorly than normal, causing the P wave to be broad and deep measuring at least 1 mm wide and 1 mm deep equivalent to one small box.
· Primary disease involving the left atrium alone is rare. Enlargement of the left atrium, therefore, is secondary to abnormalities involving the mitral valve or the left ventricle including mitral stenosis or insufficiency, left ventricular systolic, or diastolic dysfunction from several causes such as hypertension, coronary artery disease, cardiomyopathy, and aortic valve disease.
· Left atrial enlargement is a common finding in patients with left ventricular hypertrophy (LVH). The presence of left atrial enlargement is one of the criteria for the ECG diagnosis of LVH.
· Because the atria are activated circumferentially, and the electrical impulse travels through the length of the atrial wall, “enlargement” is preferred over “hypertrophy” when describing the presence of atrial enlargement. The P wave changes in the ECG do not reflect thickening or hypertrophy of the atrial wall, but rather, increase in the dimension of the atrial cavity or prolonged conduction in the atria from intra-atrial block. Additionally, when pulmonary hypertension occurs from pulmonary embolism or heart failure, the P wave changes can occur acutely. It can also regress acutely when the pulmonary pressure resolves, which is unlikely if the changes are due to atrial hypertrophy. This is in contrast to the ventricles, where electrical activation is from endocardium to epicardium. The changes in the QRS complex represent increased left ventricular mass or thickness. Thus, either “enlargement” or “hypertrophy” is appropriate in describing the increased ventricular mass, whereas atrial enlargement or atrial abnormality is more appropriate in describing the changes in the atria.
Treatment and Prognosis
· Left atrial enlargement is most often associated with abnormalities of either the mitral valve or left ventricle. The treatment and prognosis will depend on the underlying cause of the left atrial enlargement.
Left Ventricular Hypertrophy
· LVH: The sensitivity of the ECG in detecting LVH is limited; thus, several criteria have been proposed. Most of these ECG abnormalities are based on increased voltage of the QRS complex from increased mass of the left ventricle when there is LVH. These changes include the following (see Figs. 7.11 and 7.12).
Figure 7.11: Left Ventricular Hypertrophy. Twelve-lead electrocardiogram showing left ventricular hypertrophy. The P wave in V1is 1 mm wide and 1 mm deep because of left atrial enlargement. The voltage of the QRS complex is increased with deep S waves in V1 and tall R waves in V5 and V6. ST depression with T wave inversion is present in leads with tall R waves (LV strain).
o Abnormalities in the QRS complex
§ Deep S waves in V1 or V2 measuring >30 mm
§ Tall R waves in V5 or V6 measuring >30 mm
§ S in V1 + R in V5 or V6 >35 mm
§ Tall R waves in aVL measuring >11 mm
§ Tall R or deep S in any limb lead >20 mm
§ R in aVL + S in V3 >28 mm (men) and >20 mm (women)
§ The total amplitude of the QRS complex exceeds 175 mm in all 12 leads
§ Onset of intrinsicoid deflection >0.05 seconds in V5 or V6
§ Increased duration of the QRS complex >0.09 seconds
§ Left axis deviation ≥-30°
o Abnormalities in the P wave
§ Left atrial abnormality
o Abnormalities in the ST segment and T wave
§ ST depression and T inversion in leads with tall R waves (left ventricular strain)
· Increased voltage of the QRS complex: The voltage of the QRS complex is increased when there is LVH. Unfortunately, the amplitude of the QRS complex may not be a reliable marker of LVH because it can be altered by several factors other than increased thickness of the left ventricular wall.
o LVH without increased voltage: Patients with LVH may not exhibit any increase in QRS voltage because of obesity, peripheral edema, anasarca, increased diameter of the chest, lung disease especially emphysema, large breasts, biventricular hypertrophy, amyloidosis, pericardial effusion, pleural effusion, and hypothyroidism.
Figure 7.12: Left Ventricular Hypertrophy. Diagrammatic representation of the different electrocardiogram changes in left ventricular hypertrophy.
o Increased voltage not resulting from LVH: Conversely, increased voltage of the QRS complex may be present even in the absence of LVH in adolescent boys, anemia, left mastectomy, and in thin individuals.
· Left atrial abnormality: Enlargement of the left atrium is included as one of the diagnostic hallmarks of LVH. During diastole when the mitral valve is open, the left atrium and left ventricle behave as a common chamber. Thus, changes in pressure and volume in the left ventricle are also reflected in the left atrium.
Figure 7.13: Intrinsicoid Deflection. The ventricular activation time (VAT) is measured from the onset of the QRS complex to the top of the R wave. The intrinsicoid deflection is represented by the immediate downward deflection of the R wave toward baseline (A). When there is left ventricular hypertrophy, the onset of the intrinsicoid deflection (dotted lines in A and B) is delayed in V5 or V6. When there is right ventricular hypertrophy, the onset of the intrinsicoid deflection is delayed in V1 or V2.
· Ventricular activation time: Ventricular activation time represents the time it takes for the ventricular impulse to arrive at the recording electrode and is measured from the onset of the QRS complex to the top of the R or R′ wave (Fig. 7.13A, B). The thicker the myocardium, the longer it takes for the impulse to travel from endocardium to epicardium. Thus, when there is LVH, the ventricular activation time of leads overlying the left ventricle (V5 or V6) is prolonged (>0.05 seconds).
· Intrinsicoid deflection: The intrinsicoid deflection corresponds to the time that the depolarization wave has arrived at the recording electrode and is represented by the sudden downward deflection of the R wave toward baseline. If there is LVH, the onset of the intrinsicoid deflection in leads V5 or V6 is delayed (Fig. 7.13B).
· Abnormalities in the ST segment and T wave: Because depolarization of the left ventricle is abnormal, repolarization is also abnormal resulting in ST segment depression and T wave inversion in leads with tall R waves. Left ventricular strain is frequently used to describe this pattern of ST depression and T wave inversion (Fig. 7.12).
· LVH is a compensatory mechanism in response to both pressure and volume overload.
o Pressure overload: LVH from pressure overload is usually due to systemic hypertension, aortic stenosis, coarctation of the aorta, or hypertrophic obstructive cardiomyopathy. When there is pressure or systolic overload, the left ventricle becomes concentrically hypertrophied. The walls of the left ventricle are thickened although the size of the left ventricular cavity remains normal. The ECG shows tall R waves in V5 and V6 associated with depression of the ST segment and inversion of the T wave. These ST-T changes are often described as due to left ventricular “strain” (Figs. 7.11 and 7.12).
o Volume overload: This type of LVH is due to increased volume of the left ventricle as would occur when there is mitral regurgitation, aortic regurgitation, ventricular septal defect, peripheral arteriovenous shunts, anemia, and thyrotoxicosis. When there is volume or diastolic overload, the left ventricle becomes eccentrically hypertrophied. The left ventricular cavity becomes dilated. There is also increased left ventricular mass. The ECG shows prominent Q waves, tall R waves, and tall and upright T waves in V5 and V6(Fig. 7.14).
Figure 7.14: Left Ventricular Hypertrophy from Volume Overload. Twelve-lead electrocardiogram (ECG) showing tall voltage measuring >45 mm in V5 and >25 mm in V6 combined with prominent Q waves and tall T waves. This pattern of LVH is usually due to volume overload. This ECG is from a 55-year-old man with sickle cell anemia with gross cardiomegaly by chest x-ray.
· LVH associated with left ventricular strain is more common than LVH from volume overload because hypertension is the most common cause of LVH.
The ECG of LVH
· Several ECG criteria have been used in the diagnosis of LVH. These include:
o Increased amplitude or voltage of the QRS complex
§ Limb leads
§ R wave in any limb lead measuring ≥20 mm
§ S wave in any limb lead measuring ≥20 mm
§ R wave in aVL >11 mm
§ R in lead I + S in III >25 mm
§ Precordial leads
§ S wave in V1 or V2 ≥30 mm
§ R wave in V5 or V6 ≥30 mm
§ R wave in V5 or V6 >26 mm
§ S wave in V1, V2 or V3 ≥25 mm
§ R wave in V4, V5 or V6 ≥25 mm
§ SV1 + RV5 or V6 >35 mm
§ Tallest S + tallest R in V1 to V6 >45 mm
§ R wave in V6 > R wave in V5
§ Limb + Precordial leads
§ R wave in aVL + S wave in V3 >20 mm in females
§ R wave in aVL + S wave in V3 >28 mm in males
§ Total QRS voltage from all 12 ECG leads >175 mm
o Increased duration of the QRS complex
§ Delayed onset of intrinsicoid deflection ≥0.05 seconds in V5 or V6
§ Increased duration of the QRS complex ≥0.09 seconds
o Left atrial abnormality
§ Terminal negativity of the P wave in V1 measuring 1 mm × 1 mm
o Left axis deviation
o ST-T abnormalities indicating left ventricular strain in V5 or V6
§ ST segment depression
§ T wave inversion
The following are the criteria that are frequently used in the diagnosis of LVH.
· Sokolow-Lyon Index: This is the most commonly used criteria for the diagnosis of LVH.
o R in V5 or V6 + S in V1 = >35 mm
o R in aVL >11 mm
· Romhilt and Estes:
o 3 points each
§ P wave from left atrial abnormality
§ Any increase in voltage of the QRS complex
§ R or S in limb lead = ≥20 mm
§ S in V1 or V2 = ≥30 mm
§ R in V5 or V6 = ≥30 mm
§ ST-T abnormalities
§ Any shift in the ST segment (without digitalis) = 3
o 2 points
§ Left axis deviation of ≥-30°
o 1 point each
§ Slight widening of the QRS complex of ≥0.09 seconds
§ Intrinsicoid deflection in V5 or V6 of ≥0.05 seconds
§ ST-T abnormalities with digitalis
Score of ≥5 points = LVH; score of 4 points = probable LVH
· Cornell voltage criteria:
o R in aVL + S in V3 = >28 mm in men and >20 mm in women.
· Cornell product:
o Cornell voltage multiplied by the QRS duration in milliseconds = >2,440 milliseconds. (In women, 6 mm is added to Cornell voltage.)
· Total QRS voltage:
o Total QRS voltage or total amplitude of the QRS complex obtained from all 12 leads. The normal voltage averages 129 mm (range, 80 to 185 mm) with 175 mm as the upper limits of normal.
· Increased voltage of the QRS complex: Increased voltage of the QRS complex is frequently used as one of the criteria for LVH. When the ventricles are activated, the free walls of both ventricles (vector 2) are activated simultaneously from endocardium to epicardium. These forces occur in opposite directions and cancel out. Because the left ventricle is normally thicker than the right ventricle, the left ventricle continues to undergo electrical activation even after activation of the right ventricle is completed. Therefore, activation of the left ventricle continues unopposed. This vector corresponds to the main axis of the QRS complex and is oriented to the left and posteriorly. Tall R waves are normally recorded in leads V5-6 and deep S waves are recorded in lead V1 and often in V2. When there is left ventricular hypertrophy, these findings become exaggerated. The R waves become taller in left sided leads V5, V6, and aVL. Right-sided chest leads such as V1 and V2, will record deep S waves. When there is respiratory variation, the largest deflection is selected to represent the magnitude of the QRS complex.
o Pressure overload: LVH from increased systolic pressure can occur when there is aortic or subaortic obstruction or when there is systemic hypertension. This type of LVH is often called pressure overload or systolic overload and is usually characterized by the presence of a thick left ventricle with normal cavity dimension. R waves are tall in the left sided chest leads V5 or V6 and deep S waves are present in right-sided chest leads V1 or V2. The ST segments are depressed and T waves are inverted in leads with tall R waves. These ST-T abnormalities are frequently described as left ventricular strain. This type of LVH is associated with a high systolic pressure.
o Volume overload: LVH can also be due to volume overload such as valvular regurgitation, ventricular septal defect, patent ductus arteriosus, and other extracardiac leftto-right shunts. This type of LVH is often called volume overload or diastolic overload and is usually characterized by the presence of a dilated left ventricular cavity. Prominent Q waves are present in leads with tall R waves such as V5 and V6 accompanied by tall rather then inverted T waves.
· Left atrial abnormality: LVH is frequently associated with enlargement of the left atrium. When there is LVH, there is increased left ventricular end diastolic pressure or volume. This will also increase left atrial pressure or volume because the left atrium and left ventricle behave as common chamber when the mitral valve is open during diastole.
· Prolonged ventricular activation time: The ventricular activation time represents the time it takes for the impulse to activate the myocardium below the recording electrode. The thicker the myocardium, the longer it takes for the electrical impulse to travel from endocardium to epicardium. This is measured from the onset of the QRS complex to the top of the R wave. Thus, the electrodes overlying the left ventricle, such as leads V5 or V6, will record a longer ventricular activation time of >0.05 seconds when there is LVH.
· Delayed onset of the intrinsicoid deflection: The intrinsicoid deflection represents that moment in time that the impulse has reached the epicardium and is represented as a downward deflection of the R wave toward baseline. The onset of the intrinsicoid deflection signals that the whole myocardium below the recording electrode has been fully activated. Because the ventricular activation time is prolonged when there is LVH, the onset of the intrinsicoid deflection in V5 or V6 is also delayed.
· Increased duration of the QRS complex: When there is LVH, left ventricular mass is increased; thus, activation of the left ventricle will take longer. When LVH is present, the duration of the QRS complex is increased. The QRS is widened not only because of the increased muscle mass or increased ventricular activation time but intraventricular conduction delay may be present.
· Left axis deviation ≥-30°: Left axis deviation may occur when there is LVH because of increased muscle mass resulting in a more horizontal axis of the QRS complex. Additionally, LVH is frequently associated with left anterior fascicular block or incomplete left bundle branch block, which can shift the QRS axis more markedly to the left.
· ST and T wave abnormalities: The ST segment and T wave represent ventricular repolarization corresponding to phases 2 and 3 of the transmembrane action potential, respectively. Normally, when the ventricles are activated, repolarization begins immediately. During phase 2, corresponding to the ST segment, the electrical potential is normally maintained at almost 0 potential for a sustained duration; thus, there is no deflection recorded in the ECG. The T wave is inscribed only when sufficient potential is generated during repolarization corresponding to the down slope or phase 3 of the transmembrane action potential.
o ST depression: When there is LVH, ventricular activation is prolonged. Repolarization begins in some areas of the ventricle even before the whole myocardium is completely depolarized. This allows repolarization to occur relatively earlier than usual, which can reach sufficient magnitude to cause downward deviation of the ST segment in leads with tall R waves.
o T wave inversion: The T wave in LVH is inverted and is opposite in direction to that of the QRS complex. This implies that depolarization and repolarization of the myocardium occur in the same direction, which is the opposite of normal. The prolonged activation time of the thickened left ventricle allows the endocardium to recover earlier even before the whole thickness of the myocardium is completely depolarized. Thus, repolarization proceeds from endocardium to epicardium, resulting in depression of the ST segment and inversion of the T waves in leads with tall R waves. Additionally, when the left ventricle is thickened, the myocardium may outstrip its normal blood supply even in the absence of occlusive coronary disease. Thus, the whole thickness of the left ventricle becomes relatively ischemic. The endocardium, which is the first to be depolarized, will recover earlier because it had a longer time to recover.
· Although LVH is a physiologic response to pressure or volume overload, it is a marker of increased cardiovascular morbidity and is a known risk factor for sudden cardiovascular death. The presence of LVH may be a predictor of LV dysfunction within 5 years after its detection.
· Hypertension is the most common cause of LVH. In hypertensive patients, LVH occurs as a compensatory adaptation from pressure overload. LVH due to hypertension can regress with antihypertensive medications. All antihypertensive medications are generally effective in regressing LVH except hydralazine and minoxidil. There is clinical evidence to show that regression of LVH in patients with hypertension reduces cardiovascular events. A baseline ECG therefore is standard examination in patients initially diagnosed with hypertension.
· The several ECG criteria proposed for the diagnosis of LVH suggest that none of these criteria is optimal. The sensitivity of the ECG in diagnosing LVH is relatively poor and is <50%. However, when LVH is diagnosed by ECG, the specificity is high and is approximately ≥90%. The diagnosis of LVH in the ECG is primarily dependent on the presence of increased voltage. Unfortunately, voltage can be affected by many conditions other than LVH. The echocardiogram is more sensitive and more specific than the ECG for the detection of LVH, but is less readily available and much more expensive. The ECG remains the procedure of choice and is the most important modality in detecting LVH in patients with hypertension.
· When there is LVH, physical examination will show the following findings:
o Normal apical impulse: The apex of the heart is normally occupied by the left ventricle. The apex impulse, which is the lowest and most lateral cardiac impulse in the precordium, is due to left ventricular contraction and normally occupies <2 cm (the size of a quarter) and confined to only one intercostal space. In some patients, the apex impulse may not be palpable.
o Concentric LVH:When the left ventricle is concentrically hypertrophied, the left ventricular cavity is not enlarged and the apex impulse is not displaced. The area occupied by the apex impulse, however, becomes wider measuring about 2 to 3 cm or more in diameter, thus occupying an area that may involve two intercostal spaces. Furthermore, the apex impulse becomes more sustained and longer in duration compared with the short precordial tap that is normally expected when the left ventricle is not hypertrophied. A prominent 4th heart sound is usually audible if the patient is in normal sinus rhythm, which may be palpable as a prominent outward pulsation at the apex before systole. This is better appreciated when the patient is lying in lateral decubitus position.
o Eccentric LVH:When there is eccentric LVH, the left ventricular cavity is dilated. The apex impulse is displaced laterally and downward and may reach the 6th or 7th intercostal space at the left anterior axillary line. The precordial impulse becomes more diffuse involving a wider area in the precordium.
Figure 7.15: Right Ventricular Hypertrophy. There is right axis deviation, the QRS complexes are tall in V1 and P waves are peaked in II and aVF. This pattern of right ventricular hypertrophy is described as type A and is frequently seen in severe right ventricular hypertrophy often associated with congenital heart disease or severe mitral stenosis.
Treatment and Prognosis
· LVH detected by ECG is a risk factor for increased cardiovascular death. When ECG changes of LVH occur, the risk for cardiovascular morbidity and mortality increases, and the risk is even higher when ST and T wave abnormalities are also present. The treatment and prognosis of patients with LVH will depend on the etiology of the LVH. In patients with hypertension, regression of LVH with antihypertensive agents is possible. There are clinical data to show that regression of LVH in patients with hypertension decreases mortality and morbidity from cardiovascular death.
Right Ventricular Hypertrophy
· Right ventricular hypertrophy: Right ventricular hypertrophy (RVH) is recognized in the ECG by the following findings (Fig. 7.15).
o Abnormalities in the QRS complex
§ Right axis deviation of approximately ≥90°. This should always be present before the diagnosis of RVH is considered.
§ qR complex in V1
§ R wave measuring ≥7 mm in V1
§ R wave taller than the S wave in V1 (R/S ratio ≥1)
§ Delayed onset of the intrinsicoid deflection in V1 >0.03 seconds
§ rS complex from V1 to V6 with right axis deviation
§ S1 S2 S3 pattern in adults
o Abnormalities in the P wave
§ Right atrial abnormality (P-pulmonale)
o Abnormalities in the ST segment and T wave
§ ST segment depression and T wave inversion in anterior precordial leads (V1 and V2)
· In adult patients, the thickness of the right ventricle seldom exceeds that of the left ventricle even when RVH is present. Because both ventricles are activated simultaneously, the forces generated by the right ventricle are masked by the forces generated by the left ventricle. Thus, the diagnosis of RVH by ECG may be difficult unless the right ventricle is severely hypertrophied.
· Types of RVH: The ECG manifestations of RVH may be different. Three different types have been described: types A, B, and C (Fig. 7.16).
Other Patterns of RVH
· Chronic pulmonary disease: When there is chronic obstructive pulmonary disease such as emphysema or chronic bronchitis, the overinflated lungs push the diaphragm downward, causing the heart to become vertically oriented. When this occurs, the axes of the P wave, QRS complex, and T wave are all shifted rightward and inferiorly toward lead aVF (90°), resulting in the so called “lead I sign.” Because lead I (0°) is perpendicular to lead aVF, lead I and often V6 will conspicuously show small deflections (Fig. 7.17) because the P, QRS, and T waves become isoelectric in these leads. The ventricles also rotate in a clockwise fashion, causing poor R wave progression and delay in the transition zone. Other signs of type C RVH like right axis deviation and P-pulmonale are usually present.
· S1 S2 S3 pattern: S1 S2 S3 pattern implies that S waves are present in leads I, II, and III. When the S1 S2 S3 pattern is present, the direction of the mean QRS axis is superior and to the right, away from leads II and aVF. This brings the main axis of the QRS complex to the northwest quadrant, as shown in the ECG in Figure 7.18. S1 S2 S3 pattern is not specific for RVH because it can occur normally in young children without any evidence of RVH or cardiac disease. In older individuals, this pattern is suggestive of RVH, especially when other signs of RVH such as right atrial enlargement (P-pulmonale) or prominent R waves are present in V1. Additionally, the size of the S waves in leads I, II, and III are usually deeper than the size of the R waves.
Figure 7.16: Right Ventricular Hypertrophy. Three types of right ventricular hypertrophy (RVH) are shown. (A) Type A RVH. (B) Type B RVH. (C) An example of type C RVH.
Acute Pulmonary Embolism
· Acute pulmonary embolism: Acute pulmonary embolism may also result in acute right heart strain (Fig. 7.19). Most patients with acute pulmonary embolism are usually ill and restless and are therefore tachypneic and tachycardic. Sinus tachycardia and incomplete right bundle branch block are the most frequent ECG findings. The following are the ECG changes of acute pulmonary embolism.
§ Sinus tachycardia, atrial flutter, or atrial fibrillation
o Changes in the QRS complex:
§ Right axis deviation of approximately ≥90°
§ S1 Q3 T3 pattern (S wave in lead I, Q with inverted T wave in III)
§ rSR′ pattern in V1 usually of acute onset
§ V1 may also show QS, qR, or R > S pattern
§ Clockwise rotation with persistent S in V6 similar to type C RVH
Figure 7.17: Chronic Obstructive Pulmonary Disease. In chronic obstructive pulmonary disease, the heart is vertically oriented because of the hyperinflated lungs pushing the diaphragm downward. This causes the P, QRS, and T deflections to be oriented vertically toward 90° resulting in the so called “lead I sign,” where all the deflections in lead I become conspicuous by their diminutive appearance. This could also occur in V6, because V6 is also perpendicular in relation to lead aVF. In addition, the heart is rotated clockwise with peak P-pulmonale in II, III, and aVF. These changes are consistent with type C RVH.
o Changes in the P wave:
§ P-pulmonale with peaking of the P waves in leads II, III, and aVF
§ Ta waves become exaggerated in leads II, III, and aVF, causing 1 mm of ST depression in the inferior leads
o Changes in the ST segment and T waves
§ ST elevation in V1
§ Inverted T waves in V1 to V3 or up to V6
Figure 7.18: S1 S2 S3 Pattern. This pattern simply implies that an S wave is present in leads I, II, and III. The direction of the impulse is away from these leads and is usually at the northwest quadrant causing a tall R wave in aVR. S1 S2 S3 may suggest right ventricular hypertrophy in older individuals, especially when the P waves are peaked in lead II because of right atrial enlargement, when R waves are tall in V1, or the size of the S waves is deeper than the size of the R waves in all three leads.
Combined Ventricular Hypertrophy
· Biventricular hypertrophy: When both the right and left ventricles are hypertrophied, there is cancellation of the forces generated by both ventricles. Thus, the ECG may remain unchanged, and the diagnosis of biventricular hypertrophy is often difficult. Occasionally, the following ECG changes may be present as shown in Fig. 7.20.
o Tall biphasic complexes in mid-precordial leads: The transition leads V3 or V4 may show increased amplitude of the QRS complex with increased R waves combined with deep S waves (Katz-Wachtel phenomenon).
Figure 7.19: Acute Pulmonary Embolism. The electrocardiogram shows sinus tachycardia, right axis deviation ≤90°, S1Q3 T3 pattern, rR′ pattern in V1, and persistent S in the precordial leads extending to V6. These findings are usually acute in onset due to acute right heart strain.
Figure 7.20: Combined Ventricular Hypertrophy. When both ventricles are hypertrophied, the electrocardiogram changes of right and left ventricular hypertrophy cancel each other and may be difficult to diagnose. In this example, there is increased voltage of the QRS complex, especially over the transition zones V3 and V4, which shows tall R waves and deep S waves. There is also evidence of left ventricular hypertrophy and right atrial enlargement. Note also that there is voltage discordance, in that the precordial leads show tall voltages, whereas the limb leads that are bipolar leads have lower voltage.
o Right atrial enlargement combined with LVH: LVH by any standard criteria combined with P pulmonale as shown in Fig. 7.20.
o Voltage discordance: Biventricular hypertrophy may also manifest as voltage discordance between the limb and precordial leads. Precordial leads are unipolar leads and are closer to the heart than the limb leads. Thus, tall QRS complexes are recorded in the precordial leads, whereas the limb leads, which are further away especially bipolar leads I, II, and III, will record low voltages.
ECG Findings in RVH
Abnormalities in the QRS complexes
· Right axis deviation of approximately ≥90°. This should always be present before the diagnosis of RVH is considered.
· qR in V1
· R wave in V1 ≥7 mm
· Tall R waves in V1 or V2 (R/S ratio ≥1)
· Delayed intrinsicoid deflection in V1 or V2 >0.03 seconds.
· rS complex from V1 to V6 (clockwise rotation) with right axis deviation
· S1 S2 S3 pattern in adult patients
· rSR′ or RBBB in V1 with right axis deviation
Abnormalities in the P waves
· Peaked P waves in leads II, III and aVF (P-pulmonale) Abnormalities in the ST segment and T waves
o ST depression and T wave inversion in right sided precordial leads (V1)
o T wave inversion in V2 to V6
· Because of its thinner wall and smaller mass, the right ventricle does not contribute significantly to the generation of the QRS complex. Thus, when the ventricles are synchronously activated, the forces generated from the right ventricle are masked by those generated from the left ventricle. When there is RVH, the right ventricular wall becomes thickened and the right ventricular mass is increased, resulting in a larger contribution of the right ventricle in generating the QRS complex. In adults, the thickness of the right ventricle does not exceed that of the left ventricle even when RVH is present, thus the ECG changes of RVH continue to be masked by the forces generated by the thicker left ventricle. In certain types of congenital heart diseases, however, the RV wall is much thicker than the LV wall, such as in tetralogy of Fallot or in congenital pulmonary stenosis. When this occurs, the ECG findings of RVH become more obvious.
· Changes in the frontal or limb leads: RVH is better appreciated in the precordial leads than the limb leads because the precordial leads overlie the ventricles directly. Nevertheless, there are certain changes in the limb leads that may suggest RVH.
o Right axis deviation: Right axis deviation is one of the most reliable signs in the diagnosis of RVH. Because the right ventricle is anterior and to the right of the left ventricle, increase in right ventricular mass will shift the QRS axis to the right and anteriorly. Thus, the axis of the QRS complex is shifted toward 80° to 120° or further to the right when RVH is present. RVH is the most common cause of right axis deviation in the adult. The diagnosis of RVH is unlikely unless the axis of the QRS complex is shifted to the right.
o S1 S2 S3 pattern: This pattern simply means that there is an S wave in lead I, lead II, and lead III. The presence of S waves in these leads is due to the terminal forces of the QRS complex being oriented rightward and superiorly toward the northwest quadrant. This is due to activation of the posterobasal portion of the right ventricle terminally. The presence of S1 S2 S3, however, is not always diagnostic of RVH because it is also seen in normal healthy individuals, especially the younger age group. When there is S1 S2S3 pattern, RVH may be present when other changes in the QRS complex are present, such as tall R waves in V1, P-pulmonale, or when the S waves are deeper than the size of the R waves in all three leads.
o Abnormalities of the P wave: Right atrial enlargement is a frequent accompaniment of right ventricular enlargement. Thus, the presence of peaked P waves with increased amplitude (P-pulmonale), best recorded in leads II, III, and aVF suggest RVH unless the P wave changes are due to tricuspid stenosis, which is rare in adults.
· Changes in the precordial leads: Because the precordial leads are directly on top of the ventricles, more information is provided by these leads when compared with the more distal limb leads.
o Tall R waves in V1 or V2 with R/S ratio ≥1: Increased voltage in the right-sided precordial leads occur when there is increased thickness of the right ventricular wall. This will be recorded as tall R waves in V1 or V2 with R/S ratio ≥1. R/S ratio ≥1 means that the height of the R wave in V1 is equal to or higher in amplitude than the S wave, which is the reverse of normal in the adult population.
o rS complex from V1 to V6 with right axis deviation: This is also called clockwise rotation or delayed transition. Deep S waves or rS complex from V1 to V6 may be due to RVH or LVH. For RVH to be present there should also be right axis deviation. When RVH is present, the right ventricle rotates anteriorly, causing the left ventricle to rotate in a more posterior orientation. If the ventricles are viewed from below looking upward, the rotation of both ventricles will be clockwise when there is right ventricular enlargement. Because the precordial leads are recorded in their standard location from V1 to V6, the transition zone is not crossed unless the electrodes are moved to the left and more posteriorly. This type of RVH is frequently associated with chronic lung disease (type C RVH).
o Prolonged ventricular activation time with delayed onset of the intrinsicoid deflection in V1 or V2.When the ventricular activation time is prolonged, the onset of the intrinsicoid deflection is delayed. The ventricular activation time of the right ventricle is measured in V1 from the onset of the QRS complex to the peak of the R or R?Œ wave and represents the time required for the impulse to activate the right ventricular wall. The ventricular activation time of the right ventricle normally measures ≤0.03 seconds and is increased to ≥0.04 seconds when there is right ventricular hypertrophy. The onset of the intrinsicoid deflection, measured in V1 or V2, represents the time when the electrical impulse has reached the right ventricular epicardium and generally coincides with the peak of the R wave or immediately thereafter, when the R wave is deflected downward toward baseline.
· In adults, RVH can result from many different causes. RVH may be due to pressure overload such as pulmonic stenosis or primary pulmonary hypertension. This type of RVH predominantly results in increased thickness of the right ventricle. It may also be due to volume overload such as atrial septal defect and tricuspid or pulmonic regurgitations, resulting in volume overload with dilatation of the right ventricular cavity. RVH can also result from the presence of lung disease, which may distort the anatomical relationship between the heart and the chest wall. Or it may be due to left heart failure where an increase in left ventricular mass is associated with an increase in right ventricular mass. These changes may develop insidiously or abruptly, as when pulmonary hypertension occurs in the setting of acute pulmonary embolism. The ECG presentations of RVH, therefore, in these different clinical settings are not necessarily similar. Different patterns of RVH have been described which includes types A, B, and C based on the morphology of the QRS complex in the precordial leads. Types A and B are easy to recognize as RVH because the size of the R wave is taller than the S wave in V1, whereas in type C the size of the R wave is smaller than the S wave in V1 and may not be recognized as RVH. In all three types, the axis of the QRS complex is shifted to the right.
o Type A RVH: This is the most recognizable type of RVH. The R waves are tall in V1, often in V2 and V3. The R wave is usually monophasic (no S wave) in V1. If an S wave is present, the R wave is always taller than the height of the S wave with an R/S ratio >1. V5 and V6 may show deeper S waves than R waves. In type A RVH, the thickness of the right ventricle is greater than the thickness of the left ventricle, and the right ventricle is the dominant ventricle. This type of RVH is the most commonly recognized and is seen in severe pulmonic stenosis, primary pulmonary hypertension, or mitral stenosis with severe pulmonary hypertension. The axis of the QRS complex is significantly deviated to the right at approximately +120°.
o Type B RVH: The R wave in V1 is slightly taller than the S wave or the ratio between the R wave and S wave is ≥1. V1 may also exhibit an rsr′ pattern. The QRS complex in V5 and V6 is not different from normal. This type of RVH is usually due to atrial septal defect or mitral stenosis with mild to moderate pulmonary hypertension. The frontal axis is vertical at approximately 90°.
o Type C RVH: This type of RVH is difficult to recognize and is frequently missed because the R wave in V1 is not tall and is smaller than the S wave. Instead, a deep S wave is present in V1 and in V2 that extends up to V6. Thus, V1 to V6 will show rS complexes. In V6, the R wave continues to be smaller in amplitude than the S wave. The axis of the QRS complex is approximately 90° or less. This type of RVH is usually due to chronic obstructive lung disease but could also occur acutely as a manifestation of acute pulmonary embolism.
· Prolongation of the QRS complex usually does not occur when there is RVH because the thickness of the right ventricle wall usually does not exceed that of the left ventricle, even when RVH is present. Thus, the forces generated by the right ventricle are cancelled by the forces from the left ventricle. When widening of the QRS complex is present, there may be associated right bundle branch block because the right bundle branch is very susceptible to injury when there is increased right ventricular pressure.
· The right ventricle is to the right and anterior to that of the left ventricle. Pulsations from the right ventricle are not normally visible or palpable. However, when the right ventricle is enlarged or hypertrophied, a sustained systolic precordial impulse is palpable along the left parasternal area. Prominent “a” waves are seen in the neck veins. Very often, tricuspid regurgitation is also present causing a “cv” wave in the jugular neck veins accompanied by prominent pulsations of the liver or the ear lobes bilaterally. Third and fourth gallop sounds may also be audible along the lower left sternal border. Their right ventricular origin can be verified by increase in intensity of these gallop sounds with in spiration.
Treatment and Prognosis
· When RVH is present, the underlying cause should be evaluated. The treatment and prognosis will depend on the etiology of the RVH.
Ariyarajah V, Frisella ME, Spodick DH. Reevaluation of the criterion for interatrial block. Am J Cardiol. 2006;98:936-937.
Buxton AE, Calkins H, Callans DJ, et al. ACC/AHA/HRS 2006 key data elements and definitions for electrophysiological studies and procedures: a report of the American College of Cardiology/American Heart Association Task Force on clinical data standards (ACC/AHA/HRS writing committee to develop data standards on electrophysiology. J Am Coll Cardiol.2006;48:2360-2396.
Casale PN, Devereux RB, Alonso DR, et al. Improved sexspecific criteria of left ventricular hypertrophy for clinical and computer interpretation of electrocardiograms: validation with autopsy findings. Circulation. 1987;75:565-572.
Chow TC, Helm RA, Kaplan S. Right Ventricular Hypertrophy in Clinical Vectorcardiography. 2nd ed. New York: Grune and Stratton; 1974.
Conover MB. Chamber hypertrophy and enlargement. In: Understanding Electrocardiography. 8th ed. St. Louis: Mosby; 2003:407-419.
Devereux RB, Wachtell K, Gerdts E, et al. Prognostic significance of left ventricular mass change during treatment of hypertension. JAMA 2004;292:2350-2356.
Dunn MI, Lipman BS. Lipman-Massie Clinical Electrocardiography. Chicago: Yearbook Medical Publishers, Inc.; 1989.
Gardin JM, Lauer MS. Left ventricular hypertrophy: the next treatable silent killer. JAMA. 2004;292:2396-2398.
Haider AW, Larson MG, Benjamin EJ, et al. Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death. J Am Coll Cardiol. 1998;32:1454-1459.
Josephson ME, Kastor JA, Morganroth J. Electrocardiographic left atrial enlargement. Electrophysiologic, echocardiographic and hemodynamic correlates. J Am Coll Cardiol.1977;39:967-971.
Kligfield P, Gettes LS, Bailey JJ, et al. Recommendations for the standardization and interpretation of the electrocardiogram. J Am Coll Cardiol. 2007;49:1109-1127.
Marriott HJL. Chamber enlargement. In: Practical Electrocardiography. 5th ed. Baltimore: The William and Wilkins Company; 1972:56-66.
Mirvis DM, Goldberger AL. Electrocardiography. In: Zipes DP, Libby P, Bonow RO, et al., eds. Braunwald's Heart Disease, a Textbook of Cardiovascular Medicine. 7th ed. Philadelphia: Elsevier Saunders; 2005:118-125.
Nicholas WJ, Liebson PR. ECG changes in COPD: what do they mean? J Respir Dis. 1987;8:103-120.
Odom II H, Davis L, Dinh HA, et al. QRS voltage measurements in autopsied men free of cardiopulmonary disease: a basis for evaluating total QRS voltage as an index of left ventricular hypertrophy. Am J Cardiol. 1986;58:801-804.
Okin PM, Roman MU, Devereux RB, et al. Time-voltage QRS area of the 12-lead electrocardiogram: detection of left ventricular hypertrophy. Hypertension. 1998:31:937-942.
Okin PM, Devereux RB, Jern S, et al. Regression of electrocardiographic left ventricular hypertrophy during antihypertensive treatment and the prediction of major cardiovascular events.JAMA. 2004;292:2343-2349.
Romhilt DW, Estes EH Jr. A point-score system for the ECG diagnosis of left ventricular hypertrophy. Am Heart J. 1968;75:752.
Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J. 1949;37:161-186.
Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for intraventricular conduction disturbances and pre-excitation. J Am Coll Cardiol. 1985;5:1261-1275.