The Core Curriculum: Cardiopulmonary Imaging, 1st Edition (2004)

Chapter 20. Acquired Cardiac Disease

Heart disease is the leading cause of death in the United States. Patients with acquired heart disease can present with classic clinical syndromes, such as angina and myocardial infarction or with vague symptoms such as fatigue or shortness of breath. However, many patients with heart disease present with atypical clinical signs and symptoms or are entirely free of any sign of disease. Radiologists play a key role in making the initial diagnosis of heart disease in many cardiac patients. Imaging is also one of the most important tools used to assess the effectiveness of treatment of cardiovascular disease. In this chapter we cover the basic imaging features of adult acquired heart disease, with an emphasis on chest radiography. Table 20.1 provides an outline of topics covered.

Cardiac Valve Disease

Mitral Valve Disease

According to the American Heart Association 2000 statistical update (1), there were 40,000 hospital discharges secondary to mitral valve disease in the year 2000. Approximately 2,500 U.S. citizens died, and 6,100 other deaths involved mitral disease as a contributing factor. Pure mitral stenosis comprises 25% of all cases of mitral disease, pure insufficiency 37%, and combined mitral stenosis and insufficiency 39% (2). Postinflammatory disease (chronic fibrosis) commonly causes mitral stenosis, whereas floppy valve and inflammatory disease are the most common causes of mitral insufficiency.

Combined mitral stenosis and insufficiency is more common than isolated stenosis or isolated insufficiency.

The radiographic diagnosis of mitral valve disease centers on detection of a dilated left atrial chamber (Table 20.2). It should be mentioned, however, that the left atrial volume must increase more than 200% to be detected on radiography (3). The “double density” sign occurs in the frontal projection when the left atrial opacity projects through the right atrial outline (Fig. 20.1). The left atrium can be seen normally through the right atrium but should be considered enlarged when the distance between the right lateral margin of the left atrium and the bottom of the mid-point of the left main bronchus measures more than 7 cm (4). Focal enlargement of the left atrial appendage in the frontal view is an additional important sign of mitral disease (Fig. 20.2). The enlarged atrial appendage projects as a local bump along the left heart outline, below the level of the left main bronchus. This bump is often called the “fourth mogul,” because the enlarged appendage opacity is in addition to the normally found opacities of the aortic arch, left pulmonary artery, and lateral margin of the left ventricle. However, enlargement of the appendage is sometimes absent in left atrial dilatation. This lack of enlargement of the left atrial appendage sometimes indicates thrombosis of the appendage (5). The appendage is most commonly enlarged when the valve disease is rheumatic in origin and is less likely enlarged when the cause is nonrheumatic (6). In some patients the left main bronchus is displaced upward and backward, although this is not a very reliable sign (7). Posterior displacement of the upper posterior cardiac margin and carina or left lower lobe bronchus can also be seen in the lateral view (Fig. 20.3). Focal displacement of a barium-filled esophagus was used in the past, before introduction of echocardiography, to show left atrial enlargement (Fig. 20.4).

Left atrial volume must be twice that of normal to be detectable radiographically.

Focal left atrial appendage enlargement (the “fourth mogul” on a posteroanterior chest radiograph) should raise suspicion of mitral valve disease.

Table 20.1: Outline of Topics: Imaging of Adult Acquired Heart Disease

Valve disease
   Mitral
   Aortic
   Pulmonic and tricuspid
Myocardial disease
   Cardiomyopathy
   Myocarditis
Neoplastic disease
Pericardial disease
   Pericardial effusion
   Constrictive pericarditis
Coronary artery disease
   Coronary calcification
   Myocardial infarction

Table 20.2: Chest Radiograph Signs of Left Atrial Enlargement

Double density
Fourth mogul
Displaced left main and lower lobe bronchi
Posterior bulge of upper posterior cardiac outline
Displaced barium-filled esophagus

Figure 20.1 Posteroanterior chest radiograph of a 66-year-old patient with mitral valve stenosis. The left atrium can be seen as a hemispherical opacity (arrowheads) projecting through the right atrium, the so-called “double density” sign. The normal left atrium can be seen in some patients as a “double density.” To be called enlarged, the distance from the right lateral margin of the left atrium to the mid-point of the left main bronchus should measure more than 7 cm in most patients.

Figure 20.2 Posteroanterior chest radiograph of a 42-year-old patient with mitral valve stenosis. The left atrial appendage is enlarged, producing a localized bump (arrow) along the left heart margin, below the level of the left main bronchus. This bump is sometimes referred to as the “fourth mogul.” The other moguls represent the aortic arch, left pulmonary artery, and lateral margin of the left ventricle. The enlarged left atrium casts a double density behind the right atrium.

Figure 20.3 Lateral chest radiograph on the same patient with mitral stenosis shown in Fig. 20.1. The upper portion of the posterior margin of the heart, formed by the posterior wall of the enlarged left atrium, bulges posteriorly (arrowheads).

Mitral Valve Stenosis

The underlying functional abnormality in mitral valve stenosis relates to obstruction at the valve with a pressure gradient between the atrium and left ventricle. As a result of the obstruction left atrial pressure elevates, with corresponding elevation of the pulmonary venous, capillary, and arterial pressures. As capillary pressure rises, blood flow can redistribute from the bases into the upper portions of the lungs (“cephalization” or “redistribution”) (Fig. 20.5). Increased blood flow in the upper portions of the lungs produces increased diameters of arteries and veins in the upper lungs, with corresponding decreased sized vessels in the lung bases. This sign can be seen on occasion in upright patients, where blood flow ordinarily dominates in the dependent portions of the lungs. Cephalization of pulmonary blood flow can only be diagnosed in upright patients who have clear lungs at full inspiration. When pulmonary capillary pressure rises further, hydrostatic pressure in the capillary bed overcomes colloid osmotic pressure. Thus, fluid extravasates into the interstitium of the lungs, creating Kerley lines, linear opacities representing fluid in interlobular septa (Fig. 20.6). The left ventricle maintains a normal size in mitral stenosis.

Figure 20.4 51-year-old patient with mitral regurgitation. A. Posteroanterior chest radiograph shows the double density and fourth mogul signs of left atrial enlargement. B. Lateral radiograph shows posterior displacement (arrows) of the barium-filled esophagus by the enlarged left atrium. The carina is also displaced posteriorly (long arrow).

Figure 20.5 Posteroanterior chest radiograph of a 36-year-old patient with mitral stenosis. Pulmonary vessels in the upper portions of the lungs are relatively dilated compared with the lower portions of the lungs. This “redistribution” or “cephalization” of pulmonary blood flow indicates pulmonary venous hypertension secondary to elevated left atrial pressure. The enlarged left atrium is shown as a double density behind the right atrium, and there is a subtle convexity (arrow) along the left heart margin reflecting dilatation of the left atrial appendage.

Figure 20.6 Posteroanterior chest radiograph of a 45-year-old patient with severe mitral stenosis. View of the left lung shows Kerley B lines (arrows) and perihilar haze indicative of interstitial edema.

Right-sided chambers can enlarge secondary to chronic pulmonary arterial hypertension. Identification of mitral valve leaflet calcification can be helpful in diagnosing mitral valve stenosis, although large amounts of valve leaflet calcification are necessary for the calcific opacity to become visible on the lateral chest radiograph (Fig. 20.7). Most patients do not have enough calcification to be detected on radiographs. Valve calcification should be distinguished from the commonly seen “C-shaped” calcification of the mitral annulus (Figs. 20.8A and B). Calcification of the annulus is common in the elderly, possibly related to systemic atherosclerosis (8). Uncommonly, calcific deposits in the wall of the left atrium are shown on chest radiographs (Fig. 20.9) or computed tomography (CT) (Fig. 20.10). Left atrial wall calcification is often associated with a history of rheumatic fever, and the calcification is therefore likely due to rheumatic carditis (9). Mural thrombi in the left atrium can also calcify.

Figure 20.7 Lateral chest radiograph of a 73-year-old patient with mitral stenosis. There is heavy calcification in the mitral valve(arrows).

Figure 20.8 A. Posteroanterior chest radiograph of a 44-year-old patient with chronic renal failure, without valve disease, shows typical curvilinear calcification of the mitral annulus (arrows)B. 75-year-old patient with previous history of mitral and tricuspid valve repair. Lateral chest radiograph shows the prosthetic valve ring at the mitral position (arrow) surrounded by dense calcification (arrowheads) of the mitral annulus. A tricuspid valve ring is also shown (long arrow).

Mitral annulus calcification may be an indication of atherosclerosis but is not an indicator of mitral valve stenosis or insufficiency.

A calcified left atrial wall should raise suspicion of rheumatic mitral valvular disease.

Mitral Valve Insufficiency

Incompetence of the mitral valve can be due to a variety of pathologic conditions. Postinflammatory disease (usually rheumatic), floppy valve, ischemic heart disease, endocarditis, idiopathic rupture of chordae, and cardiomyopathy are etiologic possibilities. Chest radiographs show left atrial dilatation, and the degree of enlargement can be quite marked. In contrast with mitral stenosis, the left ventricle also dilates (Fig. 20.11). Left ventricular dilatation is due to the demand for increased left ventricular stroke volume in light of the regurgitant flow fraction. Redistribution of blood flow is uncommon in pure chronic mitral regurgitation, as is pulmonary edema, because left atria can be compliant with normal left atrial pressures (10). If heart failure occurs, redistribution and pulmonary edema can be seen on chest radiographs. Pulmonary edema is more apt to occur in acute mitral regurgitation due to ruptured chordae and acute ischemia of the papillary muscles, sometimes with atypical distribution of pulmonary edema predominating in the right upper lobe (Fig. 20.12) (11).

In mitral insufficiency, the left atrium and left ventricle are enlarged because of increased blood volume from the “regurgitated” blood. In contrast, only the left atrium is enlarged with mitral stenosis.

Figure 20.9 Posteroanterior chest radiograph of a 66-year-old patient with a Starr-Edwards valve placed for rheumatic mitral valve disease. Note the curvilinear calcification (arrowheads) outlining the lateral wall of the left atrium.

Figure 20.10 Computed tomography image of a 56-year-old patient who has had mitral valve replacement for mitral stenosis. Note the mural calcifications of the left atrium. An arrow points to the prosthetic valve.

Figure 20.11 A 78-year-old patient with chronic mitral regurgitation. A. Posteroanterior chest radiograph shows marked left atrial enlargement. The left atrial opacity behind the right atrium (double density) has a large diameter, and the left atrial appendage is also very large (arrow)B. Lateral chest radiograph shows enlargement of the upper posterior heart margin (arrows), representing the dilated left atrium. The inferior posterior margin of the heart, representing a dilated left ventricle (long arrows), is displaced posterior relative to the inferior vena cava (IVC).

Figure 20.12 Bedside anteroposterior chest radiograph of a 59-year-old patient with acute myocardial infarction. The patient had acute pulmonary edema secondary to papillary muscle rupture. The pulmonary edema predominates in the right lung, especially the upper portion of the right lung. This distribution of edema in the correct clinical setting should suggest the diagnosis of acute mitral valve regurgitation.

Aortic Valve Disease

The American Heart Association 2000 statistical update states that 11,600 patients died of aortic valve disease, with 24,000 having aortic valve disease mentioned as a contributing factor. There were 40,000 hospital discharges with this diagnosis. Most cases of aortic valve disease occur in conjunction with a congenital bicuspid valve or secondary to degenerative and postinflammatory diseases (12,13,14). As our population ages, the proportion of patients with a degenerative etiology is increasing (15,16).

Aortic Stenosis

The pathophysiology of aortic stenosis is based on outflow obstruction, left ventricular pressure overload, and increased myocardial wall thickness. Heart size remains normal until heart failure occurs, an ominous clinical sign. With concentric hypertrophy of the left ventricle, sometimes the left cardiac margin on the frontal view has a somewhat rounded configuration. However, the primary signs of aortic valve stenosis include poststenotic dilatation of the ascending aorta and aortic valve calcification (Fig. 20.13). Poststenotic dilation of the ascending aorta evolves with the chronic stress of a jet of blood flow that impacts the aortic wall. Calcification of the valve is common and increases with age. In fact, calcification in the aortic valve without any functional obstruction occurs in one in four or five patients over 65 years of age. The valve calcification is best seen on the lateral view, because the valve usually projects over the spine in the frontal projection. When calcification is observed on chest radiographs of younger individuals or is associated with signs and symptoms of heart failure, aortic stenosis should be suggested. Incidental observation of aortic valve calcification on chest CT occurs frequently and is usually clinically insignificant. However, abundant aortic valve calcification found on CT in patients less than 55 years of age should be considered possible aortic stenosis (17).

Aortic stenosis with left ventricular failure is a poor prognostic sign.

Aortic valve calcification is common in adults over 65 years of age. When seen in younger individuals, it should raise suspicion of aortic valvular stenosis.

Aortic Valve Insufficiency

Aortic valve insufficiency, or regurgitation, creates a volume load on the left ventricle. The causes of aortic insufficiency are listed in Table 20.3. Left ventricular stroke volume must increase to compensate for regurgitation to maintain normal forward cardiac output. By way of illustration, to maintain forward cardiac output of 5 L/min in a patient with 5 L/min of regurgitant flow, there would be a need for a left ventricular output of 10 L/min.

An enlarged left ventricle and ascending aorta should raise suspicion for aortic valvular insufficiency.

Figure 20.13 59-year-old patient with aortic valve stenosis. A. Posteroanterior chest radiograph shows abnormal protrusion of the right mediastinal outline (arrows) representing the margin of a dilated ascending aorta. Heart size is normal. The valve lies over the spine and valve calcification is obscured. B. Lateral chest radiograph shows dense calcification of the aortic valve (arrowheads).

The left ventricle dilates in cases of aortic valve insufficiency, and the thoracic aorta can dilate. The degree of aortic dilatation varies on chest radiography, but identification of left ventricular dilatation is necessary for radiologists to make a diagnosis of aortic regurgitation. The cardiac outline enlarges, and the apex in the frontal view is often displaced laterally and inferiorly toward the costophrenic angle (Fig. 20.14). In the frontal view the dilated ascending aorta can displace the mid-mediastinal outline to the right and the aortic arch can enlarge. In the lateral view, the left ventricle lies inferior and posterior relative to the other cardiac chambers. When dilated, the left ventricle projects more than 18 mm posterior to the inferior vena cava, often intersecting the diaphragm behind the inferior vena cava (18).

Aortic and mitral valvular disease commonly coexist. The valve leaflets are in direct physical continuity, permitting an inflammatory process such as rheumatic disease to involve both valves. This is known as Lutembacher syndrome.

Pulmonic and Tricuspid Valve Disease

The incidence of acquired disease confined to the pulmonic and tricuspid valves is low compared with mitral and aortic valve disease (Table 20.4). The American Heart Association 2000 statistical update reveals only 11 patient deaths due to primary disease of the right-sided cardiac valves (1). Most commonly, primary disease of the right-sided valves is due to rheumatic disease, almost always associated with disease also involving the left-sided cardiac valves. Carcinoid disease is uncommon and rarely recognized on radiographs (Fig. 20.15). Secondary disease of these valves due to pulmonary hypertension is more common (19).

Table 20.3: Causes of Aortic Valve Insufficiency

Idiopathic valve degeneration
Bicuspid aortic valve
Postinflammatory valve disease including rheumatic fever
Aortic dissection
Atherosclerotic aneurysm
Infection (bacterial, mycotic and syphilitic)

Figure 20.14 64-year-old patient with pure aortic valve insufficiency. A. Posteroanterior chest radiograph shows cardiac enlargement. The long axis of the heart (long arrow) elongates downwards toward the left costophrenic angle, a finding indicating left ventricular dilatation. The ascending aorta is dilated, presenting as a convex lateral border of the mid-right mediastinal contour (small arrows)B.Lateral chest radiograph shows posterior displacement of the inferior cardiac margin (arrows), projecting more than 18 mm behind the inferior vena cava (positive Rigler sign) (arrowheads). This configuration indicates left ventricular dilatation.

Pulmonary Hypertension

Pulmonary hypertension results in right atrial and ventricular pressure and/or volume overload, with enlargement of these chambers (Fig. 20.16). Pulmonic and tricuspid valve insufficiency are common sequelae (Fig. 20.17). Frontal chest radiographs show rounded enlargement of the left cardiac margin with upward displacement of the cardiac apex, representing right ventricular enlargement. Right atrial dilatation causes increased circumference and lateral displacement of the right cardiac margin. The pulmonary arteries are enlarged. The dilated right ventricle can be detected in the lateral view as fullness behind the sternum, although this is not a reliable radiographic sign (20).

Table 20.4: Causes of Acquired Pulmonic and Tricuspid Valve Disease

Primary disease
   Rheumatic
   Carcinoid syndrome
   Bacterial endocarditis
   Traumatic rupture
Secondary cause
   Pulmonary hypertension

 

Myocardial Disease

Cardiomyopathy

The American Heart Association reports that 29,000 patients died because of cardiomyopathy in 2000 (1). The diagnosis of cardiomyopathy was mentioned in the deaths of 53,000 individuals. The cardiomyopathies can be categorized by etiologic or functional classification schemes (Table 20.5).

Figure 20.15 61-year-old patient with carcinoid heart disease and tricuspid valve insufficiency. A. Posteroanterior chest radiograph shows normal heart size and configuration. B. Posteroanterior chest radiograph 2 months later after development of tricuspid insufficiency shows enlargement of the right atrium (arrows on left) and ventricle (arrow on right).

Figure 20.16 26-year-old patient with primary pulmonary hypertension. A. Posteroanterior chest radiograph shows rounding of the right heart margin representing a dilated right atrium. The cardiac apex is rounded and elevated secondary to right ventricular enlargement. The central pulmonary arteries are dilated. B. Lateral chest radiograph shows retrosternal fullness caused by the dilated right ventricle. The right atrium is not border forming in this view.

Figure 20.17 Computed tomography angiogram of a 56-year-old patient with pulmonary hypertension secondary to chronic pulmonary thromboembolism. The patient has pulmonic and tricuspid valve insufficiency. The right atrium (ra) and ventricle (rv) are dilated. The interventricular septum is flattened and left ventricle (lv) is displaced posteriorly because of pressure and volume overload.

Dilated Cardiomyopathy

Idiopathic dilated cardiomyopathy is a disease characterized by dilatation of both ventricles or of the left ventricle alone. The true incidence of this disease is difficult to determine, because many cases are unrecognized. The annual incidence is reported to be 36 cases per 100,000 in the United States annually, with 10,000 deaths (21). Almost half of the cases are “idiopathic,” although some investigators have implicated a viral-immune etiology in these cases. Secondary dilated cardiomyopathy can be caused by a variety of etiologies (22) (Table 20.6).

Table 20.5: Etiologic and Functional Classifications of the Cardiomyopathies

Etiologic classification
   Primary cardiomyopathy
      Pathologic process involving the myocardium, not affecting other organs
   Secondary cardiomyopathy
      Myocardial disease as one manifestation of systemic disease
Functional classification
   Dilated
      Characterized by dilated ventricles and systolic dysfunction
   Hypertrophic
      Inappropriate myocardial hypertrophy with preserved or enhanced contractile function
      Decreased wall compliance with resultant diastolic dysfunction
   Restrictive
      Infiltrative or noninfiltrative myocardial disease with normal systolic function
      Normal diastolic volumes but with stiff myocardium causing impaired ventricular filling

Pathology shows dilated cardiac chambers with normal or decreased wall thickness. The valves can be scarred, and the annuli of the mitral and tricuspid valves are often dilated. Symptoms of heart failure are usually evident, although some patients are diagnosed based on the incidental finding of cardiomegaly on chest radiography. Ninety-five percent of patients have advanced disease with severe symptoms of left-sided heart failure. Dangerous ventricular arrhythmias commonly are the cause of death in these patients, and many require placement of defibrillating devices. Prognosis is poor, as 50% of patients die within 5 years of initial diagnosis.

Table 20.6: Causes of Secondary Dilated Cardiomyopathy

Toxic
   Hydrocarbons (e.g., alcoholic)
   Drugs (e.g., chemotherapeutic agents, cocaine)
   Lead, cobalt, mercury
Inflammatory
   Connective tissue disease (e.g., scleroderma)
   Sarcoidosis
   Churg-Strauss
Neuromuscular
   Muscular dystrophy including Duchenne
   Friedrich ataxia
Metabolic
   Electrolyte abnormalities (e.g., hypocalcemia)
   Endocrine abnormalities (e.g., hypothyroidism)
   Nutritional deficiencies including thiamine
Miscellaneous causes
   Familial
   Hypertension
   Chronic ischemia
   Peripartum

Chest radiographs show generalized global cardiac enlargement (Fig. 20.18). Signs of heart failure are also commonly shown, including redistribution of pulmonary blood flow and interstitial pulmonary edema. Cross-sectional imaging can be used to characterize the morphology of the cardiac chambers and myocardium (Fig. 20.19). The diagnosis of dilated cardiomyopathy secondary to underlying disease such as sickle cell anemia can be suspected on chest radiographs (Chapter 13). The diagnosis is suspected on radiographs when there are typical osseous and cardiac abnormalities (Fig. 20.20).

Figure 20.18 Posteroanterior chest radiograph of a 35-year-old patient with idiopathic dilated cardiomyopathy. The cardiac chambers are diffusely dilated.

Figure 20.19 A, B. Sagittal black-blood proton-density magnetic resonance images of a 48-year-old patient with dilated cardiomyopathy. The ventricular chambers are dilated, and there is thinning of the myocardium.

Diffuse cardiac enlargement is the hallmark of dilated cardiomyopathy radiographically.

Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy is characterized by biventricular myocardial hypertrophy without chamber dilatation or associated causal factors such as hypertension (23). Many patients have asymmetric hypertrophy, with pronounced involvement of the interventricular septum. The disease can cause sudden death, often in patients under the age of 40. Left ventricular hypercontractility and diastolic dysfunction create vigorous emptying but poor compliance and chamber filling during diastole. Chest radiographs of adults most commonly show normal heart size, although on occasion there can be enlargement. Cardiac magnetic resonance imaging (MRI) can be helpful in diagnosis (24) (Fig. 20.21).

The heart may be normal size on radiographs in hypertrophic cardiomyopathy, because ventricular hypertrophy does not increase ventricle size (it decreases ventricular capacity).

Restrictive Cardiomyopathy

Restrictive cardiomyopathy results in diastolic dysfunction, with impaired filling of noncompliant ventricles. On cardiac catheterization, the physiologic changes are indistinguishable from constrictive pericarditis. Clinical symptoms can be due to right or left ventricular failure, and often signs and symptoms of right heart failure predominate. Left-sided failure produces symptoms of pulmonary edema, whereas right-sided heart failure can manifest as soft tissue edema and ascites. Restrictive cardiomyopathy occurs with less frequency compared with the other types of cardiomyopathy and is uncommon in the United States. The disease is much more common elsewhere in the world (e.g., equatorial Africa). The causes are multifactorial (Table 20.7) (25).

Restrictive cardiomyopathy and constrictive pericarditis are difficult to separate based on physiology and clinical presentation.

The cardiac size and configuration are usually normal on chest radiography. However, CT, echocardiography, radionuclide imaging, and cardiac MRI have been used in the diagnosis of restrictive cardiomyopathy, often to exclude the diagnosis of constrictive pericarditis.

Figure 20.20 38-year-old patient with sickle cell anemia. A. Posteroanterior chest radiograph shows generalized cardiomegaly. The ribs are sclerotic with appearance compatible with bone infarcts. B. Lateral chest radiograph shows cardiac enlargement and typical changes of sickle cell disease involving the spine.

Figure 20.21 50-year-old man with hypertrophic cardiomyopathy. Coronal magnetic resonance black-blood image shows concentric hypertrophy of the left ventricle (LV).

Table 20.7: Causes of Restrictive Cardiomyopathy

Amyloidosis
Familial
Scleroderma
Endomyocardial fibrosis
Carcinoid heart disease
Sarcoidosis
Idiopathic
Gaucher
Radiation

 

Cardiac amyloidosis is the most common form of restrictive cardiomyopathy found in the United States. Both primary and secondary amyloidosis can involve the heart, and amyloid deposits are common in the senile heart. When the disease becomes symptomatic, the myocardium is thickened with infiltrating amyloid deposition and is noncompliant. The chambers are often normal in volume but can be small or moderately dilated. The heart can dilate with the senile form of amyloid myocardial disease (Fig. 20.22). Echocardiography and technetium-99m pyrophosphate or indium-111 radionuclide imaging have been used to diagnose cardiac amyloidosis. Cardiac amyloidosis has also been diagnosed with MRI (26). Cardiac sarcoidosis can cause inflammation of the myocardium with subsequent fibrosis. Much of the time myocardial sarcoidosis is subclinical, but on occasion sarcoidosis can produce symptoms of functional impairment with diastolic dysfunction. Chest radiographs usually show a normal heart size, although the heart can enlarge when heart failure is severe (Fig. 20.23). Imaging with thallium-201 or gallium-67 can reveal abnormal uptake in cardiac sarcoidosis, and cardiac MRI can also be used (Fig. 20.24) (26).

Amyloidosis is the most common cause of restrictive cardiomyopathy in the United States.

Myocarditis

Myocarditis, inflammation of heart muscle, is usually asymptomatic. On the other hand, myocarditis can cause sudden death. Our understanding of the epidemiology of myocarditis has been limited because of its insidious nature (27). The etiology of the disease is often unknown clinically, although there are many known causes, such as infectious, toxic, and immune-related etiologies (e.g., heart transplant rejection). Tables 20.8 and 20.9 list a sampling of types of infectious and toxic etiologies. Viral myocarditis is a major cause of myocarditis in the United States, and the diagnosis can be suspected in the acute phase by demonstration of rising antibody titers. Animal studies have implicated an infectious-immune etiology for myocarditis and idiopathic dilated cardiomyopathy (28).

The findings on chest radiography in patients with myocarditis vary according to the extent of disease. The findings can be normal in patients with subclinical disease. However, generalized global cardiac enlargement with pulmonary edema can be seen in patients with extensive disease. In acute myocarditis, often viral in origin, heart failure can be so severe and progressive that artificial circulatory support, and urgent heart transplantation may be necessary (Fig. 20.25).

Figure 20.22 78-year-old patient with senile cardiac amyloid disease. Posteroanterior chest radiograph shows generalized cardiac enlargement and heart failure.

 

Pericardial Disease

There are many forms of acquired pericardial disease. The disease can be acute or chronic, clinical and physiologic findings are variable, and there are many etiologies (29,30). Table 20.10 provides an outline of the types of pericardial effusion, with examples of a few of the many causes.

Figure 20.23 Posteroanterior chest radiograph of a 52-year-old patient with sarcoid heart disease shows generalized cardiomegaly. There is diffuse interstitial lung disease secondary to sarcoidosis.

Figure 20.24 T1-weighted axial spin-echo image of a patient with known sarcoid heart disease demonstrates sarcoid infiltration of the myocardium (asterisk), with signal intensity greater than normal myocardium, involving the anterior wall of the outflow portion of the right ventricle.

Table 20.8: Causes of Infectious Myocarditis

Bacterial: Mycoplasma pneumoniae
Protozoal: toxoplasmosis
Parasitic: echinococcus granulosus
Viral: coxsackievirus and human immunodeficiency virus
Others: fungus, spirochetes, and rickettsia

Table 20.9: Causes of Toxic Myocarditis

Drug induced: cocaine, ethanol
Heavy metals: iron
Miscellaneous: radiation

Figure 20.25 Supine bedside anteroposterior chest radiograph of a 25-year-old patient with acute viral myocarditis. There is widespread pulmonary edema despite the presence of biventricular circulatory support with two extracorporeal support devices and an intraaortic balloon pump (arrowhead). Right heart support is achieved by removal of blood from the right atrium by one cannula (# 1) and return to the pulmonary artery through a separate cannula (# 2). Left-sided circulatory support is achieved by removal of blood from the left atrium through a cannula placed through the right superior pulmonary vein (# 3), with return of blood to the aorta under systemic pressure. The cannula (# 4) returning blood to the ascending aorta appears short because the distal portion of the cannula is radiolucent. The extracorporeal pumps produce constant pressure. The intraaortic balloon pump is placed to produce a more physiologic cyclical pressure waveform.

Pericardial disease with effusion can exist without physiologic abnormality and without clinical symptoms. However, abnormal physiology of acute tamponade and chronic constrictive pericarditis can produce severe and life-threatening conditions. With acute tamponade, the heart is compressed by fluid accumulation within the pericardial sac associated with elevated intrapericardial pressures. The high pressure within the pericardium inhibits diastolic filling of the ventricles, with subsequent decreased stroke volume and cardiac output. Acute tamponade is most commonly due to trauma, often iatrogenic after open cardiac surgery (Fig. 20.26). If uncorrected, death can occur. Tamponade can also occur in a subacute fashion (Fig. 20.27).

Fluid in the pericardium increases intrapericardial pressure, thereby decreasing diastolic filling of the ventricles and resulting in decreased cardiac output.

Pericardial Effusion

The pericardium normally contains approximately 50 mL of fluid. When the volume of pericardial fluid exceeds 200 to 250 mL, chest radiographs can be helpful in making the diagnosis of abnormal pericardial fluid accumulation. However, chest radiography is not particularly sensitive or specific in making a diagnosis of pericardial effusion (31). Chest radiographs of patients with large effusions can show typical features of the “water bottle” heart (Fig. 20.28). This configuration shows symmetric enlargement of the cardiopericardial outline, shaped somewhat like a chocolate candy kiss. The “hilum overlay” sign presents when fluid distension of the superior recesses of the pericardium obscures the outline of the left pulmonary artery. The epicardial “fat pad” sign is produced when the pericardial layers and fluid widen the space between the anterior epicardial fat and substernal fat stripes more than 4 mm (Fig. 20.29) (32). Echocardiography, CT (Fig. 20.30), and MRI (Fig. 20.31) can substantiate the radiographic diagnosis of pericardial effusion. In the past, before development of ultrasound, CT or MRI, carbon dioxide injection into the pericardial sac was used to make the diagnosis (Fig. 20.32). Air in the pericardial sac can be seen on chest radiographs of many patients after open-heart surgery; large hydropneumopericardium (Fig. 20.33) is rarely seen.

Table 20.10: Types of Pericardial Effusion

Serous
   Hypoalbuminemia
   Viral pericarditis
   Heart failure
Chylous
   Idiopathic
   Postsurgical
Hemorrhagic
   Postsurgical
   Postinfarction
   Traumatic
   Neoplastic
   Infectious
   Postradiation
   Systemic disease (e.g., uremia)

The radiographic epicardial “fat pad” sign is specific, but not sensitive, for pericardial effusion.

Figure 20.26 An anteroposterior supine bedside chest radiograph of a 55-year-old patient after mitral valve repair with sudden change in vital signs. The bulge of the left heart margin (arrows) was caused by a pericardial hematoma that compressed the right ventricle. The pulmonary vasculature is oligemic because of tamponade and reduced cardiac output.

Figure 20.27 Computed tomography image of a 58-year-old patient with purulent pericarditis. A loculated anterior pericardial fluid collection compresses the right ventricle and reverses the usual curvature of the ventricular septum (arrows).

Figure 20.28 Anteroposterior chest radiograph of a 76-year-old patient with a large pericardial effusion of unknown etiology. Note the enlarged cardiac outline with a globular shape mimicking a chocolate “candy kiss” or “water bottle.” The apparent heart outline overlies the left hilum including the left pulmonary artery opacity (arrowheads); this is the so-called hilar overlay sign.

Figure 20.29 27-year-old patient with systemic lupus erythematosus. A. Lateral chest radiograph shows a positive “fat pad” sign. The lucency of the epicardial fat (arrowhead) is separated from the mediastinal fat lucency (arrow) by a distance of 9 mm, indicating the presence of a small pericardial effusion. B. Follow-up lateral chest radiograph after treatment shows a normal pericardial stripe (arrow).

Figure 20.30 Computed tomography image obtained from a 74-year-old patient with chronic exudative pericardial effusion. The pericardial effusion (asterisk) is well demarcated by epicardial and mediastinal fat.

Figure 20.31 Sagittal proton-density, black-blood, magnetic resonance image of a 66-year-old patient with a simple pericardial effusion(arrows) located inferior to the heart.

Figure 20.32 84-year-old patient with myxedema heart disease and dilated cardiomyopathy. The patient was worked up in 1965, before the advent of cross-sectional imaging. A. Posteroanterior chest radiograph shows enlargement of the cardiac outline. The configuration is compatible with dilated cardiomyopathy with or without pericardial effusion. B. Posteroanterior chest radiograph obtained after injection of carbon dioxide into the pericardial sac. The air–fluid level (arrowheads) proves the diagnosis of pericardial effusion and shows the anatomy of the superior reflection of the pericardium.

Figure 20.33 64-year-old patient with hydropneumopericardium thought to have accumulated by ball-valve mechanism through a sternal suture. The air was withdrawn by percutaneous catheter insertion and did not recur. A. A posteroanterior chest radiograph shows an air–fluid level (arrows) in the pericardial sac representing the hydropneumopericardium. Note the anatomic extent of the pericardial reflection. B. Lateral chest radiograph shows the extensive pericardial air collection.

 

Constrictive Pericarditis

In chronic constrictive pericarditis (Fig. 20.34), ventricular filling is impeded by loss of compliance. The cardiac chambers are constricted by the thickened pericardium, and diastolic pressures are elevated. Elevated venous pressures, with inhibition of venous return, can lead to development of ascites and soft tissue edema. The two layers of normal pericardium measure 2 to 3 mm together (33). In constrictive pericarditis the pericardial layers are fused and thickened, typically measuring more than 4 mm (Fig. 20.35). The cardiopericardial outline can appear normal or enlarged. Approximately half of the patients with constriction have calcification of the pericardium, although calcified pericardium occurs without constriction and constriction can occur without calcification. Calcification presents as curvilinear opacity, conforming to the anatomy of the pericardial sac (Fig. 20.36). Pericardial calcification is distinguished from myocardial calcification by its distribution and its amorphous and often thick appearance. Myocardial calcification is usually confined to the left ventricle, whereas pericardial calcification can be seen along the surfaces of the other chambers, particularly along the right ventricle and in the atrioventricular groove (34) (Fig. 20.37). MRI does not show calcification but demonstrates pericardial thickening and sometimes can be used to show impaired diastolic function. Table 20.11 lists CT and MRI signs of pericardial constriction.

Figure 20.34 Posteroanterior chest radiograph of a 45-year-old patient with chronic constrictive pericarditis secondary to mediastinal radiation therapy. Heart size is normal, but somewhat small. Paramediastinal radiation fibrosis is present and there are small pleural effusions.

Pericardium at least 4 mm thick is abnormal.

Myocardial calcification is usually confined anatomically to one chamber, whereas pericardial calcification crosses the anatomic location of cardiac chambers.

Patients with constrictive pericarditis and restrictive cardiomyopathy can have similar clinical and physiologic findings. CT and MRI can be helpful in differentiating between the two diagnoses (35). The presence of pericardial thickening or other signs of constriction suggests that the abnormality is pericardial in origin, and pericardiectomy can be done in an attempt to alleviate the clinical syndrome (36). A normal pericardium with thickening of the myocardium suggests cardiomyopathy as the diagnosis, a nonsurgical disease except for transplantation.

Figure 20.35 69-year-old patient with chronic constrictive pericarditis. A. A lateral chest radiograph shows a positive epicardial “fat pad sign” indicative of thickening of the pericardium (arrows)B. Computed tomography demonstrates thickening of the pericardium(arrows) anteriorly and laterally. C. Computed tomography at the level of the diaphragm shows dilatation of the inferior vena cava (IVC) and abdominal fluid (asterisk) above the dome of the right hemidiaphragm.

Figure 20.36 73-year-old patient without clinical signs of constrictive pericarditis. Chest radiographs show extensive pericardial calcification. The diffuse pattern of distribution distinguishes pericardial from myocardial calcification. A. Posteroanterior chest radiograph shows thick pericardial calcification (arrows) along the right and inferior heart margins. B. Lateral chest radiograph shows calcification (arrows) of the anterior portion of the pericardium.

Figure 20.37 Computed tomography images on the same 73-year-old patient with nonconstrictive pericardial calcification shown in Fig. 20.36A. Computed tomography image at the inferior portions of the ventricular chambers shows calcified pericardium adjacent to the right (short arrows) and left ventricles (long arrows)B. More caudal image demonstrated abundant calcification at the inferior atrioventricular groove (asterisks).

Table 20.11: Computed Tomography/Magnetic Resonance Imaging Signs of Constrictive Pericarditis

Pericardial thickening and/or calcification
Tubular deformity of one or both ventricles
Flattening of the interventricular septum
Dilatation of one or both atria
Dilatation of inferior and superior vena cava

Ischemic Heart Disease

The American Heart Association estimates that over 12 million Americans suffer from coronary heart disease. Almost 500,000 individuals died from coronary disease in 1998, the single leading cause of mortality. Chest radiography, echocardiography, and cardiac nuclear medicine play major roles in managing patients with coronary disease. MRI and CT methods of imaging coronary artery disease are rapidly improving.

Atherosclerotic cardiovascular disease is the leading cause of death in the United States.

Imaging of the Coronary Arteries

Coronary arteriography is the accepted method used to examine the coronary arteries. Noninvasive methods using MRI and CT are under development but have not yet achieved the accuracy necessary to replace the invasive and costly catheter procedure. There are circumstances where noninvasive imaging is useful in evaluating the coronary arteries. For example, CT and MRI can diagnose ectopic origin of the coronary arteries. Chest radiography and fluoroscopy often show calcification of the coronary arteries (Fig. 20.38) (37).

This observation should not be considered clinically useful in older patients but should be mentioned if observed in young patients, under the age of 40. On occasion, a diagnosis of Kawasaki disease can be made by observation of calcified coronary aneurysms on chest radiographs (Fig. 20.39). Several authors have suggested that the incidental finding of extensive coronary arterial calcium with standard CT can have clinical implications (Fig. 20.40) (38,39). As with radiography, the standard CT finding of abundant coronary calcium in patients under the age of 40 should be mentioned on interpretation. Detection of calcium with standard CT in older patients is of doubtful clinical usefulness. Large groups of patients are now being screened for coronary artery disease by quantifying coronary calcium with electron beam or multidetector helical CT (Fig. 20.41). The resultant coronary calcium “score” is then compared with data normalized by sex and age. Abnormal increased calcium may be a signal of clinically significant disease (40).

Figure 20.38 Lateral chest radiograph of an 88-year-old patient shows calcification of the right (black arrowheads) and left circumflex coronary (white arrowheads) arteries.

Figure 20.39 23-year-old patient with Kawasaki disease. A. Posteroanterior chest radiograph shows a calcified aneurysm (arrows) of the left anterior descending coronary artery. B. Lateral chest radiograph shows the same coronary artery aneurysm (arrows).

Figure 20.40 Computed tomography image of a 60-year-old patient obtained to evaluate chronic calcified pulmonary artery thromboembolism (long arrow) demonstrates the incidental finding of calcification in the left main (arrowhead) and left anterior descending (small arrow) coronary arteries. The coronary arterial calcification was of no clinical value in this patient.

Figure 20.41 Electron beam computed tomography for coronary artery calcium of a 59-year-old man with angina demonstrates abundant calcium in the left main (arrowhead) and left anterior descending (arrows) coronary arteries.

The total coronary calcium score is a measure of total atherosclerotic burden (calcified and noncalcified plaque) and may be a useful predictor of the risk for future cardiac events, similar to the use of other risk factors such as hyperlipidemia, smoking, diabetes, and family history.

Myocardial Manifestations of Coronary Artery Disease

Acute and/or chronic ischemia can damage the myocardium. Ischemic myocardial disease can present with a variety of findings on chest radiographs. Chest radiographs can be normal or demonstrates nonspecific findings of cardiomegaly and heart failure. For example, patients with ischemic cardiomyopathy (dilated cardiomyopathy associated with severe coronary artery disease) show nonspecific cardiomegaly indistinguishable from idiopathic cardiomyopathy. Some patients with acute ischemic disease have normal heart size and extensive pulmonary edema (Fig. 20.42). Specific radiographic abnormalities can occur with myocardial damage secondary to coronary artery disease (Table 20.12).

Myocardial infarction can result in formation of a ventricular aneurysm. As an infarct heals, fibrous tissue replaces cardiac muscle (Fig. 20.43). The scarred portion of the ventricular wall can be motionless (akinetic) or can move outward instead of inward during systole (dyskinesis). If the scarred region assumes the shape of a persistent outward bulge, it is considered a true aneurysm that can sometimes be shown on chest radiographs (Figs. 20.44 and 20.45). In some patients the infarct region can calcify without forming an aneurysm, presenting as a thin curvilinear opacity over the heart on chest radiographs. Most commonly, this occurs at the left ventricular apex or anterolateral wall (Figs. 20.46 and 20.47). Pathologically, true aneurysms have remnants of myocardial wall within regions of scarring. In contrast, pseudoaneurysms represent regions of transmural infarction with rupture constrained by overlying pericardium, with no remaining elements of the ventricular wall. Pseudoaneurysms typically occur in the posterior-basal segment of the left ventricle near the posterior interventricular groove (Fig. 20.48). It is important to recognize the possibility of pseudoaneurysm because they are susceptible to rupture (41). Imaging with contrast ventriculography, CT, or MRI can be helpful in distinguishing aneurysm from pseudoaneurysm by demonstrating a relative narrow orifice or “neck” leading from the ventricular chamber to a pseudoaneurysm (42) (Fig. 20.49).

Focal calcification of the left ventricular apex indicates a calcified infarct and should raise suspicion of a ventricular aneurysm.

Figure 20.42 Bedside anteroposterior chest radiograph of a 69-year-old patient with acute myocardial infarction. There is extensive pulmonary edema with a normal heart size. In situations with acute ischemic disease the myocardium can be noncompliant, and cardiomegaly can take days to develop.

Table 20.12: Radiographic Signs of Myocardial Infarction

Calcified myocardial infarct
Left ventricular aneurysm
Left ventricular pseudoaneurysm
Ruptured interventricular septum

Figure 20.43 Double-oblique, short-axis, cine-magnetic resonance, contrast-enhanced image of a 76-year-old patient with an inferior wall left ventricular infarct. The inferior wall of the left ventricle (arrows) is thinned and demonstrates a magnetic resonance signal deficit compared with other portions of the left ventricular myocardium.

Figure 20.44 Posteroanterior chest radiograph of a 70-year-old patient with a large chronic left ventricular aneurysm (arrows).

Pseudoaneurysms are usually due to transmural infarction and are full-thickness wall ruptures contained by the pericardium.

Figure 20.45 An 86-year-old patient with a chronic calcified left ventricular aneurysm. A. Posteroanterior chest radiograph shows a rounded calcification (arrowheads) at the inferior margin of the cardiac apex. B. Computed tomography image shows the apical calcification and a well-defined rounded aneurysm (arrowheads).

Figure 20.46 Lateral chest radiograph of a 68-year-old patient with an old calcified left ventricular apical infarct (arrowheads). In this case, the infarct healed as a calcified scar, without the outward bulge of a ventricular aneurysm.

Figure 20.47 Computed tomography image of an 80-year-old patient with a calcified apical infarct. There is calcification in a region of marked myocardial thinning (arrowhead). The left ventricular chamber is dilated, but there is no well-defined aneurysm with a neck.

Figure 20.48 63-year-old patient with a history of inferior wall myocardial infarction. Left ventriculography demonstrated a posterior-inferior wall pseudoaneurysm. A. Posteroanterior chest radiograph shows the pseudoaneurysm presenting as a rounded opacity (arrows)projecting over the inferior portion of the cardiac outline. B. Lateral chest radiograph shows the typical posterior-inferior bulge of a pseudoaneurysm (arrows).

Figure 20.49 Computed tomography image of an 82-year-old patient shows an large rounded opacity representing a pseudoaneurysm (PSA) at the posterior-inferior aspect of the left ventricle (LV). The lateral margin of the pseudoaneurysm is calcified. A narrow neck(arrowheads) helps distinguish a pseudoaneurysm from a true aneurysm.

 

Neoplastic Disease

Primary neoplasms of the heart and pericardium are rare, found at autopsy in 0.001% to 0.03% of cases (43). About three-fourths of these primary lesions are benign (Table 20.13), most commonly myxomas (44). CT and MRI are very helpful in making a diagnosis, assessing the extent of disease, and planning a surgical approach. Table 20.14 lists the most common primary malignant neoplasms of the heart and pericardium. Sarcomas are the most common primary malignant neoplasm and second most common overall, after myxoma (45). Metastatic disease is far more prevalent, perhaps 40 times more common than benign tumors (Table 20.15) (46).

Cardiac malignancy is more commonly metastatic to the heart than primary to the heart.

Chest radiographs show cardiac enlargement in many cases of neoplasm, although some patients have normal heart and mediastinal contours (47). On occasion, neoplastic disease can present on chest radiographs as a mass-like contour abnormality of the cardiopericardial outline (Fig. 20.50). Benign pericardial cysts (Fig. 20.51), lipomas, and ventricular aneurysm (Fig. 20.52) can have the same appearance. Therefore, the diagnosis and extent of neoplastic disease can be better evaluated with CT (Figs. 20.5320.54 to 20.56) or MRI (Figs. 20.57,20.58, and 20.59) (48). MRI is superior to CT in many cases because of faster image acquisition, the ability to image in multiple planes, and superior contrast resolution (49). MRI relaxation characteristics allow for better soft tissue characterization of masses.

Table 20.13: Benign Primary Cardiac and Pericardial Neoplasms

Myxoma
Papillary fibroelastoma
Fibroma
Paraganglioma
Lipoma
Hemangioma

Table 20.14: Malignant Primary Neoplasms of the Heart and Pericardium

Sarcoma of mesenchymal cell origin
   Angiosarcoma (most common)
   Rhabdomyosarcoma
   Fibrosarcoma
   Osteosarcoma
Lymphoma
Pericardial mesothelioma

Table 20.15: Common Sources of Metastatic Disease to the Heart

Breast
Bronchogenic
Renal cell
Melanoma
Leukemia

Figure 20.50 Posteroanterior chest radiograph of a 61-year-old patient with a primary leiomyosarcoma of the outflow portion of the right ventricle (arrows).

Figure 20.51 Posteroanterior chest radiograph of a 73-year-old patient with a pericardial cyst (arrows).

Figure 20.52 Posteroanterior chest radiograph of a 70-year-old patient with a left ventricular aneurysm (arrows).

Figure 20.53 Computed tomography image of the heart of a middle-aged patient shows a filling defect in the left atrium (arrowheads), representing an intraluminal myxoma.

Figure 20.54 A computed tomography image of a 70-year-old patient with metastases to the myocardium (asterisks).

Figure 20.55 61-year-old woman with breast cancer and metastasis to the epicardium. A computed tomography image shows a solitary metastasis in the epicardial fat (asterisk) beneath the pericardium, compressing the apex of the right ventricle.

Figure 20.56 21-year-old patient with pericardial lymphoma. A computed tomography image shows extensive abnormal soft tissue infiltration at the superior aspect of the pericardial sac. The lymphomatous tissue surrounds the aorta (A) and pulmonary artery (PA). The superior vena cava is obliterated, and its position is shown by a venous catheter (arrow). Contrast is shown in the right atrial appendage (arrowhead).

Figure 20.57 40-year-old patient with a right atrial myxoma. Fast-cine magnetic resonance image in the two-chamber view of the right atrium and ventricle (rv) shows a polypoid myxoma in the right atrium (arrowheads).

Figure 20.58 65-year-old patient with metastatic renal cell carcinoma. Spin-echo axial magnetic resonance study shows a left ventricular polypoid metastasis (asterisk) attached to the ventricular septum.

Figure 20.59 37-year-old patient with metastatic melanoma. Proton density-weighted axial magnetic resonance image shows a metastasis (asterisk) extending from the right atrial appendage into the right atrium.

 

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