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From: Essential Cardiology: Principles and Practice, 2nd Ed.
Edited by: C. Rosendorff © Humana Press Inc., Totowa, NJ
11 Radiology of the Heart
Gautham P. Reddy, MD, MPH, and Robert M. Steiner, MD
INTRODUCTION
Imaging plays a critical role in the diagnosis of heart disease. In the past 25 to 30 yr, advanced imaging modalities such as digital angiography, echocardiography, magnetic resonance imaging (MRI), computed tomography (CT), and nuclear cardiology have become important in the evalu- ation of the heart. However, the conventional radiographic examination remains the mainstay of cardiac imaging. This chapter will discuss the role of the chest radiograph in the diagnosis of car- diac disease in adults, with an emphasis on both normal cardiovascular anatomy and pathoanatomy in a variety of diseases. Correlation will be made with cross-sectional imaging in order to illustrate important anatomic points.
NORMAL ANATOMY
The standard radiographic examination of the chest consists of upright frontal (posteroanterior) and lateral projections (Fig. 1). If a patient is acutely ill or is unable to stand upright, an antero- posterior frontal radiograph may be obtained with the patient in the supine position, and the lateral radiograph is usually omitted. It is important to ensure that the patient is properly positioned in the both the frontal and lateral views so that cardiac structures can be evaluated accurately. In the past left and right anterior oblique projections were obtained routinely, often with contrast medium in the esophagus. With the advent of echocardiography, however, the current role of oblique radio- graphs is limited.
In the normal chest radiograph, there is excellent inherent contrast between the air-filled lungs, pulmonary vessels, and mediastinum. The chest film therefore is the primary imaging study for evaluation of the lung parenchyma and vessels. However, the components of the mediastinum, including the heart, the blood, and the fat, have similar radiographic densities and cannot be easily distinguished on chest radiographs. Nevertheless, the margins of the heart and mediastinal vessels are clearly demarcated, and variation from the normal appearance suggests the presence of disease.
Left Subclavian Artery
On the frontal chest radiograph, the left subclavian artery forms the superior portion of the left mediastinal border above the aortic arch (Fig. 1A). This artery usually forms a concave border with the lung, although a convex border may be seen if there is increased blood flow, such as in coarctation of the aorta, or if the vessel is tortuous because of atherosclerosis or hypertension. A per- sistent left superior vena cava is suggested by a straight or convex left supraaortic border.
Aorta
On the frontal view, the ascending aorta forms a convex margin above the right heart border (Fig. 1A). When the ascending aorta enlarges, it projects farther to the right. On the lateral view,
the anterior margin of the ascending aorta lies above the right ventricle but is not seen in the normal individual due to an abundance of mediastinal fat.
The aortic arch or “knob” forms a convex border just below the left subclavian artery on the frontal radiograph (Fig. 1A). The aortic arch displaces the trachea slightly to the right. In a patient with a right aortic arch, the trachea is deviated slightly to the left (1). The arch is usually small in the young, healthy individual. An enlarged aortic arch is higher and wider than the normal aorta.
The ascending aorta or arch may be enlarged on the frontal view in individuals with aortic aneu- rysm, aortic regurgitation, systemic hypertension, or atherosclerosis.
Immediately below the aortic arch along the left mediastinal border, there is an indentation known as the aorticopulmonary window, bordered by the lower margin of the aortic arch and by the superior margin of the left pulmonary artery (Fig. 1A). Convex bulging of the aorticopulmonary window may reflect a ductus diverticulum, lymphadenopathy, or other mass (2).
Pulmonary Vasculature
The main pulmonary artery forms a slightly convex border along the left side of the mediastinum between the aortic knob and the left atrial appendage (Fig. 1A). A prominent convex bulge in this location indicates enlargement of the main pulmonary artery. A large main pulmonary artery may be related to pulmonary arterial hypertension; increased blood flow, as in anemia or a left-to-right shunt; or turbulent flow, as in patients with pulmonary valvular stenosis. On the other hand, the main pulmonary artery border may be flat or convex in patients with transposition of the great vessels, truncus arteriosus, tetralogy of Fallot, or pulmonary atresia. On the lateral projection the anterior border of the main pulmonary artery, located above the right ventricle, is not clearly seen due to the presence of mediastinal fat.
The left pulmonary artery is visualized as a smooth arc just inferior to the aorticopulmonary window. The left pulmonary artery arches over the left mainstem bronchus, as seen on the lateral projection (Fig. 1B). On the other hand, the right pulmonary artery is a round or oval opacity anterior to the right mainstem bronchus on the lateral view (Fig. 1B).
The intrapulmonary branch arteries parallel the airways, and gradually decrease in size toward the lung periphery. The arteries and bronchi are of approximately the same size at any given level;
comparison of arterial and bronchial diameters is therefore useful when assessing increase or redis-
Fig. 1. Normal chest radiograph in a 36-year-old woman. (A) Posteroanterior frontal projection. (B) Lateral projection. A, ascending aorta; AA, aortic arch; LA, left atrium; LP, left pulmonary artery; LV, left ventricle;
P, main pulmonary artery; RA, right atrium; RP, right pulmonary artery; RV, right ventricle; Z, azygos vein.
Open arrow = left subclavian artery; straight arrow = aorticopulmonary window; curved arrow = left mainstem bronchus.
tribution of blood flow. When a patient is upright, lower-lobe vessels are larger than upper-lobe vessels due to differences in blood flow, partly due to the effects of gravity (3).
Heart
On the posteroanterior frontal radiograph, the normal heart usually occupies no more than 50%
of the transverse diameter of the thorax (4). The respective widths of the heart and the chest can be measured to determine the “cardiothoracic ratio,” calculated as the maximum transverse diam- eter of the heart divided by the maximum width of the thorax (4). In practice, the size of the heart is usually assessed subjectively. Low lung volumes, lordotic projection of the radiograph, or pectus excavatum deformity can cause the heart to appear larger than it really is. A large heart may appear to be of normal size if the lungs are hyperinflated, as in patients with emphysema, or if the cardiac apex is displaced inferiorly. When evaluating the size of the heart, it should be kept in mind that anteroposterior frontal projections result in magnification of the cardiac silhouette by 10 to 13% (5).
LEFT ATRIUM
The left atrial appendage is identified as a smooth, slightly concave segment of the left heart border immediately inferior to the left mainstem bronchus in the frontal view (Fig. 1A). When the left atrial border is straightened or convex, atrial enlargement is suggested. It is important to recog- nize that noncardiac pathology, such as a pericardial cyst or lymphadenopathy, may mimic enlarge- ment of the left atrial appendage on the frontal radiograph. The right-side margin of the normal left atrium is visualized deep to the right atrial border as an convex “double” density. If the left atrium is severely dilated, the left atrial border may project lateral to the margin of the right atrium (6).
Elevation of the left mainstem bronchus is another sign of left atrial enlargement (7). On the lateral projection, the normal left atrium forms a slight bulge at the upper posterior cardiac border (Fig. 1B).
Enlargement of the left atrium results in posterior displacement of the esophagus, most easily seen when the esophagus is filled with contrast medium.
LEFT VENTRICLE
The borders of the left ventricle blend with the left atrial margins on both the frontal and lateral radiographs (Fig. 1). On both projections, the slightly convex left ventricular border extends to the diaphragm. The cardiac apex can be displaced inferiorly and laterally when the left ventricle is dilated due to aortic or mitral regurgitation. When the ventricle is hypertrophied because of aortic stenosis or hypertrophic cardiomyopathy, it may be rounded and the apex may be elevated.
RIGHT ATRIUM
The right atrium forms a gentle convex border with the right lung (Fig. 1A). The margins of the right atrium blend with the inferior and superior vena cavae. The border of the inferior vena cava below the right atrium is usually straight (8). On the lateral view, the right atrium is not seen directly because this chamber does not form the cardiac border.
RIGHT VENTRICLE
The right ventricle cannot be visualized directly on the frontal projection because it is not border- forming in the frontal projection. A large right ventricle can displace the left ventricle posteriorly and to the left, causing widening of the cardiac silhouette on the frontal view. On the lateral view, the right ventricle comprises the anterior margin of the heart in the subxyphoid area, occupying the inferior one-third of the thorax (Fig. 1B). A dilated right ventricle will extend further superiorly into the retrosternal space (9).
Azygos Vein
The azygos vein is an oval structure seen in the frontal radiograph at the right tracheobronchial angle (Fig. 1A). The size of the azygos vein is a good marker of cardiovascular dynamics. It enlarges in left and right heart failure, obstruction of the superior vena cava, and absence of the intrahepatic
segment of the inferior vena cava (10). A change in size of the azygos vein will parallel changes in pulmonary venous pressure, making it a useful radiographic indicator of congestive heart failure.
SPECIFIC ABNORMALITIES
Abnormal Pulmonary Blood Flow and Pulmonary Edema
Pulmonary blood flow reflects the hemodynamics of the heart itself. Increased, decreased, or asymmetrical pulmonary blood flow can be recognized on chest radiographs and correlated with other signs of disease.
The size of the pulmonary arteries is related both to blood flow and blood pressure or to pres- sure alone (4). Enlarged pulmonary arteries are present in a variety of conditions, including left- to-right shunt, increased cardiac output due to chronic anemia or pregnancy, and pulmonary arterial hypertension, which may be primary or may be secondary to conditions such as chronic interstitial lung disease, emphysema, Eisenmenger’s syndrome, or chronic thromboembolism (Fig. 2). Cen- tral pulmonary artery calcification indicates chronic, severe pulmonary arterial hypertension (11).
Elevation of pulmonary venous pressure can be due to left ventricular failure, mitral stenosis, and other causes of vascular obstruction distal to the pulmonary arterial bed. When pressure rises to between 12 and 18 mmHg, there is a redistribution of pulmonary blood flow to the upper lobes, which manifests radiographically as enlargement of the upper lobe vessels (“cephalization”) (12).
As pulmonary venous pressure increases above 18 mmHg, pulmonary interstitial edema occurs.
Radiographically, thin horizontal interlobular septal lines, called “Kerley B lines,” are visible at the lung bases (Fig. 3) (13). With elevation of pulmonary venous pressure above 25 mmHg, alveolar edema ensues. In the setting of alveolar edema, chest radiographs demonstrate opacities that typi- cally involve the central portions of the lungs, sometimes producing a “batwing” appearance. If the pulmonary edema is related to heart failure, the cardiac silhouette is enlarged (Fig. 3).
Valvular Heart Disease
Stenosis of the aortic valve is most frequently related to a congenital bicuspid valve. Less com- monly a tricuspid aortic valve can undergo degeneration, which can be due to rheumatic valvulitis.
Aortic stenosis of a mild to moderate degree causes left ventricular hypertrophy. Radiographi- cally, the valve may be calcified, and typically the right side of the ascending aorta bulges due to poststenotic dilation. The left ventricular border may be rounded or the cardiac apex may be ele- vated due to concentric hypertrophy of the left ventricle (14). More severe narrowing of the valve can lead to enlargement of the left ventricle and atrium (15), in proportion to the degree of stenosis
Fig. 2. Pulmonary arterial hypertension secondary to Eisenmenger syndrome in a 32-yr-old woman with atrial septal defect. (A) Frontal chest radiograph. The main (arrow), left, and right pulmonary arteries are enlarged.
(B) Transverse electrocardiographically gated spin echo MRI image shows a large defect (arrow) of the atrial septum. LA, left atrium; RA, right atrium.
and the severity of associated mitral regurgitation. Pulmonary venous hypertension and pulmonary edema also can develop in patients with severe aortic stenosis.
Aortic regurgitation can develop in a stenotic bicuspid valve, or it can be due to rheumatic valvulitis, infective endocarditis, or annular dilation resulting from enlargement of the ascending aorta in conditions such as annuloaortic ectasia. Aortic dissection also can cause aortic insufficiency.
With mild aortic regurgitation, the heart size usually remains normal, and the ascending aorta is normal or mildly dilated. Enlargement of the left atrium suggests coexisting mitral regurgitation.
In patients with moderate or severe aortic regurgitation, the left ventricle and the aorta are enlarged.
In contrast to aortic stenosis, diffuse dilation of the aorta can occur in patients with aortic regur- gitation. When aortic regurgitation is secondary to annuloaortic ectasia, the aortic root is dispropor- tionately enlarged. Valve calcification often occurs in patients with aortic insufficiency due to a congenital bicuspid valve or rheumatic valve disease. In chronic aortic regurgitation, the left ven- tricle becomes enlarged, but the lungs appear essentially normal (16). When aortic regurgitation is acute, such as in trauma or dissection, chest radiographs demonstrate pulmonary venous hyper- tension and pulmonary edema without left ventricular enlargement.
Fig. 3. Frontal chest radiographs in a 72-yr-old woman with a history of congestive heart failure. (A) Base- line film demonstrates moderate enlargement of the heart. (B) Radiograph performed when the patient was in acute cardiac decompensation. The cardiac silhouette has increased in size, and there is cephalization of the pulmonary vasculature. Kerley B lines (between arrows) are identified in the right lower lobe, indicating pulmonary interstitial edema. (C) Film obtained the next day shows progression of pulmonary edema with alveolar opacities.
Fig. 4. Severe tricuspid and mitral regurgitation. (A) Frontal projection reveals a markedly enlarged cardiac silhouette with global cardiomegaly. The prominent right heart border indicates severe right atrial dilation.
The elevation of the left mainstem bronchus (arrowheads) suggests left atrial enlargement. (B) Lateral view demonstrates enlargement of the right ventricle (short, wide arrow), left ventricle (long, straight arrow), and left atrium (curved arrow).
Mitral stenosis is most commonly secondary to rheumatic heart disease. Mild enlargement of the left atrium is one of the initial radiographic manifestations of mitral stenosis. When the stenosis is more severe, the left atrium dilates further, and the left atrial appendage can enlarge dispropor- tionately (17). Pulmonary venous hypertension and cephalization can develop, and the central pul- monary arteries can enlarge. The mitral valve is frequently calcified. The left ventricle appears nor- mal in most patients with mitral stenosis.
Chronic mitral regurgitation can be due to a variety of causes, including ischemic cardiomyopa- thy, rheumatic heart disease, valve prolapse due to myxomatous degeneration, and calcification of the mitral annulus. Chest radiographs exhibit enlargement of both the left atrium and left ventricle (Fig. 4). Because of volume overload and elevated pressure, chamber enlargement can be severe.
Acute mitral regurgitation can be caused by rupture of the chordae tendineae or papillary muscles, ischemic dysfunction, and bacterial endocarditis. Although the heart may be normal in size, these patients have left heart failure, which causes severe pulmonary alveolar edema. Occasionally asym- metric pulmonary edema, more severe in the right upper lobe, can result from selective retrograde flow from the mitral valve into the right upper lobe pulmonary veins (18). The valve can be evalu- ated and the regurgitant flow can be quantified with either echocardiography or MRI.
Tricuspid valve regurgitation (Fig. 4) can be due to ischemic cardiomyopathy, rheumatic heart disease, Ebstein’s anomaly, and other causes. Typically the right-sided chambers enlarge, and the right atrium can be disproportionately dilated (19). Patients with tricuspid regurgitation can have massive cardiac enlargement, known as a “wall-to-wall heart.”
Ischemic Heart Disease
Several imaging techniques can be used for evaluation of ischemic heart disease, including coro- nary angiography, radionuclide scintigraphy, echocardiography, electron-beam CT, and MRI. In patients with ischemic cardiomyopathy, the chest films can be completely normal, even in patients
who have severe disease. However, many of these patients have cardiomegaly, especially left ven- tricular enlargement. These patients may also have a left ventricular aneurysm. Pulmonary edema may be present, especially in patients who are acutely short of breath.
Dressler syndrome, or postmyocardial infarction syndrome, manifests radiographically as enlargement of the cardiac silhouette due to pericardial effusion. Pleural effusion (usually unilateral on the left side) is common, and consolidation is present in a minority of patients (20).
Occasionally left ventricular aneurysm can develop after myocardial infarction. A true aneurysm is most frequently located at the cardiac apex or on the anterior ventricular wall. On chest radio- graphs, the aneurysm appears as a focal bulge along the left heart border (21). A thin rim of cal- cification is sometimes seen within the aneurysm. A false aneurysm can arise after left ventricular rupture secondary to acute transmural infarction (22). Although most patients with cardiac rupture die immediately, in a small percentage the rupture is contained by the surrounding soft tissues, result- ing in a false aneurysm. Chest films can be normal or can demonstrate a contour abnormality, most commonly along the posterior or diaphragmatic aspect of the heart (22). Definitive diagnosis is made by MRI, CT, or echocardiography. Cross-sectional imaging can differentiate a false aneu- rysm, with its narrow neck, from a true aneurysm, which has a wide neck communicating with the ventricular chamber.
Papillary muscle rupture is an unusual complication of myocardial infarction. Chest radiographs demonstrate a wide spectrum of findings, from no abnormality to marked cardiomegaly and pul- monary edema. Echocardiography or MRI can be performed to diagnose the abnormal mitral valve leaflets and to quantify the severity of mitral regurgitation (23).
In patients with dilated cardiomyopathy and ischemic cardiomyopathy, the left ventricular ejec- tion fraction is decreased. Left ventricular and later biventricular failure develop in most of these patients. Radiographic presentation can vary from a normal heart to diffuse globular enlargement, which may simulate a large pericardial effusion. Ventricular hypokinesis and dilation of the left atrium and left ventricle are the findings at echocardiography.
Coronary artery calcification is an indicator of atherosclerosis, and the quantity of calcification correlates with the total atherosclerotic burden (24). Coronary artery calcification can be identified by various imaging modalities including radiography, fluoroscopy, and CT. CT has the highest diag- nostic accuracy for detection of coronary artery calcification (24). In the past several years, electron- beam CT and multidetector helical CT have been investigated for identification of coronary athero- sclerosis. Evidence from several recent studies seems to support the use of electron-beam CT and multidetector helical CT for risk stratification in asymptomatic individuals and for diagnosis of coronary artery disease in patients with atypical chest pain (25,26).
Pericardial Disease
On the lateral chest radiograph, the normal pericardium can be seen in some patients as a curved linear opacity between the pericardial fat and the subpericardial fat. Because of their excellent con- trast resolution, CT and MRI depict the pericardium more readily than plain radiographs do (27,28).
A small pericardial effusion often is not seen on chest radiographs. As the quantity of pericar- dial fluid increases, the cardiac silhouette may acquire a “water bottle” or globular configuration (Fig. 5). The normal bulges and indentations of the cardiac borders may become obscured, and the contours of the heart may become blunted and featureless. Because a pericardial effusion can cause enlargement of the cardiac silhouette (28), it may be difficult to distinguish pericardial effu- sion from cardiomegaly. Since the pericardium extends to the main pulmonary artery, a large peri- cardial effusion can obscure the hilar vessels, which should not occur with cardiomegaly alone.
Occasionally, pericardial effusion may been seen on a lateral chest radiograph as an opaque band between the pericardial fat and the subpericardial fat, known as the “fat pad sign” (Fig. 5C). Although this sign is specific for a pericardial effusion, its sensitivity is limited.
Echocardiography is more sensitive than plain radiographs for the diagnosis of pericardial effusion (29). When a pericardial effusion is suggested by clinical or radiographic findings, echocardiography
Fig. 5. Pericardial effusion in a 52-yr-old woman on hemodialysis. (A) Baseline frontal chest film. (B) and (C) Films performed two days later just before dialysis. (B) The cardiac silhouette has increased in size. (C) The lateral view shows the “fat pad sign.” There is a dense layer of fluid (between arrows) between the lucent epicardial and pericardial layers of fat. (D) Contrast-enhanced CT scan demonstrates a large pericardial effusion (E).
can be used for more definitive evaluation. CT and MRI also can identify pericardial effusion and are useful for the identification of a hemorrhagic effusion (Fig. 5D) (30).
Constrictive pericarditis may occur as a result of open heart surgery, radiation therapy, viral or tuberculous infection, or hemopericardium (31). The cardiac silhouette usually is normal or small, and the right heart border may be flattened (32). A pericardial effusion is present in the majority of these patients, and enlargement of the left atrium and azygous vein in a minority. In a small proportion of patients with pericardial constriction, calcification of the pericardium may be seen.
Most often due to tuberculous pericarditis, such calcification may be seen most readily along the anterior and inferior borders of the heart and in the atrioventricular and interventricular grooves (Fig. 6).
Because constrictive pericarditis and restrictive cardiomyopathy may have overlapping clinical presentations and findings, MRI and CT can play an important role in distinguishing the two diag- noses. Pericardial thickening of at least 4 mm is highly sensitive and specific for constrictive peri- carditis (30). Ancillary findings of constrictive pericarditis include enlargement of the right atrium, inferior vena cava, and hepatic veins, in addition to a narrowed, “tubular” configuration of the
Fig. 6. Calcific pericarditis in a patient with a history of tuberculosis. (A) Frontal and (B) lateral radiographs demonstrate dense calcium (arrows) in the interventricular groove.
right ventricle. Although pericardial calcification and thickening indicate chronic pericardial inflammation and can be used to support the diagnosis of pericardial constriction, the diagnosis must be based on clinical criteria in addition to imaging findings.
When a mediastinal mass is identified on chest radiography, CT or MRI may be performed for more precise evaluation (Fig. 7). A pericardial cyst appears as a smooth, well-marginated fluid-filled paracardiac structure. Because they are benign and generally asymptomatic, these cysts may be clinically important only because cross-sectional imaging must be performed to differentiate a cyst from a solid mass. Echocardiography also can be used to make the diagnosis of a pericardial cyst.
Congenital Heart Disease in the Adult
There are three groups of adults with congenital heart disease: those who were treated surgi- cally in childhood, those who were diagnosed as children but did not receive surgical intervention, and those whose disorder was not recognized until adulthood.
Fig. 7. Pericardial cyst. (A) Frontal chest film reveals a smoothly marginated round mass in the right cardio- phrenic angle. (c) (B) Contrast-enhanced CT scan demonstrates a well-circumscribed, thin-walled mass of fluid density.
COARCTATION OF AORTA
In adults, a focal juxtaductal stenosis is most common. Chest radiographs may demonstrate a characteristic abnormal contour of the aortic arch, known as the “figure 3” sign, which is a double bulge immediately above and below the region of the aortic knob (Fig. 8A) (33). Bilateral symme- trical rib notching in an older child or adult is diagnostic of coarctation. In recent years, MRI has been used for the evaluation of coarctation of the aorta before and after surgical repair or angiography (Fig. 8B) (34). Because it a noninvasive technique that provides complete anatomic and functional evaluation of the coarctation, MRI can usually be performed in place of diagnostic angiography.
LEFT-TO-RIGHT SHUNTS
Ostium secundum atrial septal defect (ASD) is the most common left-to-right shunt diagnosed in adult life, accounting for more than 40% of adult congenital heart defects (35). Although the chest radiograph may be normal in a patient with a small shunt, typically the main pulmonary artery, the peripheral pulmonary branches, the right atrium, and right ventricular borders are enlarged (Fig.
2A). Echocardiography can delineate the size and location of the ASD, as well as associated abnor- malities such as mitral valve prolapse. MRI can be performed if echocardiography does not reveal the ASD (Fig. 2B).
If a ventricular septal defect (VSD) is small, the chest film is normal. However, the pulmonary arteries, both ventricles, and the left atrium are enlarged if the left-to-right shunt is large or if there is secondary pulmonary hypertension,. Echocardiography usually will demonstrate the site of the defect. MRI is performed in certain cases to evaluate associated abnormalities or to define certain lesions such as a supracristal VSD, which may be difficult to image by echocardiography (36).
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RECOMMENDED READING
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