Radiology of the Heart: Plain Film Imaging and Diagnosis

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B, Superimposed drawing of the cardiac chambers and the major vessels.

(From Van Houten FX, Adams DF, Abrams HL: Radiology of valvular heart disease. In Sonnenblick E, Lesch M [eds]: Valvular Heart Disease. New York, Grune & Stratton, 1974.)

C, A computer-generated model in the lateral projection demonstrates the valves, chambers, and sulci.

(From Steiner RM: Radiology of the heart and great vessels. In Braunwald E, Zipes PD, Libby P [eds]: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, Saunders, 2001.)

FIGURE 5-12 Right anterior oblique projection (RAO). A, 45-degree RAO film of the chest in a normal patient. B, Computerized image of the heart in the RAO projection demonstrates the anatomic relationships of the cardiac chambers and valves.

(A, from Van Houten FX, Adams DF, Abrams HL: Radiology of valvular heart disease. In Sonnenblick E, Lesch M [eds]: Valvular Heart Disease. New York, Grune & Stratton, 1974; B, from Steiner RM: Radiology of the heart and great vessels. In Braunwald E, Zipes PD, Libby P [eds]: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, Saunders, 2001.)

FIGURE 5-13 Aortography in the LAO plane in this patient with coarctation of the aorta demonstrates to best advantage the full expanse of the aortic arch—a useful projection for the diagnosis of aortic aneurysm, dissection, tubular hypoplasia, and patent ductus arteriosus.

FIGURE 5-14 The pericardium. A, Globular or water flask mediastinal configuration due to a large pericardial effusion. B, The subepicardial fat stripe (arrowhead) in the normal patient is separated from the anterior mediastinal fat by the 2 to 4 mm line or band representing the normal width of the pericardium. C, When a pericardial effusion is present, the soft tissue stripe is widened because of the presence of increased fluid in the pericardial sac (arrowheads). D, A contrast-enhanced CT scan shows a wide band of water density enveloping the heart due to a large effusion (asterisks).

(From Steiner RM: Radiology of the heart and great vessels. In Braunwald E, Zipes PD, Libby P [eds]: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, Saunders, 2001.)

FIGURE 5-15 Pericardial effusion. A, Large cardiac silhouette in the PA chest film in a patient with suspected pericardial effusion. B, A wide pericardial stripe is visible on the lateral view confirming the pericardial abnormality.

FIGURE 5-16 Pericardial calcification. A, PA chest film shows the extensive pericardial calcification (arrows) as well as calcification of the right pleural surfaces. B, CT in the axial plane confirms the pericardial (arrows) and pleural calcification (arrowheads) in this patient with a history of tuberculous pleuritis and pericarditis.

FIGURE 5-17 Pericardial cyst. A, A bulge along the left heart border on the PA chest film. B, The abnormality is confirmed on CT as a water-density filled sharply marginated structure along the left side of the mediastinum compatible with the diagnosis of pericardial cyst (arrow).

FIGURE 5-18 Normal pulmonary vasculature. Lateral image of the chest shows the normal anatomy of the left and right pulmonary arteries in the lateral projection The RPA follows a horizontal course within the mediastinum producing an elliptical opacity. The LPA lies behind the airway and assumes a “shepherd’s crook” configuration parallel to the descending thoracic aorta.

FIGURE 5-19 Pulmonary vasculature. Two contrast-enhanced CT images with maximum intensity projection (MIP) illustrates to best advantage the relationships between the pulmonary veins and arteries in the lower and upper lung zones.

FIGURE 5-20 Increased pulmonary blood flow. PA image shows increased size of the central and peripheral pulmonary vasculature in a patient with atrial septal defect.

FIGURE 5-21 Decreased pulmonary vasculature. An adult patient with flattening of the MPA border and a high, rounded left ventricular border owing to right ventricular enlargement. The peripheral pulmonary vasculature is markedly reduced. The result is a classic boot-shaped heart in this patient with tetralogy of Fallot.

FIGURE 5-22 Pulmonary arterial hypertension. The MPA is markedly enlarged in this patient with Eisenmenger physiology due to a reversed intercardiac shunt.

FIGURE 5-23 Pulmonary venous hypertension. A, The heart is enlarged, the central pulmonary vessels are indistinct, and there is evidence of cephalization in this patient with left-sided heart failure. B and C, CT scan of the chest in the same patient showing the ground-glass pattern of pulmonary edema. D, There is preferential pulmonary edema in the right upper lobe due to acute CHF with mitral regurgitation. The focal right upper lobe pulmonary edema is thought to be due to the orientation of the regurgitant blood flow into the right upper lobe pulmonary veins. E, 4 days later the pulmonary edema pattern is symmetric as the pulmonary venous pressure rises in all lung zones.

FIGURE 5-24 Myocardial calcification. A, Curvilinear-shaped calcification (arrow) is visualized along the anterior wall of the LA in this individual with a history of rheumatic heart disease and atrial fibrillation. A, PA projection. B, coronal CT reformatted image.

FIGURE 5-25 Mitral valve calcification. PA film of the chest shows calcification in the area of the mitral valve (arrows). Valve calcification should not be confused with annular calcification, which is circular, larger, and scalloped. B, Lateral projection.

(From Steiner RM: Radiology of the heart and great vessels. In Braunwald E, Zipes PD, Libby P [eds]: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, Saunders, 2001.)

FIGURE 5-26 Aortic valve calcification. Course nodular and linear calcification conforms to the aortic annulus and the fibrotic, partially fused aortic valve leaflets in a patient with aortic stenosis secondary to bicuspid aortic valve. A, Coned—down view of the chest film in the lateral projection (arrow). B, CT in the axial plane in the same patient shows typical calcifications of the aortic valve (arrowheads).

(From Steiner RM: Radiology of the heart and great vessels. In Braunwald E, Zipes PD, Libby P [eds]: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, Saunders, 2001.)

FIGURE 5-27 A, Lateral plain film radiograph demonstrates calcification of the left anterior descending artery (LAD) as a “tram track” immediately behind the sternum, indicating externsive calcific coronary atherosclerosis of the LAD. B, Nonenhanced axial CT image shows externsive LAD calcification in the same patient as A. C, An ECG-gated angiogram in the axial plane in another patient shows extensive calcification of the LAD together with opacification of surrounding cardiac structures.

FIGURE 5-28 Aortic calcification. A and B, PA and lateral chest radiographs show a continuous thin line of calcification from the ascending aorta to the lower descending thoracic aorta in a 24-year-old patient with severe temporal cephalgia. Biopsy of a temporal artery confirmed the diagnosis Takayasu arteritis. C and D, PA and lateral chest radiographs in a 60-year-old patient with systemic hypertension shows thoracic artery dilation with a rim of calcification deep to the edge of the aortic border. This pattern is compatible with diagnosis of thoracic aortic dissection.

(From Steiner RM: Radiology of the heart and great vessels. In Braunwald E, Zipes PD, Libby P [eds]: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, Saunders, 2001.)

FIGURE 5-29 Coarctation of the aorta. A through C, PA chest radiograph, frontal, angiographic, sagittal MRI images show a zone of narrowing or constriction of the proximal descending aorta in the region of the ligamentum arteriosum—the most frequent site for aortic coarctation.

(From Steiner RM: Radiology of the heart and great vessels. In Braunwald E, Zipes PD, Libby P [eds]: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, Saunders, 2001.)

FIGURE 5-30 Atrial septal defect. A and B, PA and lateral views show enlargement of the main pulmonary artery (arrow) and prominence of the LPA and RPA in the lateral projection. C and D, Within the cardiac silhouette is the radio-opaque Amplatz ASD occluder device (arrow) in the area of the interatrial septum.

FIGURE 5-31 Pulmonary valvular stenosis. A, PA chest radiograph shows prominent MPA (arrow). The heart is not enlarged and the LPA is prominent. B, CT shows a large pulmonary artery. The LPA is asymmetrically enlarged because the blood flow pattern is directed toward the left pulmonary circulation.

FIGURE 5-32 Mitral valvular disease. A, Mitral stenosis: The left atrial appendage (arrow) is markedly enlarged in an otherwise normal cardiac silhouette related to the weakening of the LAA owing to rheumatic carditis. B, Mitral regurgitation: Large cardiac silhouette is shown in this patient with severe mitral regurgitation.

FIGURE 5-33 Nonenhanced axial CT using lung windows demonstrates the lacelike pattern of interstitial lung disease compatible with hemosiderosis of the lung, secondary to long-standing mitral stenosis.

TABLE 5-1 Cardiovascular and Pulmonary Devices and Other Appliances in the ICU Patient

CHAPTER 5 Radiology of the Heart

Plain Film Imaging and Diagnosis

Robert M. Steiner

INTRODUCTION

Imaging of the heart and the great vessels with plain film radiography dates to the earliest days of radiology. Since that time, more advanced technologies including fluoroscopy, kymography, and more recently nuclear imaging, echocardiography (ECHO), computed tomography (CT) and magnetic resonance (MRI) have revolutionized cardiac imaging.

All of these newer modalities yield anatomically detailed images of the heart and great vessels not possible with plain film radiography alone. However, the chest radiograph continues to provide valuable and often unique information concerning the structure and function of the cardiovascular system. The chest radiograph presents an opportunity to recognize subtle and/or overlooked abnormalities such as cardiac chamber enlargement, clinically important calcifications, and evidence of right and left heart dysfunction. Because the pulmonary arteries and veins are visualized in exquisite detail on a well-performed posterior-anterior (PA) and lateral chest radiograph, over and under pulmonary circulation as well as the findings of pulmonary arterial and venous hypertension can be appreciated. Adult onset congenital heart disease, often misdiagnosed or overlooked clinically, can often be identified on a plain film chest radiograph.¹^,²

The portable chest radiograph, usually performed in the anterior-posterior (AP) supine or erect position is the imaging modality of choice for the evaluation and monitoring of patients with cardiopulmonary disease in the intensive care unit (ICU) including postoperative cardiac patients and in those with implanted cardiovascular devices.³^,⁴

In this chapter, the role of plain film chest imaging including alterations of cardiovascular anatomy in a variety of disorders is discussed.

NORMAL AND ABNORMAL CARDIAC BORDERS

Chest Radiograph

The chest radiograph has the advantage of allowing predictable and precise definition of the air-filled lung and soft tissues, thereby permitting the pulmonary arteries, veins, and fissures to be clearly visualized. For this reason, the PA chest film is the ideal screening examination for the evaluation of the vascular structures, the pulmonary parenchyma, and the pleural surfaces. The heart and other mediastinal structures appear as a sharply delineated but featureless opaque silhouette. The coronary arteries, great vessels, cardiac valves and other mediastinal structures cannot be separately identified because they have similar attenuation characteristics as the remainder of the mediastinum. The goal for the image interpreter is to appreciate the normal and abnormal patterns of the cardiac silhouette in a variety of normal and abnormal states. A significant depth of training and experience is needed to recognize the range of patterns of the cardiac silhouette in both normal and abnormal patients and to use that information to establish a clinical diagnosis or suggest additional studies needed to further clarify the findings appreciated on the plain film radiograph.

It is important also to appreciate that an abnormal cardiac border may be due to a nonvascular abnormality such as a pericardial cyst, thymoma or lymphoma, or other solid or cystic masses that may alter the cardiac border. A systematic approach to identify the anatomic landmarks of the heart borders is essential to avoid missing an important, but often subtle, abnormality of the cardiac configuration.

In a well-positioned PA or frontal chest radiograph, the cardiac silhouette and other vascular structures are predictably outlined against the lung as a series of bulges and indentations along the right and left mediastinal borders (Fig. 5-1).

Left Mediastinal Border

In the normal patient, the most superior border-forming structure along the left side of the mediastinum is the left subclavian artery (LSCA). Positioned just above the aortic arch and below the left clavicle, it usually forms a concave border with the lung and lies medial to the aortic arch (see Fig. 5-1). When blood flow through the LSCA is increased, as in a postductal coarctation of the aorta, or when the vessel is tortuous because of atherosclerosis, it will lie at or lateral to the aortic knob or arch—an important clue to the diagnosis of disease. A vertical, straight, or convex, double shadow parallel to the LSCA border is found when a left superior vena cava is present (Fig. 5-2). A cervical aortic arch or the elongated aortic arch of a pseudocoarctation of the aorta may also obscure the normal LSCA border.

FIGURE 5-1 Frontal (A) and lateral (B) projection of the left and right heart borders. Line drawing (C) demonstrates the anatomic relationships of the cardiac chambers.

(From Van Houten FX, Adams DF, Abrams HL: Radiology of valvular heart disease. In Sonnenblick E, Lesch M [eds]: Valvular Heart Disease. New York, Grune & Stratton, 1974.)

FIGURE 5-2 A, Frontal chest radiograph in a patient with a cardiac pacemaker demonstrates the position of the left superior vena cava (LSVC) extending from a position above the aortic arch downward across the medial portion of the left hilum to the region of the coronary sinus. B, Axial nonenhanced thoracic CT shows the pacemaker wire in the LSVC, which lies adjacent to the aortic arch (arrow).

Aortic Arch

The aortic arch or “knob” forms a convex segment along the left mediastinal border below the LSCA border and above the main pulmonary artery border. The aortic convexity is the distal posterior portion of the arch measuring 2.0 ± 1 cm in the young adult and 2.5 to 3.5 cm in the normal middle-aged individual. A clue to the location of the medial border of the aortic arch is the right-sided displacement of the tracheal airway at the same level as the arch. Although the aortic arch border usually has smooth margins, a rounded 2 to 3 mm extension or “nipple” may be present. This structure, seen in up to 10% of normal individuals, is the left superior intercostal vein (LSIV) (Fig. 5-3). An enlarged LSIV will suggest obstruction to blood flow in the deep mediastinal venous system such as superior vena caval obstruction. A dilated LSIV is similar in significance to a dilated azygos vein.

FIGURE 5-3 A, small convex bulge or “nipple” is visible along the aortic arch border representing the left superior intercostal vein. This normal anatomic structure is usually 2 to 3 mm in diameter but will enlarge because of increased blood flow secondary to SVC or other deep venous obstruction in the mediastinum. B, Contrast-enhanced CT shows the anatomic relationship of the left superior intercostal vein (V) to the aortic arch (A).

(From Steiner RM. Radiology of the heart and great vessels. In Braunwald E, Zipes PD, Libby P [eds]. Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, Saunders, 2001.)

The left side of the descending thoracic aorta forms a clearly visualized interface with the left lung behind the left heart border on a well-penetrated frontal chest film (see Fig. 5-4). Pleural effusion and pulmonary masses, left lower lobe pneumonia, and other soft tissue opacities may obliterate the descending aortic border.

The aortic border enlarges in older patients due to a variety of abnormalities such as aortic regurgitation, systemic hypertension, aneurysm, or atherosclerosis. The ascending aorta along the right mediastinal border will also widen and the brachiocephalic arteries may become tortuous and dilate—mimicking a substernal thyroid or other superior mediastinal mass. An aberrant right subclavian artery will also widen the superior right mediastinal border. These right upper mediastinal conditions may require CT scan or MRI for a specific diagnosis.

When the aortic arch border on the left side of the mediastinum is not visible and when the trachea is displaced to the left, the presence of an aortic arch on the right side of the mediastinum will suggest the diagnosis of right aortic arch (RAA) (Fig. 5-4). It is associated in most cases with an aberrant left subclavian artery; however, RAA may occur without an associated aberrant subclavian artery in mirror image RAA with or without associated cyanotic heart disease.

FIGURE 5-4 Aberrant right subclavian vein. A, PA radiograph of the chest demonstrates a convex bulge along the upper right mediastinal border due to an aneurysmal aberrant right subclavian artery. B, Contrast-enhanced axial CT image demonstrates a partially thrombosed dilated aberrant artery corresponding to the convex bulge on the chest radiograph.

Below the aortic arch segment of the left heart border and above the main pulmonary artery border is a variable-sized concavity or indentation termed the aorticopulmonary window. This anatomic landmark is associated with several important structures including the recurrent laryngeal nerve, the ligamentum arteriosum or ductus arteriosus, and the ductus node which drains the lymphatics of the left lung. A convex bulge instead of a concave indentation will suggest important pathology such as an enlarged ductus node due to neoplasm or an inflammatory disorder such as tuberculosis or sarcoidosis. A ductus diverticulum can also create a distinct bulge in the aorticopulmonary window. Left vocal cord paralysis may occur as a result of pressure on the left recurrent laryngeal nerve from intrusion into this confined space from any of these pathologic entities.

Main Pulmonary Artery Border (see Fig. 5-1)

The normally convex main left pulmonary artery (LPA) is situated immediately below the aorticopulmonary window and extends posteriorly as it arches over the left bronchus. It will enlarge because of increased pulmonary blood flow due to a left-to-right shunt, increased pulmonary pressure in patients with obliterative lung disease or Eisenmenger physiology, pulmonary valve stenosis, or weakness of the pulmonary arterial wall in an arteritis (Fig. 5-5). The main pulmonary artery (MPA) and LPA will bulge to the left and the pulmonary artery branches will converge at the lateral border of the enlarged vessel. Alternatively, if the pulmonary artery border is flat or concave, the MPA may be absent or stenotic when truncus arteriosus, tetralogy of Fallot, pulmonary atresia, or transposition of the great vessels is present.

FIGURE 5-5 Prominent main pulmonary artery. PA image of the chest in a 58-year-old man shows a large main pulmonary artery (arrow). The heart is enlarged and the peripheral pulmonary vessels are engorged in this patient with ASD and pulmonary hypertension.

Left Atrial Border (LAA)

The LAA lies below the left main-stem bronchus in the frontal projection and is border forming with the lung. The LAA forms a smooth and slightly concave portion of the left heart border (see Fig. 5-1). Atrial enlargement should be suspected when the LAA is convex and prominent (Fig. 5-6) but the LA may enlarge significantly, even when the LAA remains small, so that enlargement of the LA may be suspected by other signs of enlargement including a double right atrial-left atrial border on the right side of the mediastinum, elevation and widening of the carinal angle, and a prominent LA bulge on the lateral projection. Nonvascular pathology may simulate enlargement of the left atrial appendage. For example, a pericardial cyst, lymphoma, thymoma, or other mediastinal or pleural neoplasms may appear as a convexity of the left atrial border (Fig. 5-7). Bulging of the LAA border may also be caused by partial absence of the pericardium.

FIGURE 5-6 Prominent left atrial appendage. A patient with mitral stenosis. The left atrial appendage border is convex due to enlargement of the appendage secondary to increased pressure and weakening due to rheumatic carditis (arrow).

FIGURE 5-7 Pericardial cyst. A, A portable erect image demonstrates an abnormal left mediastinal border characterized by a convex opacity extending from the aorticopulmonary window to the area of the left atrial appendage. B, A coronal reformatted contrast-enhanced CT image shows the nonenhanced water density structure that conforms to the abnormal left mediastinal border visualized on plain film. The diagnosis of pericardial cyst was entertained.

Left Ventricular Border (LV)

The left ventricular border continues downward seamlessly from the left atrial border. The LV is usually mildly convex in relation to the nearby lung. When the LV is hypertrophic as a result of aortic stenosis or hypertrophic obstructive cardiomyopathy, it may be round and slightly enlarged. When the left ventricle is dilated, as may occur with aortic regurgitation or other causes of decompensation, the apex is displaced downward and laterally (Fig. 5-8). An enlarged right ventricle (RV) may displace the LV border downward, thereby simulating LV dilation or aneurysm.

FIGURE 5-8 Prominent left ventricular border. A, Patient with aortic regurgitation secondary to annuloaortic ectasia in a patient with Marfan syndrome. B, CT shows the massive enlargement of the ascending aorta due to the breakdown of the walls of the vessel.

When the LV dilates because of volume overload as in patients with mitral regurgitation, the dimensions of the LV chamber increase markedly, assuming a globular or water flask appearance similar to a large pericardial effusion. The LV border may extend to the left and can reach the lateral ribs in massive LV dilation. As the LV enlarges, the LA border is obscured. In such circumstances, the left anterior oblique (LAO) projection is helpful to separate the two chambers so that their relative sizes can be discerned (Fig. 5-9). Separating the left heart chambers assumes importance when the differential diagnosis lies between ischemic cardiomyopathy (in which case the left ventricle is larger than the left atrium) and mitral regurgitation (in which case the left atrium may be larger than the left ventricle).

FIGURE 5-9 Left anterior oblique projection. A, A frontal chest radiograph in a 60-degree LAO projection. B, Superimposed drawing of the ventricular chambers and vessels. C, A computer-generated diagram in the LAO projection highlights the valve rings, the atrioventricular groove, and the anatomic relationship of the ventricular chambers.

(From Steiner RM: Radiology of the heart and great vessels. In Braunwald E, Zipes PD, Libby P [eds]. Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. Philadelphia, Saunders 2001.)

Azygos Vein

The azygos vein forms an elliptical or teardrop structure at the right tracheobronchial angle (see Fig. 5-1A). It ascends in the right paravertebral sulcus and arches forward over the right mainstem bronchus to enter the back of the SVC. The azygos vein and its left-sided equivalent, the hemiazygos vein, receive intercostal veins and act as an important collateral pathway when the deep mediastinal veins are obstructed. Normally measuring 0.7 ± 0.3 cm across in the erect and 1.0 ± 0.3 cm in the supine position, the azygos vein is a good indicator of changing cardiovascular dynamics. It is enlarged in SVC and IVC obstruction, in the absence of the intrahepatic portion of the inferior vena cava, in portal vein obstruction, and in both left- and right-sided cardiac failure. A change in diameter of the azygos vein from film to film will parallel changes in pulmonary venous pressure, which makes it a useful guide to the development of congestive heart failure on plain film radiographs. An azygos fissure can be found in 3% of the population. When an azygos fissure is present, the azygos vein is displaced laterally and superiorly and will dilate under the same conditions as a normally positioned azygos vein.