Chapter 1 The Elements of Cardiac Imaging
Cardiovascular imaging is different from that for all other organs because the dimension of time has to be included in the subsecond acquisition and analysis of images. The chest film remains the entry-level examination for most cardiac problems. Although daunting economic and scheduling constraints remain, the cross-sectional methods—echocardiography, computed tomography (CT), and magnetic resonance imaging (MRI)—are becoming the primary imaging choices to diagnose cardiac diseases because the millisecond temporal resolution and the millimeter spacial resolution can follow the beating heart and the moving blood.
The anatomic and physiologic effects of heart disease have many common imaging features. Chamber dilatation, valve calcification, and anomalous connections are morphologic signs of cardiac abnormalities. Increased or decreased blood flow and segmental wall motion disorders are physiologic signs of heart disease. The analysis for cardiovascular disease on the chest film, echocardiogram, CT scan, and MRI begins with a search for these common elements. This chapter provides a grounding in basic cardiac anatomy and physiology that is applicable to all types of modalities. A more systematic imaging examination can then be devised to address particular questions.
The chest film is often the first imaging procedure performed when heart disease is suspected, and more commonly, it is used to assess and follow the severity of cardiac disease. Because the chest film forms images by projection, this technique detects only those cardiopulmonary abnormalities that change the shape of the heart, mediastinum, and lungs and those that alter the structure of the pulmonary vasculature. Clinically silent heart disease may also be detected on a chest film taken for other reasons. Extracardial structures, particularly in the abdomen and the thoracic cage, may produce additional clues indicating heart disease. Calcification in the aortic valve, for example, identifies the abnormal structure and directs the differential diagnosis toward a particular pathologic lesion (Box 1-1).
The age of the patient greatly influences what is considered the normal appearance of the heart and lungs, and there are some normal variants that may at times mimic disease. In the infant, the thymus typically obscures the upper portion of the mediastinum and may overlay the pulmonary hilum. In rare instances it extends inferiorly, causing the transverse heart size to appear falsely large. In the first day of life, the pulmonary vasculature has a fuzzy appearance. This normally represents the complex and rapidly changing pressures and flows in the lungs, but it can also suggest pulmonary abnormalities (e.g., transient tachypnea of the newborn or respiratory distress syndrome) or cardiac disease. In sick children under prolonged stress, the thymus may shrink to a small size but usually is still partially visible. The thymic shadow is invisible in transposition of the great arteries.
In the child and adolescent, the bronchopulmonary markings become more distinguishable, and the thymic shadow regresses and becomes inapparent so the aortic arch and pulmonary trunk can be seen. A convex pulmonary trunk in girls in their late teens may suggest pulmonary artery enlargement, but in the absence of a heart murmur this is usually a normal variant (Fig. 1-1). However, an electrocardiogram (ECG) may be necessary to exclude entities such as pulmonary stenosis and left-to-right shunts. The “double density” of the pulmonary veins may mimic an enlarged left atrium (Fig. 1-2), but a large left atrium has a rounder curve and extends medially above the diaphragm.
FIGURE 1-1 Convex main pulmonary artery. The moderate convexity of the main pulmonary artery segment (open arrow) is a normal variant in this young adult even though the aortic arch (arrows) is on the right side. The space usually occupied by a left aortic arch contains the aberrant left subclavian artery.
FIGURE 1-2 Confluence of the pulmonary veins. The superior and inferior right pulmonary veins may join and connect with the left atrium as a common vein. This normal variant may look similar to an enlarged left atrium (arrow) on the frontal film (A) and a pulmonary nodule (arrow) on the lateral film (B).
In the young adult, the major changes in the cardiac silhouette are the mild prominence of the aortic arch and the vertical orientation of the heart. In the elderly, the thoracic aorta may become elongated and tortuous. The cardiac apex becomes more rounded and the overall heart size is smaller, which possibly reflects aging changes, but more likely results from the loss of heart muscle because of lack of exercise.
The determination of heart size, both subjectively and quantitatively, has been assessed from the chest film for more than 70 years. Then Danzer described the cardiothoracic ratio, which is still one of the most common measurements of overall heart size. This ratio was constructed to measure left ventricular dilatation. Because it measures the transverse heart diameter, the cardiothoracic ratio is usually normal when either the left atrium or the right ventricle is moderately enlarged because neither of these two chambers is reflected in the transverse dimension. The left atrium and right ventricle become border-forming when they are severely enlarged. Rose and colleagues noted that for the cardiothoracic ratio to reliably detect enlargement of the left ventricle (Table 1-1), changes in left ventricular volume up to 66% in excess of normal are needed.
|Patient Characteristics||Normal Ratio|
|>1 month old||<0.5|
|Sensitivity = 0.45 (Many patients with left ventricular dilatation are not detected.)|
|Specificity = 0.85 (When ratio exceeds the normal value, heart is clearly large.)|
|Accuracy = 0.59|
Modified with permission from Rose CP, Stolberg HO: The limited utility of the plain chest film in the assessment of left ventricular structure and function, Invest Radiol 17:139-144, 1982.
When the heart size is subjectively evaluated based on the configuration of the heart with respect to the thorax, the sensitivity and specificity are quite similar to the measured cardiothoracic ratio. For this reason and because quantitative measurements from tomographic imaging methods are commonly available, the cardiothoracic ratio is now used mainly as an adjunct in assessing heart size on the chest film. Although the cardiothoracic ratio is moderately variable among individuals, it is a useful indicator in an individual who is being watched for potential cardiac dilatation, such as in chronic aortic regurgitation. In this instance, an abrupt change in the cardiothoracic ratio suggests the need for urgent clinical reevaluation.
Marathon runners with heart rates in the range of 30 to 40 beats per minute occasionally have a cardiothoracic ratio between 0.50 and 0.55, reflecting the normal physiologic dilatation of the heart rather than any overall hypertrophy.
Several other measurements can be made from the standard posteroanterior and lateral chest film. Examples include total heart volume, left atrial dimension on the frontal film, width of the right descending pulmonary artery, and the distance of the left ventricle behind the inferior vena cava. These, however, are rarely used now in clinical evaluation.
Most measurements made from the chest film have poor correlation with left ventricular size from quantitative angiographic measurements. Therefore, the measurements of specific chamber diameters, volumes, and wall thicknesses should be made from techniques that show the chamber cavities (e.g., echocardiography, angiography, CT, and MRI).
Measurements of the heart and mediastinum are dramatically affected by the height of the diaphragm and the intrathoracic pressure and less so by the body position and status of the intravascular volume (Table 1-2).
|In expiration||Transverse diameter of heart and mediastinum widens|
Indistinct appearance of pulmonary hilum can be identical to that seen with pulmonary edema
|In recumbent position||Heart is broader|
Lung volumes are lower
Upper lobe arteries and veins appear more distended
|On posteroanterior film||Change in heart width between systole and diastole is typically less than 1 cm|
|On right anterior oblique film||Heart size does not change between systole and diastole|
Left ventricular apex appears akinetic
|On left anterior oblique film||Posterolateral wall motion is typically more than 1 cm|
Usually the abnormal enlargement of the heart is easily recognized by its displacement out of the mediastinum. It may also be recognized by contour changes, by a new or different interface with the adjacent lung, or by displacement of adjacent mediastinal structures.
Each chamber basically enlarges directly outward from its normal position. Except for the right ventricle, isolated chamber enlargement does not affect the position of the heart in the mediastinum or the identification of other chamber enlargement. When the right ventricle enlarges, it contacts the sternum and rotates the heart posteriorly and in a clockwise direction as viewed from below. Frequently in right ventricular enlargement, the normal left ventricle may falsely appear enlarged on both the frontal and lateral films because the entire heart is displaced posteriorly. If the right ventricle is dilated, the diagnosis of left ventricular enlargement may not be possible in the chest film (Dinsmore principle). Therefore, you should assess the size of the right ventricle on the lateral film before judging the left ventricle (Figure 1-3, Box 1-2).
FIGURE 1-3 Right heart enlargement suggesting left heart enlargement. The left ventricle is normal in this patient with Ebstein anomaly. A, The entire left heart border from the pulmonary artery to the diaphragm is the border of the huge right ventricle. B, The posterior border of the heart projected over the spine is the normal-sized left ventricle, which has been pushed backward by the anterior right ventricle touching the sternum.
In the frontal view, the right atrium is visible because of its border with the right middle lobe (see Box 1-2). Neither subtle nor moderate enlargement can be recognized accurately because there is moderate variability of its shape in normal subjects, and in expiration the right atrium becomes rounder and moves to the right (Figures 1-4, 1-5).
FIGURE 1-4 Right atrial enlargement in rheumatic heart disease. A, The unusually large right atrium compresses the right middle lobe and extends inferiorly to intersect the diaphragm. A large left atrium usually does not have a diaphragmatic interface. B, Enlargement of the right heart creates a sharp interface with the lung (arrow). The horizontal contour suggests that this is the right atrial appendage rather than the right ventricle.
The right atrium and the other three chambers enlarge because of increased pressure, increased blood volume, or a wall abnormality. Common causes of right atrial enlargement are tricuspid stenosis and regurgitation, atrial septal defect, atrial fibrillation, and dilated cardiomyopathy. Ebstein anomaly may have all of these features. In pulmonary atresia, the right atrium dilates in direct proportion to the amount of tricuspid regurgitation (Fig. 1-6).
All the signs of right heart enlargement that are implied on the chest film are directly visible on the CT scan. The right atrium and ventricle touch the anterior chest wall and rotate the heart posteriorly. The right coronary artery adjacent to the right atrial appendage lies to the left of the sternum (Fig. 1-7).
FIGURE 1-7 Right atrial enlargement in rheumatic heart disease. The appendage portion of the right atrium (RA) touches the anterior chest wall in this patient, who had a sternotomy for mitral valve replacement. The right coronary artery is visible in the fat between the right atrium and right ventricle. The left atrium is calcified and also enlarged.
On the lateral view, the normal right ventricle does not touch more than one fourth of the lower portion of the sternum as measured by the distance from the sterno diaphragmatic angle to the point at which the trachea meets the sternum. One sign of right ventricular enlargement is the filling in of more than one third of the retrosternal space. On the frontal view, the normal right ventricle is not visible, and only extreme dilatation causes recognizable signs because the heart rotates clockwise as it dilates and pushes against the sternum. In this instance, the usual contour of the left atrial appendage is rotated posteriorly and is no longer part of the left side of the mediastinum. You can recognize this sign by an unusually long convex curvature extending inferiorly from the main pulmonary artery (Fig. 1-8). In extreme instances the entire left heart border may be the right ventricle (Box 1-3).
FIGURE 1-8 Right ventricular enlargement. A, The broad convexity along the upper left heart border represents the dilated right ventricle. B, The right ventricle touches the sternum and fills one third of the retrosternal space. Shunt vascularity is also evident in this patient with atrial septal defect.
In tetralogy of Fallot when the fat pad is absent in the left cardiophrenic angle, the heart may have an uplifted cardiac apex (Fig. 1-9), which has been called the “boot-shaped heart” or the coeur en sabot. The right ventricle is not enlarged but may have hypertrophy.
Common causes of right ventricular enlargement are pulmonary valve stenosis, pulmonary artery hypertension (cor pulmonale), atrial septal defect, tricuspid regurgitation, and dilated cardiomyopathy; it can occur secondarily to left ventricular failure.
There are many clues to left atrial enlargement on the frontal and lateral chest film. One of the earliest signs of slight enlargement is the appearance of the double density, which is the right side of the left atrium as it pushes into the adjacent lung. Because a prominent pulmonary vein or varix may also cause a vertical double density, the double density should begin to curve inferiorly (Fig. 1-10). In extreme cases, the left atrium may enlarge to the right side and touch the right thoracic wall (Fig. 1-11). The etiology of this “giant left atrium” is rheumatic heart disease, mainly from mitral regurgitation.
FIGURE 1-10 Left atrial enlargement in mitral stenosis. The double density (arrow) occurs because the large left atrium pushes into the adjacent lung. The line curves inferiorly, differentiating it from a pulmonary varix. The large pulmonary artery indicates pulmonary hypertension.
FIGURE 1-11 Giant left atrium. Rheumatic mitral valve disease has caused the left atrium to enlarge so that it almost touches the right thorax wall. The carina is splayed superiorly over the atrium, and the left atrial appendage is convex.
A convex left atrial appendage on the frontal view is abnormal and usually reflects prior rheumatic heart disease. In pure mitral regurgitation, the body of the left atrium, not the appendage, enlarges.
FIGURE 1-13 Posterior displacement of the left main stem bronchus. The left bronchus should lie in a straight line with the trachea but is displaced posteriorly (arrow) by the large left atrium. The large left pulmonary artery is seen on top of the bronchus.
Common acquired causes of left atrial enlargement are mitral stenosis or regurgitation, left ventricular failure, and left atrial myxoma. Congenital causes include ventricular septal defects, patent ductus arteriosus, and the hypoplastic left heart complex. When atrial fibrillation occurs, the left atrial volume may increase by 20%.
Left ventricular enlargement exists if the left heart border is displaced leftward, inferiorly, or posteriorly. Inferior displacement may invert the diaphragm and cause this border to appear in the gastric air bubble. The chest film cannot reliably distinguish between left ventricular dilatation and hypertrophy. With hypertrophy, the apex has a pronounced rounding and a decrease in its radius of curvature. The elderly normal heart also has this shape. When massive hypertrophy is present, the left ventricular shape is large and appears similar to one that is only dilated (Box 1-5).
Common causes of left ventricular enlargement can be grouped into three categories: pressure overload (hypertension, aortic stenosis; Fig. 1-14); volume overload (aortic or mitral regurgitation, ventricular septal defects; Fig. 1-15); and wall abnormalities (left ventricular aneurysm, hypertrophic cardiomyopathy; Fig. 1-16).
FIGURE 1-14 Aortic stenosis. A, The left ventricle is enlarged to the left and inferiorly where it is seen through the stomach bubble. The ascending aorta has poststenotic dilatation. B, The posterior border of the left ventricle is significantly behind the inferior vena cava. Note moderate calcium in the aortic valve (arrow).
FIGURE 1-15 Aortic regurgitation. The left ventricle and the aorta are both large from moderate aortic regurgitation. The indentation in the descending thoracic aorta (arrow) and the absence of rib notching denote a pseudocoarctation. Because 50% of those with pseudocoarctation have a bicuspid aortic valve, this probably is the etiology of the aortic regurgitation.
Calcium in the heart is not only a marker for specific diseases but also an aid for locating structures on the chest film. Structures that calcify usually can be located easily on routine frontal and lateral films, although, in special situations, oblique views with barium may be necessary. Most of the calcium found in the heart is dystrophic and is in tissue that has had a previous inflammatory process (e.g., rheumatic mitral stenosis) or has been in a malformed structure that has degenerated (e.g., bicuspid aortic valve).
FIGURE 1-17 Location of the aortic valve on the lateral chest film. A line drawn from the junction of the diaphragm and the sternum to the carina passes through the aortic valve. The mitral valve is below and posterior.
Calcium in the aortic valve may extend from the valve into the adjacent interventricular septum and cause arrhythmias. In most cases of bicuspid aortic stenosis, the mitral valve is normal and the left atrium is not enlarged. When both the aortic and mitral valves are calcified, the cause is usually rheumatic heart disease. In a patient without rheumatic heart disease or a previous episode of infected endocarditis, calcification in a tricuspid aortic valve is rare before age 70. Patients with bicuspid aortic valves also may have had rheumatic heart disease or endocarditis and develop heavy central calcification.
The aortic valve is the only one that has a good correlation between the amount of calcium seen on a chest film and the amount of stenosis. If the patient is over age 35, heavy calcification in the aortic valve indicates severe stenosis that will probably require a valve replacement. Conversely, if no calcium is seen by fluoroscopy in the aortic valve, it is unlikely that aortic stenosis exists.
The mitral valve ring may calcify in individuals over age 60. The incidence is four times higher in women. The calcium begins to form in or below the mitral annulus at the junction between the ventricular myocardium and the posterior mitral leaflet. More severe degrees of calcification will form a pattern resembling the letter J, the letter O, or a reversed letter C (Figure 1-19).
In most instances, mitral annulus calcification has little clinical significance and is a noninflammatory chronic degenerative process. In extreme cases, the mass of calcification can grow posteriorly into the ventricular myocardium to produce heart block. It can also grow anteriorly into the leaflets of the mitral valve to cause mitral regurgitation and stenosis. Rarely, the calcification can erode through the endocardium and cause small systemic emboli. Mitral annulus calcification in the elderly is associated with a doubled risk of stroke, independent of the traditional risk factors.
Aortic stenosis and hypertension have a higher incidence of mitral annulus calcification, possibly because of increased strain exerted on the mitral valve apparatus from the left ventricular pressure overload. For the same reason, the tricuspid annulus rarely may calcify when right ventricular pressures have been chronically increased (Fig. 1-20).