Cardiothoracic Ratio

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.

TABLE 1-1 Cardiothoracic ratio

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).

TABLE 1-2 Typical variations of heart and mediastinum measurements on the chest film

Right Atrium

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.

FIGURE 1-5 Superior right atrial convexity. In Ebstein anomaly, the large right atrium has a characteristic round superior border.

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).

FIGURE 1-6 Right atrial enlargement in pulmonary atresia with intact ventricular septum. This patient had moderate tricuspid regurgitation. Note the decreased vascularity in the lungs.

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.

Right Ventricle

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.

FIGURE 1-9 Boot-shaped heart. In tetralogy of Fallot, the cardiac apex has an uplifted appearance. Other typical features are the concave main pulmonary artery segment and the right aortic arch.

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.

Left Atrium

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.

The indirect signs visible only when the left atrium is dilated at least moderately are highlighted in Box 1-4 and Figures 1-12 and 1-13.

FIGURE 1-12 Convex left atrial appendage. The large left atrial appendage and the redistribution of blood flow to the upper lobes indicate mitral stenosis.

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 Ventricle

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.

FIGURE 1-16 Left ventricular aneurysm. A and B, This angular left ventricular border with curvilinear calcification (arrow) is characteristic of an aneurysm.

Distinguishing Characteristics

Calcium in the aortic valve is seen best in the lateral view, where it projects free of the spine. You can distinguish between aortic and mitral calcification by the following methods.

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.

FIGURE 1-18 Bicuspid aortic valve calcification. A, The calcification is located in the aortic valve by following the dilated ascending aorta into the heart. B, The distinctive bicuspid valve calcification is a ring with a linear bar through it.

Calcific Aortic Stenosis

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.

Distinguishing Patterns

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).

FIGURE 1-19 Mitral annulus calcification. The characteristic oval calcification (arrows) is located below the left atrial appendage segment.

Clinical Significance

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).

FIGURE 1-20 Tricuspid annulus calcification. A, Adult tetralogy of Fallot with unusually large mediastinal collaterals to the pulmonary hila. B, The tricuspid annulus (arrows) calcified because of the chronic right ventricular hypertension.

Causes