The Elements of Cardiac Imaging

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.


Age and Its Visible Effects

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.

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.

Evaluation of Heart Size

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


Patient Characteristics Normal Ratio
Newborn <0.6
>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).

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

Circumstance Variation
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

Chamber Enlargement

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).

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).

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).

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).

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.

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.

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.

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).


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).

Aortic Valve Calcification

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.

Aortic calcification may have a specific appearance. Calcification in a bicuspid aortic valve, which never occurs before age 35, is dystrophic and involves the raphe and edges of the cusps. The calcification is linear in the raphe and may curve along the cusp edge. A nearly circular calcification with an interior linear bar in the aortic region is diagnostic of a bicuspid valve (Fig. 1-18). In older patients with bicuspid aortic stenosis, this architecture is obliterated by nodular masses of calcium; in this instance the severely calcified aortic valve looks identical to that of the three major causes of aortic stenosis: bicuspid valve, rheumatic heart disease, and degenerative calcific aortic stenosis.

Mitral Annulus Calcification

Dec 26, 2015 | Posted by in CARDIOVASCULAR IMAGING | Comments Off on The Elements of Cardiac Imaging

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