RADIOLOGY OF THE RIGHT VENTRICLE

RADIOLOGY OF THE RIGHT VENTRICLE

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CARDIAC RADIOLOGY

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RADIOLOGY OF THE RIGHT VENTRICLE Lawrence M. Boxt, MD

The right ventricle (RV) pumps desaturated blood into the low-resistance pulmonary bed at low pressure. Due to its location in the heart and chest, changes in RV morphology secondary to pathologic function may not be demonstrated by direct change in the plain film radiographic contour of the ventricle itself. Plain film evaluation of RV disease is inferential, dependent upon recognition and evaluation of changes in adjacent structures, and in the position of the heart itself. Contrast angiography provides direct demonstration of the ventricular cavity. Rapid, cine acquisition allows evaluation of functional abnormalities and direct demonstration of underlying valvular and myocardial disease. MR imaging techniques not only provide the morphologic and functional information afforded by plain film and contrast angiographic techniques, but also provide the information noninvasively, and in arbitrary tomographic section, allowing direct demonstration of local morphologic abnormalities and their sequelae. Prior to the advent of MR imaging, RV disease and its investigation had been limited and relegated to the clinical backwaters of cardiac imaging, often limited to evaluation in patients with congenital heart disease. The ability safely to visualize the chamber and its function has led to an increase in its use in evaluation of RV disease, supporting aware-

ness of RV disease and its effect on global cardiac function. This article describes the structure and function of the RV, and the changes it undergoes in patients with RV disease and other forms of cardiovascular disease that affect the RV. When sought, changes found on plain film examination are very sensitive, but not very specific. Nevertheless, they should indicate pathophysiologic changes, and suggest further investigation to narrow or refine the differential diagnosis. Use of contrast angiography provides much anatomic and morphologic information, which helps define the problem and allows assessment of its severity. The growing use of MR imaging for the evaluation of patients with RV dysfunction is a consequence of its sensitivity to change, and ability to demonstrate directly the morphologic sequelae of an underlying disease, or the disease itself. Furthermore, it does this noninvasively, without the use of ionizing radiation and intravascular contrast material administration. Thus, we have excellent means of investigating RV disease and dysfunction, and should use these tools to help in the management of this diverse group of patients. ANATOMY OF THE RV The right ventricle is a volume pump76that drives desaturated blood to the lungs for oxy-

From the Division of Cardiovascular MR Imaging, Department of Radiology, Beth Israel Medical Center, New York, New York

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genation. In the normal adult, it pumps an equivalent volume of blood as does the left ventricle, but at significantly lower pressure. The term right ventricle, however, is a misnomer. The ”rightness” of the anterior pulmonary ventricle reflects the pathologist’s description of an excised heart placed on its apex with the interventricular septum in a sagittal plane. The term morphologic right ventricle is often to define this cardiac chamber in terms of its physical characteristics, in order to allow its identification in cases of congenital heart disease in which abnormal atrioventricular or ventriculoarterial connection exists. In the normally connected situs solitus heart, the RV is an anterior, nearly midline structure. The shape of the RV cavity is complex; it is not axissymmetric like the left ventricle. Rather, it has the appearance of an asymmetric truncated pyramid. The right posterior border of the ventricle is formed by the plane of the tricuspid valve (contained within the anterior atrioventricular ring) and crista supraventricularis. The posterior and left lateral borders of the ventricle, formed by the interventricular septum, are concave toward the center of the ventricular chamber. This bowing gives the RV the appearance of draping around the left ventricle. The anterior border of the ventricle is called the free wull. It is mildly convex and extends to the superior-most aspect of the ventricle, the outflow tract and pulmonary valve. The inferior surface of the RV is nearly flat and rests on the right diaphragm, superior to the left lobe of the liver. The RV cavity is usually divided into an inlet (or sinus) and outlet portion. The inflow and outflow regions are separated from each other by complex, well-defined muscle bands that together form a not quite circular orifice. The inlet portion of the RV consists of the tricuspid valve, the chordae tendinae, papillary muscles, and the trabeculated myocardium surrounding the tricuspid valve. The outlet portion of the ventricle is also commonly referred to as the infundibulum. This, however, is a bit confusing. The infundibulum is the muscular portion of the RV that separates the semilunar (pulmonary) from the atrioventricular (tricuspid) valve. Thus, the ventricular outflow is the portion of the RV cavity surrounded (formed) by the infundibulum. Consider the analogy of a doughnut and its hole. That is, the outflow tract is the hole through which blood flows and the infundib-

ulum is the doughnut, which contains the blood. The semilunar valve rests on the RV infundibulum, separated from the tricuspid valve. The septal and parietal bands surround the outflow tract, and fuse to form the crista supraventricularis, the superior-most identifiable muscle bundle on the RV side of the interventricular septum. The crista continues along the anterior aspect of the interventricular septum toward the ventricular apex as the septomarginal trabeculation. Just proximal to the intersection of the interventricular septum with the free wall of the RV, the moderator band extends from the septomarginal trabeculation to the free wall. A number of small papillary muscles anchor the cusps of the tricuspid valve by chordae tendineae to the interventricular septum. The medial (conal) papillary muscle (often referred to as the muscle of Luncisi) originates from the junction of the septal band of the crista supraventricularis with the septomarginal trabeculation. This papillary muscle is always small. It receives chordae tendineae from the medial portion of the anterior cusp and a few chordae from the most anterior surface of the septal cusp. The anterior papillary muscle of the tricuspid valve is usually well developed, and originates from the outer, lateral third of the septomarginal trabeculation. This papillary muscle usually receives chordae tendineae from both the lateral portion of the anterior and posterolateral cusps. A variable number (usually two or three) of very small papillary muscles originate from the posterior border of the septal band of the crista supraventricularis, and receive chordae tendineae from the anterior half of the septal cusp of the tricuspid valve. Occasionally, papillary muscles arising from the interventricular septum may be rudimentary or absent. In these cases, the chordae insert directly onto the septum itself. The septal surface of the RV is divided into the posterior (or basal) portion; the muscular coarse trabecular portion; and the conal (infundibular) septum. When examined by direct inspection, RV trabeculations appear to be fewer, more coarse, and straighter than those of the left ventricle. A more reliable angiographic means of differentiating between right and left ventricles is based upon whether or not the atrioventricular and semilunar valves are separated by a muscular infundibulum; this is the observation one must make to characterize the morphologic RV (Fig. 1).

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Figure 1. Diastolic frames from a right ventriculogram in a 7-year-old boy with pulmonic stenosis. A, PA view. The opacified cavity of the ventricle extends from the filling defect of the tricuspid valve (small arrows) to the interventricular septum (open arrows), medial to the lower left heart border. The infundibulum separates the plane of the tricuspid valve from the plane of the pulmonary valve (long arrows). Right ventricular myocardial trabeculations appear as filling defects in the chamber. 6,In lateral view, the posterior aspect of the infundibulum (white arrows), separating the filling defect of the tricuspid (TV) from the pulmonary valve (black arrows), is formed by the crista supraventricularis.

The tricuspid valve is normally 10 to 12.5 cm in circumference,S2and consists of three leaflets (anterior,posterior, and septal) all separated by commissures. The pulmonary valve is supported by the infundibulum, and lies to the left, anterior, and nearly 1.5 cm cephalad to the aortic valve.82 The right coronary artery (RCA) and its branches perfuse the RV myocardium (Fig. 2). After originating from the anterior sinus of Valsalva, the RCA turns to the right to enter the anterior atrioventricular ring. The first branches from the proximal artery are the sinoatrial node branch and conus artery. The sinoatrial node branch ascends and moves posteriorly to wrap around the superior vena cava and perfuse the sinoatrial node. The conus artery is the highest marginal branch of the RCA. In nearly 50% of individual^,^^ the origin of the conus artery is from the anterior sinus of Valsalva, separate from the RCA. In nearly 10% of hearts, branches of the circumflex artery supply posterior RV myocardium.26RV free wall myocardium is perfused by marginal branches of the RCA, each originating nearly at a right angle from the trunk artery in the fat of the anterior atrioventricular ring, and coursing in a parallel fashion toward the anterior interventricular sulcus. In 85% of individuals, the posterior descending coronary artery arises from the distal RCA at the crux of the heart and per-

fuses the posterior inferior interventricular septum. Depending upon the length of the anterior descending artery, the RCA may perfuse the anterior aspect of the interventricular septum as well. PHYSIOLOGY O f THE RV

RV function changes when the newborn leaves the uterus at birth. Recognition of the change from the aquatic uterine fetal working environment of the RV to the postnatal “dryland” environment of the outside helps shed light on changes the RV faces when exposed to acquired left heart and pulmonary disease. In utero, the RV myocardium pumps against high pulmonary vascular resistance caused by the medial hypertrophy of the muscularized pulmonary arterioles. This results in relative RV hypertrophy. With the first breath at birth, the child expands their bronchial tree, brings oxygen into the lungs, and effects the first gas exchange across the alveolar bed. The increased blood oxygen concentration has a local vasodilatory effect on the pulmonary arteriolar bed, lowering pulmonary resistance. Cross-clamping the umbilical cord and removing the placenta from the newborn circulation results in a rapid increase in systemic vascular resistance.

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Figure 2. Right coronary arteriogram in a 24-year-old man with aortic stenosis. A, In left anterior oblique (LAO) view, right ventricular marginal branches (white arrows) rising from the main trunk of the right coronary artery in the anterior AV groove perfuse the right ventricular free wall. Distal to the cardiac crux, the posterior descending artery (curved arrow) is foreshortened. The continuation of the distal right coronary artery in the posterior AV groove (open arrows) is in profile. 6,In the right anterior oblique (RAO) view, the artery takes a right turn toward the anterior atrioventricular groove, in which it descends toward the diaphragmatic surface of the ventricle. The first branch from the proximal artery is the conus branch (white arrows), which perfuses the right ventricular infundibulum. A large, bifurcating marginal branch (curved arrow) perfuses the right ventricular free wall. At the intersection of the anterior AV ring and the inferior interventricular septum (open arrow), the posterior descending artery (black arrows) originates, perfusing the inferior interventricular septum.

Over the course of the next 2 months, pulmonary vascular resistance continues to fall and systemic vascular resistance rises to adult levels. The medial hypertrophy of the pulmonary arteriolar bed and the hypertrophy of the fetal RV regresses. Thus, the RV developes in a greatly afterloaded state, and subsequently functions after birth against a markedly decreased (normal) load (Fig. 3). After the newborn circulation stabilizes, the circulatory relationship between the heart and lungs is that the heart pumps equal amounts of blood to both the lungs and systemic circulation (i.e., RV output equals left ventricular output). In the adult, the thin-walled RV pumps at low pressure against low pulmonary vascular resistance, whereas the thickerwalled left ventricle pumps at higher pressure against the higher systemic vascular resistance. Because the pulmonary circulation is a low-resistance circuit with little diastolic pressure drop from pulmonary artery to pulmonary vein and left atrium, any increase in left atrial pressure has a profound effect on pulmonary artery pressure, and hence RV work. Similarly, filling of the left ventricle is dependent upon pulmonary venous return to

the left atrium, which reflects RV pump function. Thus, an abnormality affecting RV function has an affect on left ventricular function as well. The interface between the two ventricles is the interventricular septum. Normally, the septum acts as if a part of the left ventricle. Viewed in short axis, the wall segments of the left ventricle, including the interventricular septum, appear to contract radially and symmetrically during systole (Fig. 4). The curvature of the interventricular septum is convex toward the RV cavity during both ventricular diastole and systole. RV contraction is characterized by three separate mechanisms that occur more or less simultaneously. The internal trabeculae and papillary muscles contract, drawing the atrioventricular ring and tricuspid valve toward the cardiac apex, shortening the chamber longitudinal axis. A bellows-like movement of the free wall toward the interventricular septum shortens the anteroposterior dimension of the chamber. Shortening of the deep circular fibers of the left ventricle increases the curvature of the interventricular septum, augmenting the bellows-like function of the free wall contraction. Changes in the shape (geometry) of the RV

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Figure 3. Short axis spin echo view of the heart of a 5week-old girl. The thickness of the right ventricular (RV) free wall (large arrows) is nearly that of the interventricular septum and posterior wall of the left ventricle (Lv). Notice the thickened RV trabeculations (small arrows), and the straightening of the interventricular septum.

affect the shape of the interventricular septum, and are therefore at the expense of left ventricular geometry. That is, RV dilatation may straighten or even reverse the curvature of the interventricular septum toward the left ventricle (Fig. 5). In such cases, left ventricular filling and thus end-diastolic volume may be impaired, limiting left ventricular output.

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~i~~~~ 5. spinecho short MR examination of a 22year-old with a secundum atrial septal defect and normal PA pressure. The circular shape of the left ventricle (LV) is distorted by the straightened interventricular septum. Notice the right ventricular (RV) papillary muscles extending from the interventricular septum (arrows).

RADIOLOGIC EVALUATION

OF THE RV Radiologic evaluation provides information concerning the size and shape of the ventricular cavity and the trabeculation and mass of the RV myocardium. Diagnosis of RV dysfunction and conditions that result in such

Figure 4. Gradient reversal short axis MR examination of a 28-year-old man. A, At end diastole, the right ventricular chamber (RV) appears triangular. The RV free wall myocardium is very thin when compared with the interventricular septum or left ventricular (LV) free wall. B, End systolic frame. The right ventricular cavity is nearly obliterated, filled by thickened trabeculations.

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dysfunction not only depends upon direct demonstration of a RV abnormality, but identification and quantitation of associated and causative abnormalities as well. The utility of these imaging modalities is the product of their diagnostic sensitivity and specificity as well as cost and patient risk.

Plain Chest Film Little of the RV is directly visualized as a heart border-forming structure in the posteroanterior radiograph (Fig. 6 ) . The inferior aspect of the main pulmonary artery segment of the left heart border is formed by the distal portion of the RV outflow tract. On lateral view, the RV occupies the lower 40% of the retrosternal space. The posterior course of the RV outflow tract may be appreciated as the curving interface between the retrosternal density and air lucency of the lungs. Thus, the posteroanterior plain chest film is of limited value in evaluation of RV change. In fact, RV dilatation may not be directly demonstrated on plain film examination. Changes in the position of the heart in the chest and appearance of the lateral borders of the car-

diac silhouette, however, are useful as inferential signs of RV dilatation. Radiographic changes in the appearance of the heart in patients with RV enlargement result from (as viewed from below) clockwise rotation of the heart and mediastinal structures. This has the effect of altering the superior portion of the lower third of the left heart contour. As the heart rotates, the relative concavity of the left atrial appendage segment is rotated posteriorly and medially, and the RV outflow tract and anterior interventricular sulcus are displaced laterally, and come to form the middle portion of the left heart border. This portion of the left heart border appears fuller than in the normal individual (Fig. 7). This change can be differentiated from left ventricular and left atrial enlargement by recognition of the increased distance between the left main bronchus (which itself does not appear elevated on frontal examination or displaced on lateral examination) and the left heart border itself as well as the observation that the left bronchus seems to run parallel to the left heart border, rather than crossing it. In addition, in cases of RV dilatation, other signs of heart and mediastinal rotation usually occur. Most important of these is medial displacement of the superior vena

Figure 6. Normal plain chest film of a 25-year-old woman. A, PA view. The main pulmonary artery segment (P) is no greater in caliber than the aortic arch segment (Ao) and extends to the crossing of the left bronchus (long arrow) with the left heart border. B, Lateral view. The free wall of the right ventricle fills the lower retrosternal space. The right ventricular outflow begins to course away from the sternum (short arrows) just inferior to the anterior-most contour of the ascending aorta (long arrows).

RADIOLOGY OF THE RIGHT VENTRICLE

Figure 7. PA chest film of a 22-year-old woman with a secundum atrial septal defect. The pulmonary artery segment (P) is greater in caliber than the aortic arch segment (Ao). The left heart border inferior to the PA segment (white arrows) is straightened and is nearly parallel to the left bronchus (black arrows), which does not cross the left heart border. Notice the sharp, dilated pulmonary arterial branches extending far toward the pleura.

cava shadow; this results in disappearance of the vertical line of the superior vena cava over the spine. In lateral view, changes in the size of the RV chamber manifest themselves as filling of the retrostemal clear space, and posterior displacement of the left ventricle, as manifested by posterior displacement of the inferior posterior heart border toward the spine. RV dilatation may be associated with leftto-right shunt, pulmonary or tricuspid regurgitation, and RV failure. In left-to-right shunts, RV dilatation is associated with shunt vascularity. That is, there is dilatation of the main pulmonary artery segment as well as the central and parenchymal pulmonary artery segments. The level of the shunt may be inferred by analysis of cardiac and great artery changes. For example, in atrial septal defect, RV dilatation is associated with shunt vascularity, but a normal-size left atrium and left ventricle. In ventricular septal defect, left atrial enlargement is the rule, and left ventricular dilatation is variable. In patients with patent ductus arteriosus, left atrial and left ventricular dilatation is evident, but dilatation of the ascending aorta, a sign of the extracardiac shunt, is found as well. In cases of pulmonary insufficiency, RV and pulmonary artery volume overload dominate the radiographic picture. Thus, one sees RV dila-

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tation with enlargement of the main and central pulmonary artery segments in the absence of shunt vascularity. Tricuspid regurgitation may appear with only dilatation of the right atrium and ventricle (Fig. 8). In such cases, the plain film findings may be very general, and diagnosis of a tricuspid lesion may be difficult. The most common cause of tricuspid regurgitation is pulmonary hypertension, however, so changes of the latter (abrupt change from dilatation of the central pulmonary artery segments to the peripheral parenchymal branches) may tip one off to the tricuspid dysfunction. Furthermore, in many cases of tricuspid regurgitation, findings of right atrial hypertension, including dilatation of the azygos vein or inferior vena cava, may be evident. RV failure (Fig. 9) is frequently associated with evidence of moderate-tosevere right atrial hypertension. Therefore, findings of pleural or pericardial effusion, ascites, and dilatation of the superior and inferior venae cavae, as well as RV and atrial dilatation are usually present. Plain film changes in cases of RV hypertrophy are more difficult to evaluate. Because RV myocardial mass increases at the expense of ventricular chamber volume, the projected shape of the RV on plain film examination is not directly altered, and the cardiac contour may appear normal. RV hypertrophy associated with chamber dilatation usually has the radiographic appearance of RV dilatation. Al-

Figure 8. PA chest examination of a 12-year-old girl with tricuspid regurgitation. Right atrial dilatation is indicated by the marked increase in curvature of the lower right heart border. Right ventricular dilatation is indicated by the straightened left heart border (white arrows) running parallel to the left bronchus (black arrows), which does not cross the left heart border.

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Figure 9. A 54-year-oldman with chronic mitral stenosis and right ventricular failure. A, PA radiograph. Dilatation of the main pulmonary artery segment (P) and hilar right pulmonary artery (RP) associated with abrupt change in the caliber of the parenchymal pulmonary arteries indicates pulmonary hypertension. The elevated left bronchus (black arrows) and double density beneath the tracheal bifurcation indicate left atrial enlargement. Notice the calcification of the inferior border of the left atrium (open arrow). The heart is rotated into the left chest, and a moderate left pleural effusion is present. 6, Lateral examination. Only moderate right ventricular dilatation is indicated by the top of the main pulmonary artery (arrows), which barely fills more than 50% of the retrosternal clear space.

though the etiology of the ventricular hypertrophy can often be diagnosed based upon the presence of other findings (i.e., poststenotic dilatation of the main and left pulmonary artery in valvular pulmonic stenosis, pulmonary artery and right atrial changes in pulmonary hypertension with tricuspid regurgitation), direct diagnosis of RV hypertrophy may be elusive. In patients with tetralogy of Fallot, the appearance of the heart is often described as coeur en sabot or boot-shaped heart, referring to an upward turn of the cardiac apex (Fig. 10). The appearance of the cardiac apex in these patients may result from not only the characteristic RV hypertrophy found in this disease, but also associated RV dilatation, the pronounced deep inspiratory effort made by oxygen-starved cyanotic patients, as well as exaggeration of the appearance of the curvature of the lower left heart border caused by the smaller pulmonary artery segment. Angiocardiogram

Contrast right ventriculography provides a great deal of information about t h o internal structure of the RV, as well as insight into abnormalities of regional and global contrac-

tile function. In posteroanterior view, the RV appears trapezoidal, broader at the diaphragmatic surface than at the cardiac base. During ventricular diastole, the plane of the tricuspid valve is separated from the plane of the pulmonary valve, indicating the presence of the RV infundibulum. In lateral view, the RV also has the appearance of a trapezoid or truncated triangle (see Fig. 1). Using cineangiographic technique, however, one does not appreciate the curvature of the interventricular septum separating the RV cavity from the left ventricle. During ventricular systole, the RV contracts in a bellows-like manner; the inferior wall elevates and the free wall and interventricular septum move toward each other. The muscular trabeculations of the ventricle increase in size as the muscle fibers shorten during ventricular contraction (Fig. 11).In frontal projection, the contracting septa1band of the infundibulum appears as a filling defect between the tricuspid annulus and pulmonary annulus. In lateral view, the separation of tricuspid and pulmonary valve is apparent, but during systolic contraction, the size of the filling defect caused by the crista supraventricularis increases in size. A small amount of tricuspid regurgitation

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Figure 10. Two children with tetralogy of Fallot. A, The pulmonary artery segment of the left heart border is concave and the pulmonary markings are diminished. The lungs are hyperaerated. The apex of the heart appears elevated. B, In this patient, the apex of the heart points down. The appearance of the pulmonary artery segment and lungs appear the same as in A.

may be evident during power injection into the RV. This is often secondary to the induction of transient ventricular arrhythmia (causing transient RV papillary muscle dysfunction) or simply by prevention of the tricuspid leaflets from coapting normally due to the placement of a catheter across the valvular orifice. The RV lies anterior to the interventricular septum nearly in the middle of the cardiac silhouette, as viewed in posteroanterior projection. In lateral view, it is foreshortened, so that one cannot truely appreciate

how it wraps around the left ventricle. As described previously, the pulmonary valve is supported by the ventricular infundibulum, and is thus separated from the tricuspid valve, lying anterior, superior, and to the left, along the upper half of the left heart border. The RV outflow tract and proximal-most pulmonary artery course superiorly and then posteriorly so that they are best visualized in cranialized off posteroanterior (or shallow left anterior oblique) and straight lateral views. These views also have added the advantage

Figure 11. Right ventriculogram. Systolic frames from the same patient in Figure 1. A, PA view shows thickening of the myocardial trabeculations and decrease in ventricular cavity size. B, In lateral view, the right ventricular outflow is further narrowed between hypertrophied free wall musculature and the hypertrophied crista supraventricularis (CS). The jet of pulmonic stenosis (arrows) and dilated main (PA) and left pulmonary artery (LP) are evident.

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(when performing right ventriculography) of demonstrating the bifurcation of the main pulmonary artery into its left and right branches. Biplane contrast right ventriculography may be used to provide reasonable estimates ~ a~ series ,~~ of RV volume and wall m o t i ~ n .In of eight patients with coronary atherosclerosis but no evidence of RV dysfunction, RV enddiastolic volume index (RV end-diastolic volume divided by the patient’s body surface area in square meters) was found to be 76 +- 11 mL/m2. RV end-systolic volume index was found by this method to be 2 6 k 6 mL/m2, yielding a RV stroke volume index of 5 0 k 6 mL/m2 and RV ejection fraction of 0.66 k 0.06. Large bolus radiographic contrast administration in patients with RV disease (and especially in patients with associated pulmonary hypertension), however, is not without significant risk.20,56 The linear dimensions of the RV increase when it dilates. RV volume as assessed by cineangiography is of limited value because the shape of the dilated RV may not represent the model utilized for quantitative analysis from projection angiographic images. In fact, the error of volume estimation from cineangiograms of the RV increases with the ventricular volume itself. Identification of thickened myocardial trabeculation reflects increased myocardial mass. Estimation of myocardial mass, however, is limited to qualitative evaluation, and the ability to estimate serial changes after intervention or over time is limited. MR Imaging

The complex shape of the RV is difficult to visualize in its entirety by conventional imaging techniques. Furthermore, the unpredictability of changes in its dimensions and shape under pathologic conditions makes quantitative analysis, typically based on modification of left ventriculawmodels, less accurate. MR imaging examination allows detailed direct tomographic visualization of the shape and internal morphology of the RV.7,31,53 The high contrast resolution of spin echo acquisition allows confident differentiation between rapidly moving cavitary blood and myocardium, allowing detailed analysis of the epicardial and endocardial borders (Fig. 12).43 Acquisition of gradient reversal cine imagery

in the axial and horizontal short-axis planes displays the character of RV contraction, including the orientation of the interventricular septum, and the status of the tricuspid valve. The high temporal resolution of cine gradient reversal acquisition allows acquisition of ventricular imagery at both end-diastole and end-systole. From these acquisitions, ventricular cavitary volumes,53, 87 and myocardial mass45may be calculated. Because the MR imaging technique makes no assumptions about the shape of the RV chamber, ventricular chamber volume is obtained directly by calculating the sum of ventricular cavity areas times slice thickness through the entire chamber (Fig. 13). In a population of 10 volunteers without history of heart disease, and in whom echocardiographic examination was RV end-diastolic volume index (67.9 k 13.4 mL/m2, divided by the patient body surface area) was found to be not significantly different than left ventricular enddiastolic volume index (68.9 & 13.1 mL/m2). Similarly, RV end-systolic volume index (27.9 k 7.5 mL/mz) was not significantly different than left ventricular end-systolic volume index (27.1k7.8 mL/m2). Thus, RV stroke volume index (40.1 k9.7 mL/m2) and RV ejection fraction (0.59& 0.09) were found not to be significantly different than left ventricular stroke volume index (41.8 k 10.9 mL/ m2) and left ventricular ejection fraction (0.60 k 0.11). These values are consistent with those obtained by others using spin and gradient reversals0techniques. In a similar manner, RV myocardial mass can be obtained by summing the volume of myocardium in each image slice over the entire heart. For each tomographic slice, the ventricular volume is the difference between the areas of the epicardial border and the endocardial border times the slice thickness. The sum of the volumes of myocardium times the specific gravity of myocardium (1.05 g/mL) is the myocardial mass. In a population of 10 healthy v0lunteers,4~right and left ventricular mass was determined in this manner. In this report, the myocardium of the interventricular septum was assigned to the left ventricle. RV myocardial mass index (RV mass divided by patient body surface area) in these normal subjects was 23.3 & 1.4 g/m2. RV DYSFUNCTION The RV dilates in face of a volume load, and hypertrophies in face of an afterload. Su-

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Figure 12. Spin echo MR examination. A, Axial section through the tricuspid valve. The free wall myocardium is thin and difficult to separate from the increased signal of the epicardial fat. The interventricular septum bows toward the right ventricular (RV) chamber. Notice the moderator band (arrow) extending from the interventricular septum to the RV free wall. 5, In short axis section, the right ventricle (RV) appears trapezoidal. In this patient with mild pulmonary hypertension, there is mild thickening of the RV free wall. C,In coronal section through the fat of the anterior AV ring, the relative narrowing of the right ventricular outflow tract (OT) just below the pulmonary valve and main pulmonary artery (PA) is seen. The anterolateral aspect of the left ventricle (LV) is to the left of the RV cavity. The right atrial appendage (arrow) is seen in cross section to the right of the AV ring.

perimposition of the two leads to RV failure. Assessment of RV disease requires evaluation of changes in the size and thickness of the RV as well as associated cardiovascular abnormalities reflecting the underlying etiology for the RV dysfunction itself. RV cardiac dysfunction may be caused by left heart disease, pulmonary disease, and primary or secondary RV myocardial disease. The response of the RV to increased pulmonary resistance is to p u d p at higher pressure, resulting in RV myocardial hypertrophy. The rate at which RV hypertrophy developes in response to pulmonary hypertension is not known.55RV ven-

tricular hypertrophy is defined pathologically as thickening of the interventricular septum to greater than 5 mm. This measurement, however, is insensitive to the severity of pulmonary hypertension.” 69 The most reliable and traditional means of estimating RV hypertrophy is by direct demonstration of the ratio of the weight of the RV free wall to the combined weight of the interventricular septum plus left ventricular free wall.33 By this technique, the RV weight is less than 65 g, and the left ventricle-septum/RV free wall ratio is between 2.3 and 3.3. In patients with pathologic evidence of right-sided heart fail-

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Figure 13. Quantitation of RV volume from gradient reversal short axis sections. A, End diastolic frame. B, Systolic frame. C, The white line is the hand-planimetered right ventricular endocardial border. D, From the same image as A, the endocardial and epicardial of the right ventricular myocardium is traced (white line). €, The endocardial border of the right ventricle is hand-traced (white line) from the frame in B.

RADIOLOGY OF THE RIGHT VENTRICLE

ure, 93% of cases had RV weight greater than 150 g, 64% of cases had RV weight of 100 to 150 g, and 27% of cases had RV weight between 75 and 99 g.67In addition, the shape of the RV changes with increasing mass. The RV is less C-shaped and appears more concentric (left ventricularization of the RV). Left Heart Disease The most common cause of right-sided heart failure is chronic left-sided heart failure7O including coronary atherosclerosis with ischemic cardiomyopathy and chronic mitral regurgitation associated with systolic contractile dysfun~tion.~ Chronic systemic hypertension or aortic stenosis leading to concentric left ventricular hypertrophy and restrictive cardiomyopathy have impaired left ventricular filling, resulting in increased left ventricular diastolic pressure in face of preserved systolic Restrictive cardiomyopathy may present with RV failure, but generally involves both left and right ventricles. In these diseases, left atrial pressure rises, resulting in chronic elevation of pulmonary resistance against which the RV must generate increased pressure. Chronic rheumatic mitral stenosis (see Fig. 9) results in long-standing, gradual elevation of left atrial pressure and pulmonary resistance, resulting in RV hypertension, subse-

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quent ventricular hypertrophy, and ultimately, dilatation and 70 In general, the pulmonary hypertension found in patients with mitral stenosis is more severe than that found secondary to left ventricular dysfunction.37Congenital valvular mitral stenos~~ sis16,83 and supravalvar mitral s t e n ~ s i result in reduced left atrial outflow, but usually present in childhood. In cor triatriatum (Fig. 14),’*, 64 pulmonary venous return to the left atrium is segregated from the atrial cavity and mitral valve by a partially obstructing fibromuscular membrane. This results in increased pulmonary venous pressure in face of normal left atrial pressure. Left atrial hypertension secondary to obstructing left atrial m ~ x o m aor~ ~ thrombusB8is very much less commonly found. Congenital pulmonary venous obstruction9 is usually diagnosed in childhood. Mediastinal g r a n ~ l o m a t aand ~~ metastatic tumor involving the pulmonary veins2*,54 result in pulmonary venous hypertension and increased pulmonary resistance. Left atrial hypertension varies depending upon involvement of the left atrium itself. Pericardial disorders, namely cardiac tamponade and pericardial con~triction,4~ most commonly mediate diastolic RV dysfunction. Pulmonary Disease

RV changes in patients with pulmonary disease are mediated by increased pulmonary

Figure 14. Chest radiograph from a 3-year-old boy with cor triatriatum. A, PA radiograph shows convexity of the left heart border and rotation of the heart into the left chest. The left heart border parallels the left bronchus (arrows). The pulmonary artery segment (PA) is enlarged, and the arterial segments are indistinct. B, Lateral examination demonstrates filling of the retrosternal air space. The left bronchus (arrows) is normal, indicating a normal size left atrium.

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Figure 15. Axial spin echo MR examination in a 56-yearold man with emphysema. The anteroposteriordimension of the chest is increased. Not only are the right ventricle (RV) and right atrium (RA) dilated, but the RV free wall myocardium is thickened, and the interventricular septum is bowed toward the left ventricular cavity (LV).

resistance and the increased RV systolic pressure generated in response to it. In these circumstances, maintenance of RV myocardial wall stress is achieved by increased myocardial mass and wall thickness. That is, the RV myocardium hypertrophies. Chronic RV hypertrophy and increased pulmonary resistance often go on to cause RV dilatation and failure. Cor pulmonale is the syndrome of RV hypertrophy, dilatation, and failure resulting from pulmonary hypertension secondary to lung disease.14 Pulmonary diseases that have this effect may be classified into two categories: (1) those conditions that result in alveolar hypoventilation (hypoxia); and (2) those with pulmonary vascular occlusion. Among the former include parenchymal and restrictive lung diseases. Obstructive airway diseasez8is the most common parenchymal lung disease resulting in cor pulmonale (Fig. 15). In these patients, mucosal inflammation, bronchiolar smooth muscle contraction, bronchiolar edema, or mucus plugging obstructs small airways, decreasing vital capacity and causing nonuniform distribution of inspired oxygen. Local hypoxemia causes pulmonary arteriolar vasoconstriction, leading to the vicious cycle of increased resistance and RV failure. Capillary destruction in patients with pure emphysema reduces the cross-sectional area of the vascular bed, increasing pulmonary resistance. Typically, these patients develop cor pulmonale late in their clinical course.'l Prior

to the onset of their clinical symptoms, their RV performance is usually maintained. Subsequently, they exhibit signs of vascular bed obstruction and elevated pulmonary artery pressure, including pulmonary artery dilatation. There is a loose correlation between increased RV mass19,57 and emphysema symptoms. RV ejection fraction varies widely in these patients; but in all individuals with clinical evidence of cor pulmonale it is depressed. Patients with asthma, chronic bronchitis, and cystic fibrosis all have a similar clinical picture. Cystic fibrosis is the most common cause of chronic lung disease in children in the United States and resulting in hypoxia, sustained pulmonary hypertension, RV hypertrophy, and cor pulmonale. RV failure is a common complication of cystic fibrosis (Fig. 16).46Nearly one third of patients who die with the diagnosis of cystic fibrosis demonstrate overt signs of RV failure within the last 2 weeks of life.s5Autopsy data in 37 of a series of 51 patients who died in hospital with cystic fibrosis showed that all had RV hypertrophy; 19 of 37 had right ventricular dilatation, and 13 of the 37 had left ventricular dilatation as well. These investigators found a trend toward increasing incidence of overt RV failure with increasing age, perhaps related to more prolonged exposure of the RV

Figure 16. Axial spin echo MR examination in a 22-yearold man with cystic fibrosis. The left lung is collapsed and there is hyperaeration of the right lung, with displacement and rotation of the heart into the left chest. Notice the fan-like distribution of increased signal in the right lung, representing perivascular edema. The free wall of the right ventricle (RV) is hypertrophied and the right atrium (RA) is mildly dilated. The interventricular septum is flattened (arrows).

RADIOLOGY OF THE RIGHT VENTRICLE

to increased afterload, and the development of irreversible myocardial damage. In patients with interstitial lung disease, thickening of the alveolar or capillary membrane by transudate, exudate, or granulomatous tissue impairs oxygen diffusion across the alveolar capillary bed. Most cases are of unknown etiology.Is Increasing severity of the lung disease results in extrinsic compression and fibrotic entrapment of small pulmonary z9 causing thrombosis and arterial fibrous organization and a decrease in the cross-sectional area of the pulmonary vascular bed. Eventually, arterial hypoxemia occurs at rest. Pulmonary artery hypertension reflects the severity of the hypoxemia, and is usually modest until late in the disease. If hypoxemia is marked, then severe pulmonary hypertension and RV failure occur. Conditions that express themselves in this manner include chronic pneumonia, pulmonary fibrosis secondary to rheumatoid derm a t o m y ~ s i t i s ,advanced ~~ sarcoidosis and hemosider0sis,6~and systemic lupus erythem a t o ~ u s Pulmonary .~~ hypertension is found in nearly one third of patients with progressive systemic sclero~is.~~ Similar pulmonary vascular changes are found in approximately 9?'0~~ of scleroderma patients with CREST syndrome (Fig. 17).78Cor pulmonale and RV failure are major causes of death in this disease.n People w&o live at altitudes greater than 10,000 feet are chronically exposed to de-

Figure 17. Axial spin echo examination in a 59-year-old woman with scleroderma. Right atrial (RA) and ventricular (RV) dilatation has resulted in rotation of the heart into the left chest. The interventricular septum is bowed toward the left ventricle (LV). A large pericardial effusion (e) is seen adjacent to the RA and behind the LV. The lung signal is increased bilaterally.

393

creased oxygen tension and are relatively hypoxic, with increased pulmonary vascular resistance, and mild pulmonary hypertension. Descent to sea level returns their pulmonary resistance and pressure to Diseases of the pulmonary vasculature may be acquired, as in the case of pulmonary thromboembolism, or primary, as in the case of primary pulmonary hypertension. In both categories of disease, there is a reduction in the cross-sectional area of the pulmonary vascular bed, causing increased pulmonary resistance, pulmonary hypertension, and RV hypertrophy. Normally, the lungs filter particulate material (usually small bland thrombi that have detached from somewhere in the venous circulation). In patients who have experienced bony trauma, marrow (fat) may embolize to the lungs. Tumor thromboemboli may also lodge in the lung. Most commonly, these emboli are small and occlude only a small portion of the pulmonary arterial bed. These emboli do not elicit symptoms. Clinical pulmonary thromboembolism is a common complicationz3of lower extremity or deep pelvic vein thrombosis.17,z3 Recurrent thromboembolism occurs in about 30% of patients with embolic disea~e.~, 81 Occlusion of segmental pulmonary arterial branches may cause pulmonary infarction. In a smaller number of patients, multiple small thromboemboli lodge in the peripheral branches of the pulmonary arterial tree over a period of many years, progressively decreasing the cross-sectional area of the pulmonary bed. This increases pulmonary resistance and arterial pressure. The multiple pulmonary vascular obstructions found in chronic pulmonary thromboembolic diseaseboare different than the obstructing thrombi found in acute pulmonary embolism. Although pulmonary hypertension may be acute, as seen in sudden, massive pulmonary 31 it most often develops thromboembolism,29~ chronically, resulting from hypoxia-induced pulmonary arteriolar vasoconstriction or fibrosis of the pulmonary vascular bed.28,29 A massive, acute pulmonary embolus must occlude more than half the pulmonary arterial bed before hemodynamic changes and clinical symptoms develop. Additional occlusion of a small portion of the pulmonary arterial tree has a hemodynamically significant effect if there is underlying pulmonary hypertension. In patients with chronic pulmonary hypertension, adequate RV cardiac output is

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Figure 18. PA radiograph of a 40-year-old woman with pulmonary hypertension secondary to chronic pulmonary emboli. The heart is rotated into the left chest. The pulmonary artery segment (PA), and hilar right (RP) and descending left (arrows) pulmonary arteries are dilated. Right ventricular function is maintained in this woman. There is no pleural or pericardial effusion or azygos dilatation, indicating right heart failure.

maintained by the hypertrophied RV in face of the elevated pulmonary vascular resistance (Fig. 18). Faced w i t h 3 sudden acute increase in pulmonary vascular resistance caused by massive pulmonary embolus, the hypertrophied RV cannot maintain adequate cardiac output. The acute increase in RV afterload caused by acute, massive pulmonary embolism (Fig. 19) often results in acute RV failure. In chronic, recurrent pulmonary thromboem-

Figure 19. Maximum intensity sagittal projection reconstructed from a contrast enhanced CT examination in a patient with acute shortness of breath. The nearly occlusive thrombus (arrow) is seen in the proximal left pulmonary artery (LP). The ascending aorta (Ao) is opacified as well. (Courtesy of A. de Olivera, Jr, MD, and D. Madeira Moreira, MD, Rio de Janeiro, Brazil.)

bolism, emboli lodge repeatedly in the pulmonary arterial tree over a period of years. These patients experience neither pulmonary infarction nor sufficient acute occlusion of the pulmonary vascular bed to cause an acute RV insult. Gradual occlusion of the pulmonary arterial bed is accompanied by a progressive increase in pulmonary vascular resistance, allowing the RV to adapt. Primary pulmonary hypertension (PPH) is a rare, progressive disease of unknown etiology7*,94 characterized by obstructive changes at the level of the precapillary pulmonary arterioles (pulmonary arteriopathy) or pulmonary veins and venules (pulmonary veno-occlusive disease). Histologic changes in patients with pulmonary arteriopathy may be further divided into those patients with plexogenic and thrombotic pulmonary arteriopathy. Plexogenic pulmonary arteriopathy is typical but not pathognomonic of PPH, because similar changes are found in patients with chronic, severe pulmonary hypertension of various other etiologies. In these patients, there is medial hypertrophy, intimal thickening, and fibrosis. The typical plexiform lesion appears as a multichanneled outpouching of the pulmonary arteriolar wall, and indicates advanced disease. Examination of the pulmonary arterioles of patients with thrombotic pulmonary arteriopathy reveals eccentric intimal fibrosis and medial hypertrophy with fibroelastic intimal thickening. The plexiform lesions seen in the plexigenic variety of PPH are not found. Rather, one finds scattered evidence of old recanalized thrombus, usually appearing as fibrous webs in the small vascular channels. Pulmonary veno-occlusive disease appears to be a distinct subset of patients with PPH. It seems to represent a syndrome of fibrosis of the pulmonary venous bed. Changes in the vein intima presumably lead to thrombosis, and promotion of further vascular occlusions. Microscopic evidence of PPH is found inciPulmonary dentally in 0.02% of hypertension of unexplained etiology (i.e., in the absence of pulmonary disease, an extracardiac or intracardiac shunt or valvular lesion) is found in fewer than 1%of patients undergoing cardiac catheterization.62A familial incidence is found in nearly 7% of all cases seen in the National Institutes of Health Registry on PPH.” The clinical course in PPH is highly variable and cannot be predicted on the basis of clinical presentation and initial hemodynamic data. Asymptomatic or mildly

RADIOLOGY OF THE RIGHT VENTRICLE

symptomatic individuals have elevated pulmonary vascular resistance and RV and pulmonary artery pressure. RV function, however, is maintained. Progression of the disease and clinical deterioration are associated with decreasing RV function. Increased accuracy in evaluating RV changes in patients with pulmonary hypertension is afforded by using MR imaging techniques for direct quantitative analysis (see Fig. 13) of right and left ventricular volume8 and m a ~ s . 4In~ a series of 11 patients (mean age, 24.9 k 12.9 years; range, 5.1 to 49.9 years) with primary pulmonary hypertension undergoing MR imaging evaluation as possible candidates for lung transplantation, mean RV end-diastolic volume index (121k 45 mL/ m2) and RV end-systolic volume index (70.1 k41.6 mL/m2) were found to be significantly greater than in normal subjects. Mean RV stroke volume index (50.9227.8 mL/m2) was greater than in normals, but not significantly so. Interestingly, in these patients, mean left ventricular end-diastolic volume index (44.9 k 9.7 mL/m2), left ventricular endsystolic volume index (24.4 8.6 mL/m2), and left ventricular ejection fraction (0.46 k 0.15) were all found to be decreased when compared with normals. Right and left ventricular mass calculated from MR imaging data in 13 patients with primary pulmonary hypertension undergoing evaluation for possible lung

*

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transplantation showed significant increase in RV mass index (62.7k8.2 g/m2) when compared with normal subjects, but no significant difference in left ventricular myocardial mass index (146.0 k 16.3 g/m2). The response of the RV myocardium to the increased pulmonary resistance of lung disease is to hypertrophy in order to maintain RV wall stress within normal limits. So long as the ventricular myocardium can maintain this hypertrophic response, RV function is maintained. This favorable adaptation to lung disease, however, is limited. RV enlargement of any etiology causing tricuspid annular dilatation results in tricuspid regurgitation (Fig. 20). Furthermore, RV hypertension changes the geometry of the interventricular septum, further distorting the tensor apparatus of the tricuspid valve, exaggerating tricuspid regurgitation. Thus, pulmonary hypertension is the most common cause of tricuspid regurgitation, which increases the preload as well as the afterload on the RV. Tricuspid regurgitation increases right atrial pressure, limiting myocardial perfusion. Elevated right atrial pressure is transmitted into the coronary sinus. Thus, the difference between aortic diastolic pressure and coronary sinus pressure, the myocardial perfusion gradient, is decreased, causing RV (and left ventricular) myocardial ischemia and systolic dysfunction. When the RV myocardium is no longer

Figure 20. Early systolic axial gradient reversal MR image from a 42-year-old man with pulmonary hypertension. The heart is rotated into the lefl chest. A fan-shaped signal void jet of tricuspid regurgitation is seen extending from the tricuspid valve into the dilated right atrium. Loculated pericardial effusions at the cardiac apex (arrow 7) and along the right atrial border (arrow 2) are seen.

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able to hypertrophy adequately to overcome ventricular dilatation and maintain systolic ventricular function, RV failure ensues. RV Disease

RV myocardial infarction in the absence of left ventricular myocardial infarction is rare, occurring in fewer than 5%of autopsy cases.ys On the other hand, it is found in nearly one quarter of cases with inferior wall left ventricular myocardial infarctions!* Only about one half of these patients have associated abnormalities of RV d y s f u n ~ t i o n . ~ ~74, Patients with RV infarction usually present with signs and symptoms of RV failure disproportionate to left ventricular failurelS(i.e., cardiac output is low, and both right atrial and RV enddiastolic pressures are elevated). RV involvement in hypetrophic (left ventricular) cardiomyopathy is common, but not usually clinically apparent. Occasionally, isolated RV involvement by a hypertrophic cardiomyopathy may be seen,l, 59 wherein signs of RV outflow obstruction present. Although left ventricular impairment is usually more apparent, the RV myocardium is frequently involved in dilated cardiomyopathies. In cases where RV involvement predominates?O the RV appears dilated, with regions of scattered fibrosis and inflammatory infiltrates. These patients may present with low cardiac output and systemic venous congestion. We are now becoming aware, however, of the significant incidence of sudden onset of ventricular tachycardia and sudden death in apparently healthy young people, who are subsequently found to have RV abnormalities. Arrhythmogenic RV dysplasia is a cardiomyopathy of unknown etiology characterized by ventricular tachycardia originating from the RV, ST changes in the right-sided precordial leads of the surface electrocardiogram, nonspecific regional and global RV contractile abnormalities, as well as thinning and fibrofatty replacement of the RV free wall r n y o c a r d i ~ mSevere . ~ ~ RV dilatation, reduced RV ejection fraction, and RV failure as well as left ventricular dysfunction have been reported.51,96 Most individuals, however, have only localized or patchy areas of segmental RV thinning and akinesia or dyskinesia. Save for syncopal or sudden death episodes, these individuals are frequently only minimally symptomatic. RV dysplasia can be differentiated from pathologic adiposity of the heart

(which is associated with aging) on histologic and clinical grounds. In RV dysplasia, fat extends from the epicardial surface through the interstitium displacing myocardial fibersso; pathologic adiposity is a natural process of aging, and does not cause clinical symptoms. RV dysplasia is inherited as an autosomal dominant disorder with variable penetrance and expression.61It is usually diagnosed in individuals between 20 and 50 years of but may be found in young persons65,8y as well. The disease is found predominantly in men, and symptoms are frequently induced by increases in heart rate, such as during exercise. The disease must be differentiated from RV outflow tract tachycardia,lO, which carries a significantly lower risk of sudden death. Pathologic changes of RV dysplasia are similar to those found in Uhl’s anomaly. ECG-gated cardiac MR imaging has been found to be a useful means of assessing RV free wall myocardial thinning and fatty infiltration, as well as global and regional wall motion abnormalities3,6 , 71 in patients suspected of harboring RV dysplasia. In axial and horizontal short-axis section, the free wall of the normal RV should appear as a nearly homogeneous, intermediate signal intensity extending from the fat of the anterior atrioventricular ring toward the anterior extension of the interventricular septum. There is usually a thin and tapering deposit of epicardial fat extending from the atrioventricular ring along its proximal surface, immediately subjacent to the pencil-thin line of the pericardial space.47The myocardium of the free wall is not always demonstrated in all sections because it is relatively thin and cannot always be resolved spatially. The diaphragmatic RV wall is best viewed in horizontal short-axis section, and should appear slightly thicker than the free wall, but thinner than the interventricular septum. In patients with RV dysplasia, the shape and volume of the RV chamber may appear normal, or dilated to the eye (Fig. 21). The myocardium of the free wall may appear diffusely thin, or have loci of absent myocardium, representing local areas of marked thinning. Furthermore, on T1-weighted images, loci of increased intramyocardial signal intensity, representing fatty infiltration, are observed in both the diaphragmatic and free wall. Although these changes may be identified with conventional body coil acquisitions, dedicated chest coil or surface coil acquisitions often provide exquisite demonstration

RADIOLOGY OF THE RIGHT VENTRICLE

397

Figure 21. Two patients with syncope. A, Axial spin echo image obtained using a torso phased array chest coil in a 34-yearold woman. The right ventricle (RV) appears enlarged. The myocardium of the right ventricular free wall is thin, of increased signal intensity, and towards the apex, it cannot be separated from epicardial fat. €I Axial , gradient reversal acquisition in systole obtained from a 40-year-old woman. The cavity of the right ventricle (RV) appears to extend to the pericardium (arrow) because of failure of infiltrated myocardium to thicken.

of free wall myocardial changes. Care must be exercised to place the coil over the anterior aspect of the heart. The center of the coil should be applied about 5 cm to the left of midline, just medial to the nipple. Use of gradient reversal acquisition for cine examination of the RV in this condition may be helpful in identifying focal areas of free wall myocardium, which fails to thicken during systole, resulting in apparent expansion of the RV cavity. In a similar syndrome, RV outflow tract tachycardia, similar findings of focal RV myocardial wall thinning or excavation or wall motion abnormalities may be identified. Localization of dyskinesia to the RV outflow tract, however, helps in differenti-

ating RV dysplasia from RV outflow tract ta~hycardia.'~ SUMMARY

RV changes may be generalized into dilatation and hypertrophy. Increased preload results in ventricular dilatation. Increased afterload causes hypertrophy. Change in the shape of the RV resulting from increased afterload and myocardial hypertrophy induces tricuspid regurgitation, which superimposes changes of chamber dilatation onto those of hypertrophy. Sustained ventricular dilatation and hypertrophy frequently pro-

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gresses to RV failure. In these cases, RV systolic function decreases in association with elevation of RV and right atrial diastolic pressure. Changes in the wall thickness and shape of the RV are variable, and depend upon the severity of the volume or pressure load presented, as well as its duration and rate of progression. Because the RV is an anterior cardiac structure, it occupies little of any heart border. Therefore, the sensitivity of plain film examination to RV disease is limited. Inferential diagnosis of RV disease can often be made based upon identification of other radiographic changes, notaMy the state of the pulmonary circulation, and the position of the heart in the chest. Conventional contrast right ventriculography may be used to assess the size and position of the RV, as well as associated acquired and congenital lesions that result in RV dysfunction. Due to the unusual shape of the RV cavity, however, and the unpredictable manner in which it dilates, accurate quantitative analysis by this technique is limited. Furthermore, the common association between RV disease and pulmonary hypertension limits the applicability of this imaging technique for evaluating patients with RV disease. Multiplanar MR imaging allows direct demonstration of changes in RV size and wall morphology. Furthermore, application of Simpson’s rule to tomographic slices acquired at ventricular diastole and systole allows direct, accurate, and reproducible quantitative analysis of ventricular volume and myocardial mass, allowing radiographic assessment in patients for diagnosis, as well as longitudinally during medical management or after surgical treatment for congenital and acquired diseases that result in RV dysfunction.

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