Infarction With Tricuspid Insufficiency
Chronic Right Heart Failure
DONALD D. ZONE, MD ROBERT E. BOTTI, MD, FACC Cleveland,
A patient with chronic right heart failure and probable tricuspid insufficiency associated with an inferior myocardial infarction is described. Angiograms demonstrated total occlusion of the right coronary artery at its origin, a patent venous bypass graft to the mid-rlght coronary artery and hypokinesia of the inferior wall of both the right and left ventricles. Clinical data indicated a greater impairment of right than of left ventricular function. It Is proposed that infarction of the right ventricle resulted in chronic right heart failure and tricuspid insufficiency.
The effects of ischemia on the right ventricle have only begun to be elucidated.ry2 One recent report3 provides clinical, hemodynamic and pathologic evidence of right ventricular infarction and acute right ventricular dysfunction occurring during the first few days after a myocardial infarction. No instances of chronic dysfunction from ischemit disease of the right ventricle have been noted, and angiographic evidence of right ventricular infarction has been lacking. The clinical, hemodynamic and angiographic data presented here suggest that, in a patient with an inferior myocardial infarction, right ventricular infarction occurred and led to chronic tricuspid insufficiency and right heart failure. Case
From the Department of Medicine, University Hospitals, and the Case Western Reserve University School of Medicine, Cleveland, Ohio. Manuscript accepted January 3, 1975. Address for reprints: Robert E. Botti, MD, Department of Medicine, University Hospitals of Cleveland, 2065 Adelbert Rd.. Cleveland, Ohio 44106.
A 48 year old white woman was referred to University Hospitals of Cleveland for evaluation of continuing right-sided congestive heart failure. She had been well until July 20, 1971, when she was hospitalized at another institution after having an acute inferior myocardial infarction. Complete heart block developed, and a transvenous cardiac pacemaker was inserted. Shortly thereafter cuff arterial pressure became unobtainable despite treatment with vasopressor agents. Cardiac catheterization was performed while an intraarterial pressure of approximately 60/40 mm Hg was maintained with an infusion of levarterenol. Coronary arteriograms demonstrated total occlusion of the proximal right coronary artery and a normal left coronary system. At surgery, it was noted that the rightventricle and posterior aspect of the left ventricle were akinetic. A saphenous vein bypass of the right coronary artery was performed, and the patient was maintained on cardiopulmonary bypass until contractility of the ventricle improved and sinus rhythm had replaced complete atrioventricular block. The patient’s condition gradually improved and she was discharged. The patient then did well until &lay 1972 when she was hospitalized elsewhere and treated for predominantly right-sided congestive heart failure. She was hospitalized again in February 1973 for a similar problem. Past history disclosed that the patient had had an abnormally low radioiodine thyroid uptake in 1966 and had been treated since with levothyroxine. There was no history of rheumatic fever. Physical examination disclosed a regular heart rate of 70 beatslmin and a blood pressure of 142/80 mm Hg. Xanthelasma was present. A prominent V wave was observed in the pulse of the jugular vein, which was 15 cm vertically above the angle of Louis. The apical impulse was located slightly outside the
March 4, 1976
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RA MEAN 14
v3 AVR v4 AVL v5
FIGURE 1. Electrocardiogram 20 months after bypass surgery showing a transmural inferior myocardial infarction and T wave inversions in the precordial leads.
left midclavicular line, and a grade 2/6 pansystolic murmur was heard along the left sternal border. A similar murmur was heard at the apex and radiated to the axilla. An early decrescendo diastolic murmur and fourth sound gallop were noted at the apex. The liver edge was pulsatile and was felt four fingerbreadths below the right costal margin in the midclavicular line. The electrocardiogram revealed a tiansmural inferior myocardial infarction of undetermined age (Fig. 1). A chest X-ray film disclosed cardiomegaly and pulmonary vascular congestion. No valvular calcifications were seen on cardiac fluoroscopy. Fasting serum triglyceride level was 195 mg/dl and the cholesterol level 195 mg/dl; the electrophoretic pattern suggested type IV hyperlipoproteinemia. Cardiac catheterization (Fig. 2) performed on March 20, 1973 revealed a prominent V wave (21 mm Hg) in the right atria1 pressure tracing, indicating probable tricuspid insufficiency. The right ventricular end-diastolic pressure (18 mm Hg) was increased disproportionately in relation to the mild increase in left ventricular end-diastolic pressure (19 to 21 mm Hg) and pulmonary arterial pressure (mean 18 mm Hg). The pulmonary capillary wedge pressure was normal (mean 14 mm Hg). The venous bypass graft to the right coronary artery was widely patent, filling the artery distally and also proximally almost to the aortic orifice (Fig. 3). The left coronary artery was normal. Injection into the superior vena cava with the patient supine revealed no significant increase in the pericardial shadow, thus excluding significant pericardial effusion. A similar injection made with the patient in the right anterior oblique position filled the right ventricle well. The right ventricle appeared larger than normal and had a hypokinetic inferior wall (Fig. 4A). Clearing of contrast medium from the right ventricle was extremely slow. A moderate degree of tricuspid insufficiency was noted with the catheter through the tricuspid valve and with the tip free in the right ventricular cavity. A left ventricular injection
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The American Journal of CARDIOLOGY
FIGURE 2. Pressure tracings taken 20 months after inferior myocardial infarction. A, right atrium (RA). Prominent V waves indicate tricuspid insufficiency. The mean pressure is increased (14 mm Hg. normal - 1 to +8). B, right ventricle (RV). The end-diastolic pressure is increased (18 mm Hg, normal 0 to 8). C, tracing taken as the catheter was pulled back from pulmonary wedge position (PCP) to the main pulmonary artery (PA). Both mean pressures are normal. (Normal mean pulmonary capillary wedge pressure 6 to 15 mm Hg, normal pulmonary arterial mean pressure 10 to 22.) D, left ventricle (LV). The end-diastolic pressure is increased (normal 4 to 12 mm Hg).
FIGURE 3. Frame of coronary cineangiogram. The venous bypass graft (b) was injected with a contrast agent and noted to be widely patent. The right coronary artery (a) fills proximally almost to its origin.
RIGHT VENTRICULAR INFARCTION-ZONE AND BOTTI
FIGURE 4. Contraction plots traced from the diastolic(solid line) and systolic (dotted Ilne) frames of the ventricular cineangiograms. A, right ventricle. The motion of the inferior wall is poor, especially near the tricuspid valve. The ribs and wire suture were used as markers in superimposing the frame. B, left ventricle. There is poor motion of the inferior wall. C, right ventricle of a patient with a transmural inferior myocardial infarction and no right ventricular failure. There is good motion of the inferior wall. D = diaphragm.
revealed an akinetic inferior wall with a minimal increase in the total volume of the ventricle (Fig. 4B). A minimal degree of mitral regurgitation was noted. Since cardiac catheterization, the patient has been maintained on a regimen of digoxin and diuretic agents with good control of her right ventricular failure. Comments Incidence of right ventricular infarction: There have been only a few published reports of right ventricular infarction. In 1948, Wartman and Hellerstein4 reported on the prevalence of heart disease in 2,000 consecutive autopsies. Myocardial infarction was found in 160 cases, but involved the right ventricle in only 22. In only four instances was the right ventricle alone involved, and in each instance the right main coronary artery was involved. In 1952 Zaus and Kearns5 reported a case of massive infarction of the right ventricle and analyzed 11 previously reported instances of primary infarction of the right ventricle. Their report focused on correlation of the electrocardiograms with the pathologic findings. None of the four patients for whom clinical data were available survived more than 2 weeks after the clinical episode of infarction. In 1963 Laurie and Woods6 described 46 cases of right ventricular infarction in their series of 300 autopsies on patients with coronary artery disease. Of these, 13 demonstrated gross evidence and 33 cases only microscopic evidence of right ventricular infarction. They concluded that, despite the high incidence rate of main right coronary artery disease, the right ventricle was damaged much less often and much less severely than might be expected. Three basic hypotheses have been offered to explain the relative immunity of the right ventricle to infarction. In 1940 Blumgart et al7 reasoned that this immunity occurs because the “right ventricle is thinwalled and derives considerable nourishment from the blood content within its cavity,” In 1956 Wood8 emphasized that the right ventricle is supplied by the two largest arterial branches of the right coronary artery and that it offers little resistance to systolic coronary flow. Laurie and Wood& reemphasized the ex-
cellent blood supply of the right ventricle as the probable reason for the lack of ischemic damage to this chamber. They noted that the anterior third of the right ventricle near the septum is supplied by a high branch of the left anterior descending coronary artery and the right conus branch and that the remaining two-thirds is equally well supplied from the right main coronary artery within a few millimeters of its orifice, usually proximal to areas of narrowing. Right ventricular infarction and right ventricular failure: Early reports also expressed the concept that peripheral congestive failure is not immediately related to failure of the right ventricle.5*g-11 This observation was based on cases studied post mortem in which some right ventricular failure may have been present, but only terminally and in the presence of severe left ventricular dysfunction, thus making the role of right ventricular function difficult to assess. It was also noted that severe damage to the right ventricle of the dog did not result in acute right ventricular failure.1°J2 In contrast to previous findings, right ventricular dysfunction was recently demonstratedls after cauterization of the canine right ventricle. Other reports1v2 have also confirmed that right ventricular dysfunction, demonstrated hemodynamically and echocardiographically, is common in acute inferior myocardial infarction and that its occurrence is disproportionate to changes in left ventricular function. Hemodynamic features of right ventricular infarction: Cohn et al3 recently reported the clinical and hemodynamic features in six patients with a diagnosis of right ventricular infarction supported by autopsy studies in two cases and in all cases by right and left heart pressure data and clinical evidence of right heart failure. They noted a unique syndrome in which the right ventricle is unable to maintain adequate left ventricular filling, and they treated three patients effectively with plasma volume expansion or sodium nitroprusside. The four patients who survived were asymptomatic at the time of discharge, and the two patients who underwent recatheterization were noted to have significant improvement of
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their hemodynamic status. Rackley and Russelli have summarized the role of right ventricular function in acute myocardial infarction. We believe our case represents an instance in which ischemic disease of the right ventricle caused persistent hemodynamic alterations and tricuspid valve dysfunction. The disproportionate impairment of right as compared with left ventricular function was demonstrated by end-diastolic pressure data and ventriculograms. It was also gauged clinically by the great preponderance of right over left ventricular failure. These findings suggest that infarction of the right ventricular myocardium was a significant factor in our patient’s symptoms. Right ventricular failure in this patient may also be explained, in part, by the presence of a significant degree of tricuspid insufficiency. The exact cause of the lesion is uncertain, but enlargement of the right ventricular chamber or papillary muscle dysfunction, or both, may well account for the valvular dysfunction. Although right ventricu-
lar failure itself may explain the prominent V wave in the right pressure pulse, the systolic murmur and angiographically demonstrated reflux of dye through the valve make the diagnosis of tricuspid insufficiency more likely. Since studying this patient we have performed eight more right ventricular angiograms in patients with old inferior myocardial infarction diagnosed by electrocardiogram and left ventriculogram. In all but one case contraction of the inferior wall of the right ventricle was good (Fig. 6) in contrast to the finding in the patient described herein. The one patient whose right ventricular contraction was poor did not have signs of tricuspid insufficiency or right ventricular failure. Acknowledgment We thank Dr. Nestor Banez for allowing us to participate in this patient’s care and Mrs. Patricia J. Miller for typing the manuscript.
References 1. Al-Sadir J, Foiicov R, Zahavi I, et al: Right ventricular dysfunction in acute inferior myocardiai infarction (abstr). Circulation 48:Suppl IV:iV-59, 1973 2. Gomez G, Fresch D, Grismer J, et al: Hemodynamic and echocardiographic correlation of right ventricular dysfunction in acute mvocardial infarction (abstr). Clin Res 21:420, 1973 3. Cohn JN, Gulha NH, Broder MI,.et al: Right ventricular infarction: clinical and hemodynamic features. Am J Cardiol 33:209215, 1974 Wartman WD, Hellerstein HK: Heart disease in 2,000 consecutive autopsies. Ann intern Med 28:41-65, 1948 Zaus EA, Kearns WM: Massive infarction of the right ventricle. report of a case. Circulation 6:593-598, 1952 Laurie W, Woods JD: Infarction (ischemic fibrosis) in the right ventricle of the heart. Acta Cardiol 18:399-411, 1963 Biumgart HL, Schlesinger MJ, Davis D: Studies on the relation of the clinical manifestation of angina pectoris, coronary thrombosis and myocardial infarction to the pathological findings. Am Heart J 19:1-91, 1940
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8. Wood P: Diseases of the Heart and Circulation, third edition. Philadelphia, Lippincott, 1968, p 839 9. Starr I: Our changing viewpoint about congestive failure. Ann Intern Med 30: l-23, 1949 10. Bakos AR: The questions of the function of the right ventricular myocardium, an experimental study. Circulation 1:724-732, 1950 11. Wade WG: The pathogenesis of infarction of the right ventricle. Br Heart J 21545-554, 1959 12. Starr I, Jeffers WH, Meade RH Jr: The absence of conspicuous increments of venous pressure after severe damage to the right ventricle of the dog, with a discussion of the relation between clinical congestive failure and heart disease. Am Heart J 29: 291-301,1943 13. Gulha NH, Limas C, Cohn J: Predominant right ventricular dysfunction after right ventricular destruction in the dog. Am J Cardiol 33:254-258, 1974 14. Rackley CE, Russell RO Jr: Right ventricular function in acute myocardial infarction. Am J Cardiol33:927-929, 1974