Ventricular Septal Rupture and Mitral Regurgitation in a Patient with an Acute Myocardial Infarction

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CLINICAL CONFERENCE IN CARDIOLOGY

Ventricular Septal Rupture and Mitral Regurgitation in a Patient with an Acute Myocardial Infarction Clinical Conference in Cardiology from the Departments of Medicine and Surgery, Emory University School of Medicine and Grady Memorial Hospital, Atlanta Joel M. Eelner, M.D. Associate Professor of Medicine (Cardiology) and Teaching Scholar, American Heart Association Daniel Arensberg, M.D. Assistant Professor of Medicine (Cardiology)

Thomas P. Meyer, M.D. Fellow in Medicine (Cardiology) Panagiotis N. Symbas, M.D., F.C.C.P. Professor of Surgery(Thoracic Surgery) Robert C. Schlant, M.D. Professor of Medicine and Director, Division of Cardiology

Dr. Daniel Arensberg: Ventricular septal defect after infarction is a rare and highly lethal complication of acute myocardial infarction. The incidence of this mechanical complication is approximately 1 to 2 percent and results in a mortality of up to 80 percent with medical therapy alone.' Acute severe mitral regurgitation occurring in the setting of acute myo-

pulse rate of 130 beats per minute, and labored respirations at a rate of 321 min. The veins in his neck were distended to the angle of the jaw at 300 , and there was a palpable thriU at the lower left sternal border that was also felt at the apex. A gradeS16 holosystolic murmur was heard at the cardiac apex; six hours later, this murmur was heard over

cardial infarction is another ominous complication of ischemic heart disease," The incidence of these two lesions in the same patient with acute myocar-

dial infarction is unknown. When ventricular septal rupture and acute severe mitral regurgitation occur together after myocardial infarction, they represent a formidable therapeutic challenge to the physician. Today, Dr. Meyer will present the findings in a patient who underwent successful repair of a ventricular septal defect and severe mitral regurgitation due to papillary muscular dysfunction that developed following acute myocardial infarction. Dr. Thomas P. Meyer: The patient under discussion is a SO-year-old man who was admitted to Grady Memorial Hospital, Atlanta, complaining of pain in the chest on exertion, which became progressively more severe over a six-day period and was accompanied by profound weakness and dyspnea. On admission, he had blood pressure of 90170 mm Hg, Reprint reqU88t8: Dr. Feiner, Department of. Butler Street, Atlanta 30303

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the entire precordium. Coarse roles were heard

throUghout tM pulmonary fields. The electrocardiogram on admission showed sinus tachycardia with ST-segment elevation and abnormal Q waves in leads VItO V 5. The chest x-ray film showed a normal cardiacsilhouette with diDuse pulmonary edema. InitiaUy, a Swan-Ganz catheter was inserted and advanced to the pulmonary wedge position, where the mean pressurewas 19 mm Hg with a regurgitant v wave of 40 mm Hg. On pullback the pulmonary arterial pressure was 51/15 mm Hg. Samples for determining oxygen saturation were not obtained due to technical difficulties. Because of arterial hypotension, morphine sulfate was not administered. An infusion of a low dosage of sodium nitroprusside resulted in a decrease in pulmonary capillary wedge pressure to 12 mm Hg and an increase in the blood pressure to 105165 mm Hg. An echocardiogram was performed at that time, which showed findings consistent with a flail posterior mitral valvular leaflet (Fig 1). During the MXt 18 hours, the patient's condition CHEST, 75: 5, MAY, 1979

1. M·mode scan from mitral valve (MV) to aorta (Ao) and left abium (LA). There is echo from Swan-Ganz catheter (C) iD enlarged right ventricle (RV). IntervenbicuIar septum (IVS) moves normally but is difBcult to see in this view. Motion of mitral valve is abnormal. Posterior leaflet moves posteriorly, into left abium, throughout systole and moves anteriorly or paradoxically during diastole (fU'oo toWS). Aorta and aortic valve are normal, but left abium is dilated. FIGURE

improved, with a further iflCf'ease in blood pressure; however, at that time, his pulmonary capillary wedge pressure increasedto 25 mm Hg, his systemic blood pressure feU to 8O/6Q mm Hg, and an infusion of dopamine (12pg/kglmin) was added to the infusion of nitroprusside. The patient's vital signs improved and stabilized. The patient remained on therapy with dopamine and sodium nitroprusside until the fourth day of hospitalization. On the fourth day of hospitalization, the patient underwent cardiac catheterization, which revealed the following abnormalities: (1) a ventricular septal defect with a 2.3:1 pulmonic-systemic flow ratio; (2) severe mUral regurgitation, with a regurgitant 1) wave of :Il mm Hg and a flail posterior leaflet; (3) generalized hypokinesia of the left ventricle, with an apical aneurysm and a left ventricular end-diastolic pressure of 18 mm Hg; (4) total occlusion of the left anterior descending coronary artery proximal to the first septal perforating artery; (5) multiple highgrade lesions in the diagonal branch; (6) a large left circumflex-marginal system with minor luminal irregularities; (7) minor wall abnormalities of the proximal right coronary artery; and (8) a posterior descending coronary artery arising from both the distal right coronary artery and distal circumflex coronaryartery supplying the posterior wall. Following cardiaccatheterization,intra-aortic balloon pumping was sta1'ted, and within 12 hours the patient was weaned from therapy with dopamine and nitroprusside. He continued in a stable condition on daily therapy with digoxin and intra-aortic balloon pumping (but without infusion of dopamine and nitroprusside) from the 5th to the 27th day of hospitalization, when he underwent open-heart surgery. At surgery the ventricular septal defect was repaired, the left ventricular aneurysm was plicated

CHEST, 75: 5, MAY, 1979

and excluded, and a single saphenous vein graft was inserted to the bifurcation of the left anterior descending coronary artery and diagonal coronary artery. The mitral valvular leafletswere explored from above and below, and no intrinsic abnormality could be found. The ventricular aneurysm did not appear to involve the base of either papillary muscle. The patient had an uneventful postoperative course, and the intra-aortic balloon was removed on the fourth day after surgery. He was discharged on therapy with digoxin in stable condition on the 64th day of hospitalization. Two months after surgery, the patient was readmitted and underwent repea: cardiac catheterization. There was no evidence of a residual left-toright shunt by angiographic studies or inhalation of hydrogen. An insignificant amount of mitral regurgitation was seen, and the v wave on the tracing of the pulmonary capillary wedge pressure was 9 mm Hg (Fig 2). There was no evidence of a flail mitral valve. The cardiac index was 2.4 L/minlsq m. Anterolateral hypokinesia was noted, with a left ventricular end-diastolic pressure of 15 mm Hg. Basilar contraction was normal. The mean rate of shortening of circumferential fibers was only slightly reduced, representing an almost normal midaxis shortening and indicating that the eiection fraction of 35 percent was secondary to the abnormality of anterolateral contraction. The coronary arteriogram revealed no change in the native circulation, and the saphenous vein was widely patent. A repeat echocardiogram was normal. Dr. Joel M. Felner: The therapeutic methods employed in this case and the hemodynamic responses achieved illustrate the following important clinical points: (1) the efficacy of controlled and monitored vasodilator therapy (at times in combination with

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POST-OPERATIVE

2. Preoperative and postoperative tracings of pulmonary capillary wedge pressure. Preoperative tracing reveals regurgitant v wave of 37 mm Hg, consistent with mitral regurgitation. Postoperative tracing is normal, with v wave of 9 mm Hg, FIGURE

dopamine to increase myocardial contractility) for the mechanical complications of myocardial infarction; (2) the ability of the intra-aortic balloon pump to stabilize a patient in cardiogenic shock for a prolonged period of time; and (3) the correction of severe mitral regurgitation (produced by coronary heart disease) by plication of a left ventricular aneurysm, combined with surgery for coronary arterial bypass. The degree of shunting across a ventricular septal defect is determined by the ventricular pressures, the size of the defect, the compliance of the two ventricles, the duration of systole, and the ratio of pulmonary vascular resistance to systemic vascular resistance (Qp/QS).8 Synhorst et al:' have shown experimentally in dogs that a decrease in systemic vascular resistance may result in up to a 42 percent reduction of shunt How. The use of afterload reduction with an infusion of sodium nitroprusside enabled us to reduce the pulmonary capillary wedge pressure, increase the systemic blood pressure, improve the urinary output, and correct the acute pulmonary edema. The administration of nitroprusside simultaneously reduced the aortic outflow impedance and reduced the Howacross both the ventricular septal defect and the incompetent mitral valve. The net result of these actions was a rise in aortic blood flow and arterial blood pressure. Because of systemic arterial hypotension, neither diuretic therapy nor therapy with positive end-expiratory pressure was employed. Diuretic therapy would have caused further hypotension because of intravascular volume depletion, without affecting the abnormal

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egress of blood from the left ventricle. Similarly, therapy with positive end-expiratory pressure was not used because of its propensity to impair venous return to the left side of the heart and further reduce cardiac output. The combination of therapy with dopamine and nitroprusside may provide greater improvement in selected patients with congestive heart failure than with either agent alone, since the positively inotropic effects of dopamine are augmented by the reduction in afterload and preload produced by nitroprusside.t The beneficial effects of the intra-aortic balloon pumping include reduction of left ventricular afterload and augmentation of coronary blood flow.' In our patient, we were able to discontinue all inotropic and vasodilator drugs following insertion of the intra-aortic balloon pump. The patient remained relatively stable with intra-aortic balloon pumping alone for 22 days, despite severe left ventricular dysfunction, mitral regurgitation, and a ventricular septal defect. There was no complication associated with the intra-aortic balloon pumping, during which time there was continuous monitoring of the pulmonary capillary wedge pressure, the intra-arterial blood pressure, and the distal pulses of the extremities for adequacy of perfusion, and frequent checking of the position of the balloon catheter.

Dr. Robert C. Schlant: Mitral regurgitation may be caused by abnormalities of any portion of the mitral valvular apparatus, which includes the leaflets, chordae tendineae, anulus, papillary muscles, and left ventricular wall. Mitral regurgitation secondary

CHEST, 75: 5, MAY, 1979

to papillary muscular dysfunction associated with coronary arterial disease has also been well de-

§l!rlbM.' Und~rwooJ el JI anJ MIH:J J all have

IJarclion. Il appears thai tlssue strong enough to hold sutures may be found three weeks after septal rupture. Of course, if no satisfactory hemodynamic stabilization can be accomplished with the intraaortic balloon pump and other pharmacologic support, the surgical procedure should be performed earlier, with the knowledge that the risk will be bigh. In our patient the ventricular septal defect was closed through the infarcted left ventricular wall by means of a Teflon patch and pledgetted sutures, without comprising normal myocardium. Mter closure of the cardiotomy, the left ventricular aneurysm was excluded from the left ventricle. With the judicious use of the intra-aortic balloon pump and the use of inotropic agents and peripheral vasodilator drugs, the emergency surgical closure of ventricular septal defects after myocardial infarction can be converted from a dismal complication to a potentially reversible condition.

shown experimentally in dogs that papillary muscu-

lar infarction alone does not lead to mitral regurgitation, but that papillary muscle infarction or ischemia in combination with ischemia or infarction of the ventricular waIl at the base of the papillary muscle will produce severe mitral regurgitation. In this patient the mitral regurgitation probably was produced by severe papillary muscular dysfunction due to ischemia of the left venbicular wall. This opinion is based on the fact that moderately severe mitral regurgitation was present before surgery, that the mitral apparatus appeared grossly normal at surgery, and that the degree of mitral regurgitation was only minimal after left ventricular plication and surgery for coronary arterial bypass. This further emphasizes the importance of the left ventricular wall and coronary blood supply to the normal function of the mitral apparatus.

Dr. Arensberg: Before closing, I wonder whether Dr. Symbas could make some comments as to the surgical aspects of this case, in view of the prolonged dependence this patient had on the intra-aortic balloon pump.

REFERENCES

Dr. Panagiotis N. Symbas: The surgical mortality following closure of a ventricular septal defect during the first month after a myocardial infarction varies and may be as high as 50 percent.P This high mortality can be attributed to the hemodynamic instability that results in metabolic imbalances, to the incomplete closure of the ventricular septal defect, to disruption of the suture line in the early postoperative period, and to the extent of the original myocardial infarction. The intra-aortic balloon pump minimizes the first three of these factors; ie, it improves the hemodynamic and metabolic status of the patient and allows time for formation of fibrous tissue at the margins of the ventricular septal defect so that surgical closure can be complete and lasting. Therefore the surgical procedure is performed in a patient with an overall better risk. Although it has been stated that one should wait two to three months after the occurrence of a ventricular septal rupture before surgical repair is per-

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formed, it is reasonable to expect healing of the wound to occur two to three weeks after myocardial

1 Sanders R], Kern WH, Blount SC: Perforation of interventricular septum complicating myocardial infarction: a report of eight cases. Am Heart J 51:736, 1956 2 Merlin G, Giuliani E, Pluth J, et al: Surgery for mitral valve incompetence after myocardial infarction. Am J CardioI32:322, 1973 3 Schrire V, Vogelpoel L, Beck W, et a1: Ventricular septal defect: The clinical spectrum. Br Heart J 27:813, 1965 4 Synhorst DP, Laver RM, Doty DB, et a1: Hemodynamic effects of vasodilator agents in dogs with experimental ventricular septal defects. Circulation 54:472, 1976 5 Miller RR, Awan NA, Joye JA, et al: Combined dopamine and nitroprusside therapy in congestive heart failure. Circulation 55:881, 1977 6 Scheidt S, Wilner G, Mueller H: Intra-aortic balloon counterpulsation in cardiogenic shock. N Eng} J Med 228:979 1973 7 Cheng TO: Some new observations on the syndrome of papillary muscle dysfunction. Am J Moo 47:924, 1969 8 Underwood FO, Sybers RG, Fenier FL, et a1: Cine.. angiographic studies of the pathophysiology sequelae of experimental papillary muscle damage in dogs. Am J Roentgenol Radium Ther Nucl Med 108:702, 1970 9 Mittal AK, Langston M Jr, Cohn KE, et al: Combined papillary muscle and left ventricular wall dysfunction as a cause of mitral regurgitation. Circulation 44:174, 1971 10 Oldham HN, Scott SM, Dart CH Jr, et al: Surgical correction of ventricular septal defect following acute myocardial infarction. Ann Thorac Surg 7: 193, 1969

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