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Ann Thorac Surg 1997;63:1508-1509
© 1997 The Society of Thoracic Surgeons
As Originally Published in 1989:
Updated in 1997 by James E. Lowe, MD, and Stanley A. Gall, Jr, MD
Division of Thoracic Surgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina
The treatment of postinfarction ventricular septal defect (PIVSD) has evolved considerably since the first successful surgical repair was reported by Cooley and associates in 1957 [1]. This group of patients present difficult management decisions regarding operative timing and type of repair. Many factors are associated with survival after PIVSD, including the location and size of the infarct, location of the PIVSD, right and left ventricular function, the presence of shock requiring ventricular support from either ventricular assist devices or inotropic agents, delay in referral for operation, and type of procedure performed [2–4]. The most important factor contributing to shock is the typically large infarct present in patients with PIVSD [5]. Interestingly, the size of the left-to-right shunt is inversely correlated with the extent of infarction and directly correlated with residual ventricular function. In our original study [6], the patients who survived operative repair had larger shunts on average than the nonsurvivors (3.75 versus 3.0 L/m2). This finding suggests that survivors had better left ventricular function preoperatively and therefore could shunt more blood through their PIVSDs. The actual size of the ventricular septal defect did not differ between survivors and nonsurvivors. Statistical analysis of the clinical characteristics at the time of diagnosis has consistently identified shock as a multivariate predictor of postoperative death [3–6]. Right ventricular function was an additional significant independent predictor of survival [5].
Table 1
summarizes our initial report and three recent series. These additional studies characterize their operative populations, but not the patients managed medically. Especially significant is that none of these series specified criteria used to define "cardiogenic shock." We have previously defined cardiogenic shock as "(1) systolic blood pressure less than 80 mm Hg or mean arterial pressure less than 60 mm Hg, with evidence of end-organ hypoperfusion (obtundation, decreased urine output, elevated levels of creatine or blood urea nitrogen, or cool, clammy skin), or (2) the requirement for mechanical or pharmacological interventions to maintain blood pressure and end-organ perfusion" [6]. Patients not offered operation have essentially a 100% mortality within 1 year [6].
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The following case report demonstrates the potential value of our current strategy. A 62-year-old man, who had undergone coronary artery bypass grafting after myocardial infarction in 1988, presented with an acute inferior myocardial infarction complicated by cardiogenic shock. Physical examination revealed a mean blood pressure of 57 mm Hg, bilateral rales, and a new, harsh holosystolic murmur. Transesophageal echocardiography confirmed the diagnosis of a posterior PIVSD. The patient was intubated for respiratory insufficiency and treated with dopamine and an intraaortic balloon pump for cardiogenic shock. Cardiac catheterization revealed total occlusion of the native right and circumflex coronary arteries with total occlusion of a saphenous vein graft to the right coronary artery and a 95% stenosis in a saphenous vein graft to a large circumflex marginal coronary artery. The left ventricular ejection fraction was 0.25. Because of neurologic obtundation, pulmonary edema, and renal insufficiency, immediate surgical repair was not undertaken. After 7 days of intensive medical treatment, the patient's neurologic, respiratory, and renal status improved and he subsequently underwent operative repair of the PIVSD and bypass grafting to the circumflex coronary artery. The postoperative course was complicated by respiratory insufficiency, but the patient recovered and was discharged in functional class II.
Our current technique for repair of PIVSD consists of infarct exclusion with a patch of preserved bovine pericardium and bypass grafting of any large coronary arteries that have significant stenoses and perfuse viable myocardium. The combined operative mortality in four modern series is 25%, ranging from 13% to 42%, with the mortality of patients in shock ranging from 44% to 58% [3, 4, 6, 7]. This variability in operative mortality most likely results from patient selection. Long-term survival in operative survivors ranges from 66% to 70% at 1 year, 62% to 64% at 3 years, and from 58% to 62% at 9 to 10 years. The majority of these surviving patients remain in New York Heart Association functional class I or II.
In summary, patients with PIVSD typically have had large infarcts and will frequently present with cardiogenic shock with end-organ dysfunction. The survival of these patients is predicted by their left ventricular function, just as in any myocardial infarction. Importantly, the degree of left-to-right ventricular shunting does not appear to be the major cause of cardiogenic shock. Early operative closure of PIVSDs should be undertaken in patients without shock but appropriately delayed in those with cardiogenic shock.
Footnotes
Address reprint requests to Dr Lowe, PO Box 3954, Duke University Medical Center, Durham, NC 27710.
References
This article has been cited by other articles:
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  V. Menon, J. G. Webb, L. D. Hillis, L. A. Sleeper, R. Abboud, V. Dzavik, J. N. Slater, R. Forman, E. S. Monrad, J. D. Talley, et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry J. Am. Coll. Cardiol., September 1, 2000; 36(3_Suppl_A): 1110 - 1116. [Abstract] [Full Text] [PDF]
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