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Ann Thorac Surg 2000;70:2185
© 2000 The Society of Thoracic Surgeons
a Department of Thoracic and Cardiovascular Surgery, Jichi Medical School, Yakushiji 3311-1, Minami-Kawachi, Tochigi, 329-0498, Japan
e-mail: tcvmisa{at}jichi.ac.jp
To the Editor
We read with great interest the article by Cury and associates [1]. The authors mentioned myocardial infarction extending to the papillary muscles in patients who died after partial left ventriculectomy for repair of dilated cardiomyopathy. Nine of 11 patients had myocardial infarction extending to the papillary muscles, 4 of the 9 had infarction of both anterior and posterior papillary muscles, and 3 had postoperative episodes of arrhythmias.
We treated a 72-year-old man with idiopathic dilated cardiomyopathy. He had been repeatedly admitted to several hospitals over the prior 7 years because of recurrent congestive heart failure before admission to our hospital. His New York Heart Association functional classification was IV. The left ventricular end-diastolic and end-systolic volume indexes were 257 and 215 mL/m2, respectively, with a left ventricular ejection fraction of 16%. Left ventricular end-diastolic pressure was 30 mm Hg, mean pulmonary artery pressure was 45 mm Hg, and mean pulmonary capillary wedge pressure was 31 mm Hg. Grade II/IV aortic valve regurgitation and grade III/IV mitral valve regurgitation were also recognized. He consented to undergo partial left ventriculectomy associated with both aortic and mitral valve replacement. Surgery was performed under a moderate hypothermic condition with initial antegrade and subsequent intermittent retrograde infusion of blood cardioplegic solution. Ischemic time was 187 minutes. The resected myocardium of the left ventricle weighed 54 g. The aortic and mitral valves were replaced with mechanical prostheses. He could not be weaned from cardiopulmonary bypass. Echocardiographic examination revealed hypokinetic contraction of the entire ventricle. Mechanical circulatory assist with extracorporeal membrane oxygenation was initiated along with intraaortic balloon pumping. Ventricular arrhythmias were not observed; sporadic sinus bradycardia required electrical pacing. Unfortunately, 2 weeks of mechanical assistance did not aid his recovery from hemodynamic deterioration. Autopsy findings showed myocardial infarction along the suture line, and the papillary muscles were not affected.
Cury and associates indicate that operative procedures resulting in scarification of the coronary arteries on the lateral wall of the left ventricle may cause postoperative myocardial infarction and that the induced infarction can lead to low cardiac output syndrome with ventricular arrhythmias. We agree with Cury and associates that myocardial infarction extending to the papillary muscles can indeed lead to postoperative low cardiac output syndrome with ventricular arrhythmias. However, papillary muscle damage is not always the cause of unsatisfactory results after partial left ventriculectomy. As with their 2 patients showing limited areas of myocardial infarction, our patient showed myocardial infarction limited to the myocardial suture line. The cause of dire outcomes in such patients after partial left ventriculectomy remains unclear.
Preoperative and operative evaluations may contribute to positive clinical outcomes. Conventionally, the lateral wall of the left ventricle is resected during partial left ventriculectomy. Preoperative evaluation in our patient showed severely reduced left ventricular wall motion with an akinetic inferior wall; postoperative studies revealed that the inferior and lateral walls had become akinetic. Perhaps, our patient ought to have had the posterior wall resected, leaving the lateral wall intact. The relationship between preoperative evaluation and clinical outcome is still unclear. To confirm the legitimacy of partial left ventriculectomy, further studies incorporating both Batista’s findings and preoperative evaluations of left ventricular function are needed.
References
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