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Ann Thorac Surg 2004;78:e77-e78
© 2004 The Society of Thoracic Surgeons

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Case report

Survival After Simultaneous Left Ventricular Free Wall, Papillary Muscle, and Ventricular Septal Rupture

^a Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio, USA

Accepted for publication September 10, 2003.

^* Address reprint requests to Dr Gillinov, Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, F25, 9500 Euclid Ave, Cleveland, OH 44195, USA
gillinom{at}ccf.org

	Abstract

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Cardiac rupture is a catastrophic complication of acute myocardial infarction. The three potential sites of rupture are the left ventricular free wall, interventricular septum, and papillary muscle. Without rapid surgical correction, each of these complications typically leads to cardiogenic shock, multiorgan failure, and death. Postmortem analysis has identified a small number of cases in which myocardial infarction led to rupture at more than one of these sites; however, there are no reports of survival from such an event. We report a case involving rupture at all three sites in the same patient, emphasizing the importance of transesophageal echocardiography and surgical management.

	Introduction

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Cardiac rupture accounts for 10% to 15% of deaths in patients with acute myocardial infarction (MI). The ischemic left ventricular myocardium tends to rupture at three sites: (1) the left ventricular free wall (85%), (2) the interventricular septum (10%), or (3) a papillary muscle (5%) [1]. When left ventricular rupture occurs it generally involves only one of these sites and becomes manifest 3 to 10 days post-MI [2]. Patients present with cardiogenic shock and usually die without surgical repair [3]. Cardiac operation in a patient with left ventricular rupture carries substantial mortality. The case reported in this article describes the course of a patient suffering all three of these mechanical complications of MI 5 days after a large postero-inferior infarct. This case highlights the periodic occurrence of more than one site of rupture in a single patient.

A 71-year-old man who was previously healthy was admitted to a local hospital after a posterior–inferior MI. On the fifth morning after his MI, he suddenly arrested. He was resuscitated with cardiopulmonary resuscitation and standard protocols. Emergent transthoracic echocardiogram revealed laminated thrombus around the heart suggestive of left ventricular free wall rupture, and then he was immediately transferred to the Cleveland Clinic Foundation. On arrival, the patient was receiving dopamine (20 cg/kg/min) and norepinephrine (10 µg/min). His systemic blood pressure was 70/40 mm Hg. He was immediately transported to the operating room with no further evaluation.

Emergency sternotomy and evacuation of the pericardial clot allowed the blood pressure to recover. Examination revealed transmural infarction of the posterior and inferior walls with no ongoing bleeding. Transesophageal echocardiography by color flow Doppler at this time demonstrated a very small ventricular septal defect (VSD) and no mitral regurgitation. The initial operative plan was to repair the site of the free wall rupture. Cardiopulmonary bypass was instituted, and the heart was arrested with cold blood cardioplegia given antegrade and then given retrograde. A large bovine pericardial patch was sewn to the posterior and inferior left ventricular epicardium, and Bioglue (Cryolife, Inc, Kennesaw, GA) was placed beneath the patch. An intraaortic balloon pump was placed, and the patient was weaned from cardiopulmonary bypass.

Repeat transesophageal echocardiography revealed that the VSD had enlarged significantly; therefore cardiopulmonary bypass was reinstituted to facilitate repair of the VSD. The previously placed patch was taken down and the left ventricle was opened through the infarct. The mitral valve was examined; although the posteromedial papillary muscle was ischemic, it was unruptured. The septal defect, located postero-inferiorly, was repaired using a modified Daggett technique with an autologous pericardial patch. The left ventricle was closed with a second pericardial patch. A vein graft was anastomosed to a large marginal branch of the right coronary artery. The patient was weaned again from cardiopulmonary bypass.

Fifteen minutes later, pulmonary artery pressures suddenly increased and repeat transesophageal echocardiography demonstrated rupture of the posteromedial papillary muscle and severe mitral regurgitation. For the third time, cardiopulmonary bypass was reinstituted. The mitral valve was replaced with a bioprosthesis through a combined superior and transseptal approach. Final transesophageal echocardiography confirmed no residual mitral regurgitation or VSD.

The patient's recovery was slow as expected. Tracheostomy was placed for prolonged ventilatory wean. He was transferred to the regular nursing floor after 27 days in the intensive care unit. His tracheostomy was decannulated, he was advanced to regular diet, and he began to ambulate in the hallways. On postoperative day 40 he was transferred to a rehabilitation facility in preparation for his return home.

	Comment

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Since Cooley and colleagues [4] reported the first successful surgical repair of a postinfarction VSD in 1957, much attention has been devoted to the pathologic features and technical management of cardiac rupture. Popular opinion holds that acute occlusion of a single vessel at the patient's initial infarction predisposes to rupture given the lack of existing scar and collateral flow [5]. Post-MI ventricular rupture may affect the left ventricular free wall, the interventricular septum, or a papillary muscle. Each of these complications has been described individually, but the rate at which they occur simultaneously is low, and survival in such a case very unlikely. Autopsy studies reveal that these complications do occasionally occur together. Edwards and colleagues [6] reported a 20% incidence of left ventricular free wall and papillary muscle perforation in 53 patients who died from complications of acute VSD. There are few reports, if any, describing patients surviving more than one of these complications.

In our case, the patient developed left ventricular rupture at all three sites. Although the initial effort centered on treating the left ventricular free wall, it became necessary to address ruptures of the interventricular septum and papillary muscle. In retrospect, a decision to repair the VSD during the first pump run would have been advisable. The patient's precarious hemodynamic status and the very small size of the VSD led to the initial decision to address only the free wall rupture. This case underscores the necessity of careful echocardiographic examination in any patient presenting with post-MI left ventricular rupture. Identification of a single site of rupture does not eliminate the possibility of additional ruptures, and transesophageal echocardiography should be used to search for these entities. Although simultaneous repair of each of these complications carries a high mortality, failure to address them will almost certainly result in death. Using standard surgical techniques, successful outcome is possible.

	References

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1. Cercek B, Shah P. Complicated acute myocardial infarction heart failure, shock, mechanical complications. Cardiol Clin. 1991;9(4):569–593[Medline]
2. Hackel DB, Wagner GS. Acute myocardial infarction with papillary muscle rupture. Cardiol Clin. 1993;16:59–64[Medline]
3. Cummings RG, Califf R, Jones RN, Reimer KA, Kong YH, Lowe JE. Correlates of survival in patients with post infarction ventricular septal defect. Ann Thorac Surg. 1989;47:824–830[Abstract/Free Full Text]
4. Cooley DA, Belmonte BA, Zeis LB, Schnur S. Surgical repair of ruptured interventricular septum following acute myocardial infarction. Surgery. 1957;41:930–937[Medline]
5. Pohjola-Sintonen S, Muller JE, Stone PH, et al. Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size. Am Heart J. 1989;117(4):809–816[Medline]
6. Edwards BS, Edwards WD, Edwards JE. Ventricular septal rupture complicating acute myocardial infarction: identification of simple and complex types in 53 autopsied hearts. Am J Cardiol. 1984;54:1201–1205[Medline]

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Peter A. Walts Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Walts, P. A. Articles by Gillinov, A. M. Search for Related Content PubMed PubMed Citation Articles by Walts, P. A. Articles by Gillinov, A. M. Related Collections Myocardial infarction