Delayed ventricular septal rupture complicating acute inferior wall myocardial infarction
© Cho et al.; licensee BioMed Central Ltd. 2013
Received: 16 January 2013
Accepted: 20 March 2013
Published: 28 March 2013
Ventricular septal rupture is a potentially fatal complication of acute myocardial infarction. Its incidence has declined with modern reperfusion therapy. In the era of percutaneous coronary interventions, it occurs a median of 18–24 hours after myocardial infarction and is most commonly associated with anterior myocardial infarction. We present a case of delayed ventricular septal rupture complicating acute inferior wall myocardial infarction.
A 53-year-old Caucasian male presented with epigastric pain for three days and electrocardiographic evidence for an acute inferior wall myocardial infarction. Coronary angiography revealed a total occlusion of the proximal right coronary artery. Reperfusion was achieved by balloon angioplasty followed by placement of a bare metal stent. On hospital day six, the patient developed acute respiratory distress, a new loud pansystolic murmur, and hemodynamic instability. Echocardiography revealed the presence of a large defect in the inferobasal interventricular septum with significant left-to-right shunt consistent with ventricular septal rupture. The patient underwent emergent surgical repair with a bovine pericardial patch.
Ventricular septal rupture after myocardial infarction should be suspected in the presence of new physical findings and hemodynamic compromise regardless of revascularization therapy.
KeywordsMyocardial infarction Echocardiography Ventricular septal rupture Surgery
Ventricular septal rupture (VSR) is a potentially fatal complication of acute myocardial infarction. Without surgical repair, patients with VSR have an in-hospital mortality rate of 90%. With surgical repair, the in-hospital mortality rate is still 33-45%[1, 2]. Before the era of reperfusion therapy, the incidence of VSR was 1-3%, declining to 0.2-0.3% with the advent of thrombolytic therapy. In the modern era of ubiquitous percutaneous coronary interventions (PCI), VSR has become a rare finding in patients with acute myocardial infarction. With reperfusion therapy, the median time from the onset of myocardial infarction to the diagnosis of VSR has shortened to 18–24 hours as opposed to 5 days in the pre-reperfusion era[3, 5, 6]. We present the case of delayed ventricular septal rupture complicating acute inferior wall myocardial infarction.
Rupture of the ventricular septum is a rare but well recognized complication of acute myocardial infarction. Reperfusion therapy usually prevents extensive myocardial necrosis thus decreasing the incidence of VSR. Without reperfusion, myocardial necrosis develops within 3–5 days. In the SHOCK Trial Registry, the median time from myocardial infarction to VSR was 18 hours (interquartile range, 5 hours to 36 hours) after thrombolytic therapy. However, PCI sometimes can cause reperfusion injury and induce more damage to the infracted myocardium, especially in cases with total occlusion of the infarct-related artery and minimal collateral circulation[5, 7]. VSR occurs in the setting of anterior myocardial infarction 70% of the time and complicates inferior myocardial infarction in 29% of the cases. The culprit vessel was the left anterior descending artery in 64% of patients and the right coronary artery in 28% of patients in the GUSTO-I Trial. The location of VSR was apical in 66% and basal in 34% of patients who developed VSR after acute myocardial infarction. Our patient developed symptoms 3 days prior to seeking medical attention and rupture of the inferobasal septum, which is supplied by the right coronary artery occurred six days after revascularization. The late-onset VSR in the setting of acute inferior myocardial infarction is a rare finding in view of reperfusion therapy with PCI. Both TTE and TEE are effective imaging modalities to establish the diagnosis and exclude other mechanical complications of myocardial infarction with similar clinical presentation. The sensitivity and specificity of color Doppler echocardiography for detecting a shunt at the ventricular septal level have been reported as high as 100%. Risk factors for the development of VSR include old age, female gender, anterior myocardial infarction, and single vessel disease, specifically left anterior descending artery[3, 5]. The treatment of VSR is emergent surgical repair but even with surgical repair, the in-hospital mortality rate is in the 33-45% range[1, 2]. Recently, transcatheter ventricular septal closure has shown promising results in the treatment of VSR with a 30-day mortality rate of 35%. It can be considered as an alternative to surgical repair in hemodynamically stable patients. In our patient, surgery was selected because of hemodynamic instability.
Although the incidence of VSR has significantly decreased in the modern era of PCI, septal rupture after myocardial infarction should be suspected in the presence of new physical findings and hemodynamic compromise regardless of revascularization therapy.
Written informed consent was obtained from the patient for publication of this Case Report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Ethical approval is not applicable as this manuscript is not based on experimental research.
- Moreyra AE, Huang MS, Wilson AC, Deng Y, Cosgrove NM, Kostis JB: Trends in incidence and mortality rates of ventricular septal rupture during acute myocardial infarction. Am J Cardiol. 2010, 106: 1095-1100. 10.1016/j.amjcard.2010.06.013.PubMedView ArticleGoogle Scholar
- Noguchi K, Yamaguchi A, Naito K, Yuri K, Adachi H: Short-term and long-term outcomes of postinfarction ventricular septal perforation. Gen Thorac Cardiovasc Surg. 2012, 60: 261-267. 10.1007/s11748-011-0882-1.PubMedView ArticleGoogle Scholar
- Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ: Ventricular septal rupture after acute myocardial infarction. N Engl J Med. 2002, 347: 1426-1432. 10.1056/NEJMra020228.PubMedView ArticleGoogle Scholar
- Thiele H, Kaulfersch C, Daehnert I, Schoenauer M, Eitel I, Borger M, Schuler G: Immediate primary transcatheter closure of postinfarction ventricular septal defects. Eur Heart J. 2009, 30: 81-88.PubMedView ArticleGoogle Scholar
- Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS, Vahanian A, Califf RM, Topol EJ: Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation. 2000, 101: 27-32. 10.1161/01.CIR.101.1.27.PubMedView ArticleGoogle Scholar
- Menon V, Webb JG, Hillis LD, Sleeper LA, Abboud R, Dzavik V, Slater JN, Forman R, Monrad ES, Talley JD, Hochman JS: Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK?. J Am Coll Cardiol. 2000, 36: 1110-1116. 10.1016/S0735-1097(00)00878-0.PubMedView ArticleGoogle Scholar
- Piot C, Croisille P, Staat P, Thibault H, Rioufol G, Mewton N, Elbelghiti R, Cung TT, Bonnefoy E, Angoulvant D: Effect of cyclosporine on reperfusion injury in acute myocardial infarction. N Engl J Med. 2008, 359: 473-481. 10.1056/NEJMoa071142.PubMedView ArticleGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.