**1. Introduction**

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J Med 2012;367:1287-96.

Acute myocardial infarction (AMI), despite advances in health care delivery systems, educa‐ tion, and primary prevention still remains a significant problem. Fortunately, with these ad‐ vances and early interventions, there has been a decline in the incidence of mechanical complications. Unfortunately, while becoming less common, when mechanical complica‐ tions occur and despite advances and evolving techniques in the surgical management of these problems, morbidity and mortality remain high. Post-myocardial infarction ventricu‐ lar septal rupture (PI-VSD) has challenged and intrigued clinicians for years. The timing of presentation can be quite variable, as they tend to occur in patients several days after their initial cardiovascular insult (acute PI-VSD) – and unfortunately, they can occur in patients who appear to otherwise be doing well. In addition, while less common, some patients might not present until weeks, if not longer, after their AMI with symptoms prompting a work-up that might reveal a chronic PI-VSD. Early PI-VSDs tend to be catastrophic and can result in death. The pathology is also variable and complex, but common themes include:


Definitive management remains surgical, however, controversies continue to exist regarding the timing of surgery, the role of concomitant coronary revascularization, and the evolving

role of percutaneous closure devices. Unfortunately, despite early repair and improvement in techniques and peri-operative management, the short and long-term outcomes remain less than ideal.

Risk factors include gender, with men at a greater risk than women (3:2 ratio), increasing age, and current smoking history. In the GUSTO trial, the mean age of presentation with a

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The diagnosis of a PI-VSD must be considered in any patient presenting with hypotension, cardiogenic shock, or respiratory failure, particularly in the setting of a patient who other‐ wise had been doing well, either during or after an AMI. A PI-VSD presents in a similar manner as other mechanical complications of AMI, such a papillary muscle rupture with acute mitral regurgitation, free wall rupture with tamponade, or severe LV failure and pul‐ monary edema. The initial diagnosis must be suspected during initial investigations during

Patients often complain of recurrent chest pain. The characteristics of the pain are often dif‐ ferent than their initial presentation and are typically related to the onset or recurrence of myocardial necrosis. Often a new systolic murmur will develop and it can be harsh, pansys‐ tolic, and often-best auscultated at the left lower sternal border. Patients can often have a bundle branch block from disruption of the septal conduction system. Hemodynamic deteri‐

**Figure 1.** Representative cardiac catheterization in which contrast is injected during left ventriculography crosses the defect into the right ventricle. Contrast flowing into the pulmonary artery is then diagnostic for a ventricular septal

oration can be quick and there can be a rapid progression to cardiogenic shock.

PI-VSD was 62.5 years and ranged from 44 to 81 years [13].

**4. Diagnosis**

defect.

a comprehensive work-up.

### **2. History**

Post-myocardial infarction ventricular septal defects (PI-VSD) were described first at autop‐ sy [30]. It was not until 1923 that the pre-mortem pathophysiology was understood [7]. [40], described the association with coronary artery disease and acute myocardial infarction [40]. The first report of a surgical repair came in 1956 when Denton Cooley described a patient 9 weeks after the initial diagnosis who underwent operative intervention [12]. With advances in the peri-operative and intra-operative management of the cardiovascular surgery patients there were reports of survival in what was previously felt to be an inherently fatal problem. Most of the successful operative cases occurred in patients who presented in congestive heart failure weeks after their initial acute event. Based upon these experiences, for many years it was the belief that operative management should be delayed as long as possible to allow for scaring of the necrotic myocardium to provide for a more stable repair. As experi‐ ences grew early repair was advocated, particularly in stable patients before hemodynamic deterioration and associated multi-organ failure.
