Anterior Ischemic VSD Repair After Failed Percutaneous Device Closure

Complications of acute ischemic heart disease include ventricular septal rupture resulting in a defect and sudden left to right shunt. This results in pulmonary overcirculation and heart failure. The incidence has declined significantly in the era of rapid percutaneous intervention—from 1 to 3 percent of ST-segment elevation myocardial infarctions down to 0.17 to 0.31 percent (1,2). Presentation is typically after delayed presentation or reperfusion. The rupture may be posterior or anterior, depending on the ruptured coronary obstruction. A left anterior descending coronary artery obstruction would be expected to lead to an anterior septal rupture, while a posterior rupture may occur with a distal circumflex or right posterior descending coronary artery obstruction, depending on dominance. Sudden onset of heart failure symptoms and a new murmur should raise clinical suspicion. Diagnosis may be made with an echocardiogram, a left ventriculogram, and calculation of a shunt fraction with left and right heart catheterization. Ventricular septal rupture carries a high risk of mortality with surgical intervention ranging from 60 percent with early intervention and decreasing with time from presentation (3). At three weeks from presentation, the operative mortality decreases to 10 percent (1). It is even higher with medical and percutaneous intervention, up to 90 percent mortality (4). Multiple surgical approaches for repair have been described, and most involve exclusion or patch repair of the defect to eliminate the shunt (5). Concomitant coronary bypass may be required (3). The video shows an anterior approach using a single patch technique for a ventricular septal rupture presumed to be from an ischemic event after a failed percutaneous device closure. The Patient An eighty-two-year-old female was admitted with new heart failure symptoms. She had an episode of cough and fatigue one week prior when she was treated for possible pneumonia. On admission, her EKG did not show ischemic changes and her cardiac enzymes were negative. She had a new systolic 6/6 murmur and an echocardiogram confirmed an anterior and apical ventricular septal defect. Her coronary angiogram was negative for obstructive lesions. Her Qp:Qs was calculated at 2.14 via left and right heart catheterization. A cardiac MRI was negative for myocardial ischemia or infarct as well as myocarditis. The patient’s heart failure symptoms were initially managed with diuresis and blood pressure control, a