Repair of a Large Posterior Left Ventricular PSA Involving the Mitral Apparatus
A sixty-two-year-old former smoker with chronic obstructive pulmonary disease presented to the authors’ institution with multiple recent embolic strokes and worsening heart failure symptoms. Careful diagnostic evaluation revealed a large postmyocardial infarction left ventricular (LV) pseudoaneurysm (PSA). Multimodality imaging was used to further characterize the PSA, demonstrating a large outpouching of the posterior LV wall (8 x 5 centimeters) with mural thrombus and calcifications. LV function was estimated to be reduced with LV ejection fraction less than 35 percent. There were no significant valve lesions.
A coronary angiogram demonstrated a chronic total occlusion of the right coronary artery with left-to-right collaterals. Given the presence of ongoing embolic events and persistent heart failure symptoms, the patient was brought to the operating room for repair.
Following median sternotomy, cardiopulmonary bypass was initiated via aortic and bicaval cannulation. Care was taken not to manipulate the heart prior to aortic cross clamping to avoid dislodging any LV thrombus. The aorta was clamped and the heart arrested with antegrade and retrograde cardioplegia. A vent was then placed across the atrial septum. Adhesions between the inferoposterior LV wall and the diaphragmatic surface were taken down and the heart retracted to expose the PSA. A longitudinal incision was then made over the PSA parallel to the posterior descending artery. A large amount of LV thrombus was extracted with copious irrigation. A triangular Dacron patch was fashioned and anchored to the fibrous scarred myocardium at the edges of the PSA with the mitral annulus at the base of the triangle patch. Care was taken not to disrupt the geometry of the subvalvular apparatus of the mitral valve to avoid mitral valve dysfunction after repair. The PSA sac was then closed over the patch with two Teflon felt strips.
The patient was easily weaned off cardiopulmonary bypass. Post-repair intraoperative transesophageal echocardiography demonstrated reduction of the LV cavity, no new mitral regurgitation, and a modest improvement in LV function.
The patient’s postoperative course was notable for complete heart block requiring a pacemaker. She was discharged home 16 days following surgery. At the most recent follow up, her heart failure symptoms were much improved with ongoing titration of guideline-directed medical therapy. Follow up imaging showed an intact repair with reduction in LV dimension. The patient has not experienced any more embolic events.
LV PSAs represent a rare but serious mechanical complication of acute myocardial infarction. The mechanism is thought to be secondary to acute myocardial infarction leading to free wall rupture contained by pericardium. In the acute setting, patients are at high risk for rupture. For large, chronic PSAs, patients are at risk for heart failure and LV thrombus formation with embolization. Repair of posterior LV PSAs requires recognition of the relation between the mitral valve apparatus and the edge of the PSA to avoid disruption of the subvalvular apparatus geometry and postoperative mitral regurgitation. Surgical repair with patch closure as described in this report is a reproducible and effective technique.
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