Echocardiography revealed a dilated left ventricle and severely impaired global cardiac function. The anterior septum and the anterior and lateral walls of the left ventricle were akinetic. Thrombus lined the akinetic anterior wall of the left ventricle. Left ventricular filling was impaired, which was consistent with high left atrial pressures. The inferior and posterolateral walls contracted normally. The patient had moderate-to-severe mitral valve regurgitation and severe tricuspid valve regurgitation. The estimated ejection fraction was 0.20.

Cardiac catheterization revealed a hemodynamically significant lesion in the proximal left anterior descending coronary artery and severe pulmonary hypertension, with pulmonary artery pressures (75/30 mmHg) that were nearly equal to systemic pressures. Nuclear stress testing with adenosine thallium revealed severe, fixed perfusion defects in the anteroseptal and apical regions.

Despite medical management with aggressive diuresis and optimal β-blocker therapy, symptoms of congestive heart failure (such as severe dyspnea and limited exercise tolerance) persisted. Surgical remodeling of the ventricle in combination with coronary artery bypass grafting and mitral valve repair was recommended to the patient.

After the induction of anesthesia but before the operation, transesophageal echocardiography was performed. This confirmed marked dilation of the left ventricle; left ventricular ejection fraction of approximately 0.20; akinesis of the anterior wall, apex, and septum; and severe mitral insufficiency. Of note, the transesophageal echocardiogram showed only mild tricuspid valve regurgitation.

Coronary artery bypass grafting was done through a median sternotomy. Even in light of the preoperative nuclear stress test findings that had shown an anteroseptal perfusion defect, the left anterior descending coronary artery, measuring 2.0 mm in diameter, was bypassed with a single graft—without cardiopulmonary bypass—to recruit possibly hibernating myocardium in the septal and anterior walls. The proximal graft anastomosis was performed while the aorta was partially occluded with a cross-clamp; the distal anastomosis was performed using standard off-pump stabilization techniques and a “flow-through” intracoronary cannula after completion of ventricular remodeling. Then the proximal anastomosis was performed, the aorta was cannulated, and a single venous cannula was placed in the right atrium.

Surgical ventricular remodeling and mitral valve repair were performed during cardiopulmonary bypass, without ischemic arrest or aortic occlusion. A left ventriculotomy was performed from the apex to the transitional zone of viable myocardium at the base of the posterior papillary muscle (Fig. 1). The transitional zone between contracting and noncontracting myocardium was identified visually and by palpation. The mitral valve, which was clearly visible through the ventriculotomy, was repaired through the ventriculotomy using a suture annuloplasty technique to shorten the mural leaflet.^2,3 An Alfieri-type stitch was placed, approximating the mid-portions of the mitral leaflets. Four centimeters of the akinetic anterior wall extending from the apex to the transitional zone were removed. The resection margins included the apex and the free lateral wall to the base of the posterior papillary muscle. Ventricular remodeling was achieved using a prosthetic low-porosity Dacron patch that was reinforced with overlying portions of the free ventricular wall by using Cooley's endoaneurysmorrhaphy technique (Fig. 2). Aneurysmorrhaphy was performed with a prosthetic low-porosity woven patch secured along the margin of viable and nonviable tissue by a running 3-0 polypropylene suture reinforced with interrupted pledgeted sutures. The margins of the left ventricular wall over the site of the aneurysmorrhaphy were reapproximated linearly between 2 long Teflon felt pledgets secured with a 2-0 silicone-coated polyester (Ticron) suture (Fig. 2). Before weaning the patient from bypass, a prophylactic intra-aortic balloon pump was inserted percutaneously to provide counterpulsation support. This support and the administration of epinephrine at 0.01 μg/kg/min resulted in uneventful weaning.

Postoperative transesophageal echocardiography revealed a significantly diminished left ventricular volume and improved left ventricular systolic function overall. Only trace mitral valve regurgitation was seen, as characterized by a mildly increased mitral valve gradient of approximately 4 mmHg at a heart rate of 75 beats/min.

During the first 24 hours after surgery, the patient was weaned from intravenous epinephrine. Cardiac function was excellent, with a cardiac index of 2.5, a creatine kinase-MB index of 4.6, and a troponin T level of 0.817 ng/mL. No electrocardiographic changes were noted during this period. On postoperative day 2, the patient was extubated and the intra-aortic balloon pump was removed. Because of the patient's history of myocardial infarction and the presence of a wide QRS complex on the electrocardiogram, a biventricular implantable cardioverter–defibrillator was implanted on postoperative day 10. The patient's subsequent recovery was uneventful, and he was discharged from the hospital on day 12.

The present case is notable for its complexity. Yet, despite the concomitant presence of coronary artery disease, pulmonary hypertension, severe congestive heart failure, and severe mitral regurgitation, appropriate surgical management of each condition resulted in an excellent outcome overall. This combined approach is controversial, however. Similar controversy in the past has surrounded revascularization of the left anterior descending coronary artery in combination with ventricular aneurysm resection. In cases such as the one presented here, our preference has been to 1) revascularize all vessels affected by hemodynamically significant lesions, even in the face of poor nuclear stress test findings, in order to allow maximal recruitment of possibly hibernating myocardium and 2) correct concomitant mitral insufficiency surgically in order to maximize the forward output of the severely compromised left ventricle. Mitral regurgitation frequently accompanies the disordered ventricular anatomy and physiology that are associated with ischemic cardiomyopathy. Annuloplasty of the posterior annular ring can be performed through the ventricle and without cross-clamping the aorta. When this technique is combined with an Alfieri-type valvuloplasty, long-term correction of mitral regurgitation can be achieved.

In this patient, we chose to remodel the left ventricle with a patch rather than with a commercial rigid prosthesis in order to avoid the potential for mechanical disruption of the left ventricle with a resultant pseudoaneurysm. Our repair technique, which is patterned after Cooley's technique for endoaneurysmorrhaphy, provides a flexible yet secure ventricular repair that decreases left ventricular volume, optimizes ventricular anatomy, and maximizes ventricular function while minimizing operative time.⁸