Alfred W.H. Stanley

Surgical anterior ventricular endocardial restoration (SAVER) in the dilated remodeled ventricle after anterior myocardial infarction

OBJECTIVES The goal of this study was to evaluate the safety and efficacy of surgical anterior ventricular endocardial restoration (SAVER). The procedure excludes noncontracting segments in the dilated remodeled ventricle after anterior myocardial infarction. BACKGROUND Anterior infarction leads to change in ventricular shape and volume. In the absence of reperfusion, dyskinesia develops. Reperfusion by thrombolysis or angioplasty leads to akinesia. Both lead to congestive heart failure by dysfunction of the remote muscle. The akinetic heart rarely undergoes surgical repair. METHODS A new international group of cardiologists and surgeons from 11 centers (RESTORE group) investigated the role of SAVER in patients after anterior myocardial infarction. From January 1998 to July 1999, 439 patients underwent operation and were followed for 18 months. Early outcomes of the procedure and risk factors were investigated. RESULTS Concomitant procedure included coronary artery bypass grafting in 89%, mitral valve (MV) repair in 22% and MV replacement in 4%. Hospital mortality was 6.6%, and few patients required mechanical support devices such as intraaortic balloon counterpulsation (7.7%), left ventricular assist device (0.5%) or extracorporeal membrane oxygenation (1.3%). Postoperatively, ejection fraction increased from 29 +/- 10.4 to 39 +/- 12.4%, and left ventricular end systolic volume index decreased from 109 +/- 71 to 69 +/- 42 ml/m2 (p < 0.005). At 18 months, survival was 89.2%. Time related survival at 18 months was 84% in the overall group and 88% among the 421 patients who had coronary artery bypass grafting or MV repair. Freedom from readmission to hospital for congestive heart failure at 18 months was 85%. Risk factors for death at any time after the operation included older age, MV replacement and lower postoperative ejection fraction. CONCLUSIONS Surgical anterior ventricular endocardial restoration is a safe and effective operation in the treatment of the remodeled dilated anterior ventricle after anterior myocardial infarction.

Reduction of hospital mortality rate of acute myocardial infarction with glucose-insulin-potassium infusion.

Free fatty acids (FFA), the predominant myocardial energy substrate, are present in increased quantities immediately following acute myocardial infarction (AMI) and may cause deleterious alterations in cardiac rhythm, oxygen consumption, and mechanical performance. In an attempt to suppress FFA and simultaneously increase the availability of carbohydrate as a myocardial substrate, 70 patients with unequivocal AMI were administered a right atrial infusion of glucose-insulin-potassium (GIK) (300 gm. of glucose, 50 U. of regular insulin, and 80 mEq. of KC1 per liter of H2O) at a constant rate of 0.5 to 2.0 ml. per kilogram per hour for 48 hours. A dramatic fall in FFA (944 +/- 57 to 289 +/- 16 muEq per liter, p less than 0.0005) occurred during GIK infusion, and FFA rebounded to 420 +/- 39 muEq per liter (p less than 0.005) when GIK was discontinued. The hospital mortality rate in the 70 GIK recipients was compared to that of 64 untreated patients (controls) from the same coronary-care unit during the previous year. GIK and control groups had similar severity of infarction as assessed by prognostic scales of Killip, Peel, and Norris, respectively. The hospital mortality rate was reduced in the GIK recipients compared to the control group (11/70 vs. 19/64, p less than 0.05). In patients without history of prior myocardial infarction, the mortality rate was reduced four-fold in GIK recipients compared to controls (6 vs. 24 per cent, p less than 0.05). Complications of GIK infusion were infrequent and included chiefly hyperglycemia and hyperkalemia, both of which dictated meticulous monitoring of serum chemistries. The data suggest that suppression of plasma FFA with GIK infusion may be associated with a significant reduction in the hospital mortality rate of acute myocardial infarction.

Surgical Ventricular Restoration: The RESTORE Group Experience

Congestive heart failure may be caused by late left ventricular (LV) dilation following anterior infarction. Early reperfusion prevents transmural necrosis, and makes the infarcted segment akinetic rather than dyskinetic. Surgical ventricular restoration (SVR) reduces LV volume and creates a more elliptical chamber by excluding scar in either akinetic or dyskinetic segments.The international RESTORE group applied SVR in a registry of 1198 post-infarction patients between 1998 and 2003. Early and late outcomes were examined and risk factors identified.Concomitant procedures included coronary artery bypass grafting in 95%, mitral valve repair in 22%, and mitral valve replacement in 1%. Overall 30-day mortality after SVR was 5.3% (8.7% with mitral repair vs. 4.0% without repair, p < .001) Perioperative mechanical support was uncommon (< 9%).Global systolic function improved postoperatively, as ejection fraction increased from 29.6 ± 11.0% to 39.5 ± 12.3% (p < .001) and left ventricular end systolic volume index decreased from 80.4 ± 51.4 ml/m2 to 56.6 ± 34.3 ml/m2 (p < .001). Overall 5-year survival was 68.6 ± 2.8%, Logistic regression analysis identified EF ≤ 30%, LVESVI ≥ 80 ml/m2, advanced NYHA functional class, and age ≥75 years as risk factors for death. Five-year freedom from hospital readmission for CHF was 78%. Preoperatively, 67% of patients were class III or IV, and postoperatively 85% were class I or II.SVR improves ventricular function and is highly effective therapy in the treatment of ischemic cardiomyopathy with excellent 5-year outcome.

Angiotensin-converting enzyme inhibitor therapy affects left ventricular mass in patients with ejection fraction > 40% after acute myocardial infarction.

OBJECTIVES We tested the hypothesis that angiotensin-converting enzyme (ACE) inhibitor therapy decreases left ventricular (LV) mass in patients with a left ventricular ejection fraction (LVEF) > 40% and no evidence of heart failure after their first acute Q wave myocardial infarction (MI). BACKGROUND Recently, ACE inhibitor therapy has been shown to have an early mortality benefit in unselected patients with acute MI, including patients without heart failure and a LVEF > 35%. However, the effects on LV mass and volume in this patient population have not been studied. METHODS Thirty-five patients with a LVEF > 40% after their first acute Q wave MI were randomized to titrated oral ramipril (n = 20) or conventional therapy (control, n = 15). Magnetic resonance imaging (MRI) performed an average of 7 days and 3 months after MI provided LV volumes and mass from summated serial short-axis slices. RESULTS Left ventricular end-diastolic volume index did not change in ramipril-treated patients (62 +/- 16 [SD] to 66 +/- 17 ml/m2) or in control patients (62 +/- 16 to 68 +/- 17 ml/m2), and stroke volume index increased significantly in both groups. However, LV mass index decreased in ramipril-treated patients (82 +/- 18 to 73 +/- 19 g/m2, p = 0.0002) but not in the control patients (77 +/- 15 to 79 +/- 23 g/m2). Systolic arterial pressure did not change in either group at 3-month follow-up. CONCLUSIONS In patients with a LVEF > 40% after acute MI, ramipril decreased LV mass, and blood pressure and LV function were unchanged after 3 months of therapy. Whether the decrease in mass represents a sustained effect that is associated with a decrease in morbid events requires further investigation.