Late survival after valve operation in patients with left ventricular dysfunction.

BACKGROUND: Left ventricular dysfunction is a predictor of hospital mortality after cardiac valve operation. We evaluated late survival in a large cohort of these patients. METHODS: From 1980 to 1993, 257 patients with a preoperative ejection fraction of 0.40 or less underwent aortic (n = 177), mitral (n = 72), or combined (n = 8) valve operation, with or without concomitant coronary artery bypass grafting. RESULTS: Hospital mortality was 12.5%. Follow-up was 98% complete. Logistic regression analysis showed that an ejection fraction of less than 0.30, mitral regurgitation, concomitant coronary artery bypass grafting, emergency operation, and reoperation were independent correlates of hospital mortality (all at p < 0.05). Kaplan-Meier survival curves of the 220 hospital survivors showed a 65% 5-year survival. Multivariate analysis revealed preoperative use of diuretics, male sex, reoperation, age exceeding 60 years, and aortic regurgitation to be independent predictors of poor late outcome (all at p < 0.05). CONCLUSIONS: The liability of left ventricular dysfunction with regard to diminished long-term survival is not completely reversed by valve operation. If operation is not performed before left ventricular dysfunction develops, postoperative medical treatment of these dilated, remodeled ventricles should be considered.

Coronary microvascular reactivity after ischemic cold storage and reperfusion.

BACKGROUND: The coronary microvascular system is important in the regulation of myocardial perfusion. Preservation of microvascular reactivity may be important in those hearts undergoing ischemic storage for transplantation. Endothelium-dependent relaxation of right and left ventricular coronary microvessels was examined in a canine model of heart transplantation. METHODS: Canine hearts underwent topical cooling, antegrade arrest, and 3 hours' ischemic cold storage at 4 degrees C using crystalloid cardioplegia (n = 8), Roe's solution (n = 8), and University of Wisconsin solution (n = 8). All groups underwent 1 hour of reperfusion in an isolated heart circuit. Noninstrumented canines were used as controls (n = 10). Coronary microvessels (100 to 200 microns in diameter) were examined in a pressurized, no-flow state with video microscopic imaging and electronic dimension analysis. RESULTS: Endothelium-dependent microvascular relaxation was examined in response to the receptor-dependent acetylcholine and to the receptor-independent calcium ionophore. Microvascular relaxation to acetylcholine in Roe's solution and University of Wisconsin solution was preserved (p = not significant) in the left ventricle, whereas crystalloid cardioplegia failed to preserve (p < 0.05) microvascular relaxation when compared with the control groups. Right ventricular microvascular relaxation was always (p < 0.05) less than left ventricular microvascular relaxation. Endothelium-independent microvascular relaxation to nitroprusside was similar to that in controls, indicating normal smooth muscle responsiveness. CONCLUSIONS: Ischemic cold storage with Roe's solution and University of Wisconsin solution preserved microvascular relaxation in the left ventricle, whereas crystalloid cardioplegia failed to preserve microvascular relaxation. Right ventricular microvascular relaxation was impaired in all groups, but University of Wisconsin solution was superior to crystalloid cardioplegia and Roe's solution. This suggests that microvascular dysfunction may be partially responsible for right ventricular dysfunction after heart transplantation. The choice of preservation solution may be important in preservation of the microvascular endothelium.

Leukocyte depletion of blood cardioplegia attenuates reperfusion injury.

BACKGROUND: Leukocytes are associated with myocardial injury during reperfusion after ischemia. Short periods of leukocyte depletion during reperfusion result in persistent attenuation of postischemic myocardial dysfunction. METHODS: Leukocyte depletion was examined in a canine model of regional myocardial ischemia and reperfusion. The extracorporeal circuit and cardioplegia circuits underwent leukocyte depletion by mechanical filtration. Animals were instrumented for baseline global function before 90-minute occlusion of the left anterior descending coronary artery. Global function during ischemia and at 5, 30, 60, and 90 minutes after a 60-minute cardioplegic arrest using continuous blood cardioplegia was assessed in leukocyte-depleted (n = 9) and control (n = 10) groups. RESULTS: No significant difference between groups was seen for systemic leukocyte counts, global function, or water content. Endothelial function was significantly protected as assessed by response to both calcium ionophore (endothelial-dependent, receptor-independent relaxation: leukocyte-depleted, 72% +/- 19% of endothelin-induced constriction versus control, 46% +/- 14%; p < 0.05) and acetylcholine (endothelial-dependent, receptor-dependent relaxation: leukocyte-depleted, 83% +/- 11% versus control, 44% +/- 15%; p < 0.05). CONCLUSIONS: Leukocyte-mediated endothelial reperfusion injury can be attenuated by leukocyte depletion during reperfusion.

Microvascular reactivity after crystalloid, cold blood, and warm blood cardioplegic arrest.

BACKGROUND: The effects of three techniques of cardioplegic arrest on endothelium-dependent microvascular function of the right and left ventricles were examined in a canine model of cardiopulmonary bypass. METHODS: Oxygenated cold crystalloid cardioplegia and cold blood cardioplegia groups, (n = 11 each) had hypothermic cardiopulmonary bypass (28 degrees C), topical cooling, antegrade arrest, and intermittent antegrade delivery. A warm blood cardioplegia group (n = 11) had normothermic cardiopulmonary bypass (37 degrees C), antegrade arrest, and continuous antegrade delivery. All groups underwent cardioplegic arrest for 1 hour followed by 1 hour of reperfusion. Dogs that did not have instrumentation were used as controls (n = 10). Coronary microvessels (100 to 200 microns in internal diameter) were examined in a pressurized, no-flow state with video microscopic imaging and electronic dimension analysis. RESULTS: Ischemic arrest with cold crystalloid cardioplegia significantly (p < 0.05) impaired endothelium-dependent relaxations in both ventricles to acetylcholine (left ventricle, 69% +/- 4%, and right ventricle, 73% +/- 5%, versus control left ventricle, 100% +/- 0.3%, and control right ventricle, 100% +/- 0.3%) and the calcium ionophore (left ventricle, 70% +/- 6%, and right ventricle, 68% +/- 3%, versus control left ventricle, 98% +/- 1%, and control right ventricle, 98% +/- 1%). In the cold blood cardioplegia group, endothelium-dependent relaxations to acetylcholine (left ventricle, 96% +/- 1%, and right ventricle, 87% +/- 4%) and the calcium ionophore (left ventricle, 88% +/- 3%, and right ventricle, 78% +/- 7%) were preserved. In the warm blood cardioplegia group, endothelium-dependent responses to acetylcholine (92% +/- 3%) and the calcium ionophore (96% +/- 1%) were preserved in the left ventricle, but the right ventricle showed reduced (p < 0.05) reactivity to the endothelium-dependent acetylcholine (77% +/- 8%) and the calcium ionophore (69% +/- 8%). Endothelium-independent relaxation to sodium nitroprusside was similar to controls in all groups for both ventricles, thus indicating normal smooth muscle responsiveness. CONCLUSIONS: Cardioplegic arrest with cold blood cardioplegia preserved the endothelium-dependent response in the right and left ventricles, whereas cold crystalloid cardioplegia impairs this response. Warm blood cardioplegia preserved the endothelium-dependent response in the left ventricle, but this response was reduced in the right ventricle. This suggests that blood cardioplegia and hypothermia may be important in protection of microvascular endothelium and that the right ventricle may be more vulnerable to damage than the left ventricle.