Safeguard and management of the heart vales in congenital heart disease procedure / 中华外科杂志

<p><b>OBJECTIVE</b>To summarize the experience in performing reoperation of valve dysfunction after congenital heart disease procedure.</p><p><b>METHODS</b>From 1994 to 2001 we reviewed the data of 13 patients with valve dysfunction after congenital heart disease operation, in which 8 patients after ventricular septal defect, 3 after atrioventricular canal and 2 after respectively tetralogy of Fallot and atrial septal defect were corrected. Before the first operation, 6 patients had presented the mild to moderate mitral regurgitation, 1 had aortic regurgitation. Other 6 patients had valves dysfunction occurring after the first operation, among them, 2 suffered from respectively residual shunt of the ventricular septal defect, 2 had anterior chordae rupture of tricuspid valve, one had an operative injured aortic valve and one had surviving of right ventricular outlet obstruction. Thirteen patients were reoperated, including mitral valve replacement in 6, tricuspid valve replacement in 2, aortic valve replacement in one, aortic valve replacement consists with mitral valve repair and tricuspid valve repair in one and tricuspid valve repair in 3. Concomitant procedures were performed.</p><p><b>RESULTS</b>Low cardiac output occurred in 3 cases and there were 2 early deaths, due to cerebral air-embolism, respiratory and circulatory failure respectively. Other 11 cases discharged and were followed up well.</p><p><b>CONCLUSIONS</b>It is important to safeguard and repair the valvular construction and function during the operation in congenital heart disease. Reoperation should be performed timely for obtaining recurrent and a good results.</p>

Effect of cariporide on immature rabbit heart / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the protective effects of Cariporide on immature rabbit heart, and to search for the protective mechanism of the Na(+)/H(+) exchange inhibitor on immature rabbit hearts.</p><p><b>METHODS</b>New Zealand immature rabbits were randomly divided into two groups (n = 12 in each group). The isolated rabbit heart model was involved in this study. The hearts were submitted to 60 minutes of normothermic ischemia with cardioplegia per 20 minutes of reperfusion. Group I received St. Thomas No2 as cardioprotective solution. Group II received St. Thomas No2 with addition of cariporide (10 micro mol/L). The left ventricular function was recorded, including left ventricular systolic pressure (LVSP), left ventricular dystolic pressure (LVDP), coronary artery flow (CAF), mean aortic pressure (MAP), aortic flow (AF) and dp/dt max. The levels of creatine phosphokinase (CK), lactic dehydrogenase (LDH) of coronary sinus venous solution were measured. The ventricular cardiomyocytes isolated from other 6 immature rabbit hearts were subdivided into 3 groups of each heart, which were attained by means of collagenase-perfusion. All cells were incubated with calcium fluoresence indicator Fluo-3/AM, and then the intracellular free calcium was measured under the laser scanning con-focal microscopy. The baseline was measured after isolation without anoxic/re-oxygenation. The control group received anoxic conditions for 60 minutes and re-oxygenation for 30 minutes, then was measured. The experiment group received the same conditions as control group with addition of Cariporide (1 micromol/L).</p><p><b>RESULTS</b>After ischaemia/reperfusion, the percentage of recovery of myocardial function in group II was much better than group I; the LVDP, LVSP, MAP, AF, CAF and dp/dt max showed markedly better recovery in group II. The release of CK, LDH was significantly increased in Group I. After anoxic/re-oxygenation, the intracellular free calcium of isolated immature rabbit ventricular myocytes in control group increased significantly than baseline (P < 0.01); there were no significant difference of immature myocardial [Ca(2+)]i between experiment group and baseline (P > 0.05); and the experiment group myocardial [Ca(2+)]i reduced significantly than control (P < 0.01).</p><p><b>CONCLUSIONS</b>Cariporide demonstrates significant cardio-protective effects for immature myocardium ischemia/reperfusion, and the protective mechanism may be due to the inhibition of the intracellular free calcium overload.</p>