Treatment strategy of mechanical hemolysis after mitral valve repair / 医学研究生学报

Objective　In recent yaers, mitral valve repair has been widely used in the surgical treatment of congenital and secondary mitral valve lesions. To investigate the mechanism and treatment strategy of mechanical hemolysis after mitral valve repair.　Methods　A total of 451 consecutive patients registrated in general hospital of southern theatre command who underwent mitral valve repair surgery between August 2010 and June 2018,of whom 16(3.5%) had complicated mechanical hemolysis(hemoglobinuria, jaundice, anemia), were retrospectively analyzed. Echocardiographic examination showed that there were 3 cases of mild mitral regurgitation(MR), 9 cases of moderate MR and 4 cases of severe MR, among which 75% of mitral regurgitation flow were rapid regurgitant jets (Vmax>4m/s). According to the treatment strategy,all cases were divided into two groups: the aggressive reoperation group（n=10）,patients received re-repair procedures within 1 week after hemolysis diagnosis. The conservative treatment group(n=6), patients received symptomatic treatment of hemodialysis, blood transfusion, diuresis, alkalization of urine, liver protection and oral metoprolol et al. All patients were followed up for 2 to 36 months, with an average (16±7.5) months, and the postoperative echocardiographic results, hemolysis symptom improvement and cardiac function were compared.　Results　No death occurred in the two groups after operation. The symptoms of patients in the aggressive reoperation group receded rapidly and discharged from hospital. 4 patients in the conservative treatment group received reoperation 3~11 weeks after surgery due to poor treatment effect (1 patient underwent re-repair and 3 patients underwent replacement), the other 2 patients received long-term conservative treatment. The cardiac function of the patients undergoing reoperation was maintained at level I~II. Echocardiographic examination showed that mild MR(n=10), mild~moderate MR(n=3), and no recurrence of mechanical hemolysis. Two patients with long-term conservative treatment, mild~moderate anemia, urinogen +~++, moderate MR, cardiac function at level II, were in a subclinical hemolytic state.　Conclusion　Mechanical hemolysis frequently occurs immediately or soon after mitral valve repair. Hemoglobinuria, jaundice, anemia and postoper echocardiography found the mitral regurgitant flow with high-shear stress, these helpful to the diagnosis. Surgery is an important factor affecting hemolysis. Hemolysis can be a sign of surgical failure, re-repair operation is the best treatment as soon as possible after the hemolysis has been diagnosed.Conservative treatment is not the priority choice.

Risk factors for early postoperative death after total correction of tetralogy of Fallot: analysis of 20 cases / 南方医科大学学报

<p><b>OBJECTIVE</b>To identify the risk factors of early postoperative death after total correction of tetralogy of Fallot (TOF).</p><p><b>METHODS</b>A retrospective analysis was conducted among 356 patients undergoing total correction of TOF by opening heart surgery and cardiopulmonary bypass. Of these patients, 20 died in the early postoperative period, and the possible risk factors for early postoperative death were analyzed in view of the surgical indication, surgical approaches, myocardial protection and postoperative management.</p><p><b>RESULTS</b>Of the 20 fatal cases, death occurred due to low cardiac output syndrome in 11 cases, respiratory failure in 4 cases, kidney failure or multiple organ failure in 3 cases, acute left heart failure in 1 case, and cerebrovascular accident in 1 case.</p><p><b>CONCLUSION</b>Young age at repair and poor development of the pulmonary vessels and left ventricle are high risk factors for postoperative low cardiac output syndrome. Postoperative death following surgical correction of TOF is associated mainly with the surgical skills and approaches. Appropriate cardiopulmonary bypass and effective measures for myocardial protection are critical to ensure the surgical success, and proper postoperative management and close monitoring may help reduce postoperative death in surgical patients with TOF.</p>

Detection of gene mutations of SCN5A in 7 patients with Brugada syndrome / 中华心血管病杂志

<p><b>OBJECTIVE</b>Brugada syndrome is linked to sodium channel mutations and could induce arrhythmias that even lead to sudden death. The purpose of this study was to detect if there was gene mutation of SCN5A in 7 patients with Brugada syndrome and explore the molecular genetic characteristics of this disease.</p><p><b>METHOD</b>Genomic DNA was extracted from peripheral blood of all 7 patients with Brugada syndrome and 41 pairs of PCR primers were designed to amplify all the 28 exons of SCN5A.</p><p><b>RESULT</b>There was no novel mutation in exons of Gene SCN5A in these patients with Brugada syndrome.</p><p><b>CONCLUSION</b>Brugada syndrome might associated gene mutation or other mechanisms independent of SCN5A gene mutation.</p>

Time course change in the high mobility group box-1 after myocardial infarction in rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the time course change in myocardial high mobility group box-1 (HMGB1) after myocardial infarction in rats.</p><p><b>METHODS</b>Myocardial infarction (MI) was induced in SD rats by ligation of the anterior descending coronary artery. At 1, 2, 4, and 8 weeks after MI, the cardiac function of the rats was examined, and the expressions of HMGB1 at mRNA and protein levels in the myocardium were detected using real-time RT-PCR and Western blotting, respectively.</p><p><b>RESULTS</b>Cardiac function test confirmed that the MI model was successfully induced. The expression of HMGB1 mRNA was increased in early stage (1 week) after MI, while significantly down-regulated in later stage (4-8 weeks after MI). HMGB1 protein showed a similar biphasic pattern of changes, and was up-regulated early (1-2 weeks) after MI (P<0.05) and decreased markedly (P<0.01) at 8 weeks.</p><p><b>CONCLUSIONS</b>As an inflammatory regulator, HMGB1 can modulate inflammatory response early time after MI and functions later as a transcriptional modulator, thus contributing to the myocardial repair after MI. Interventions targeting HMGB1 in different stages after MI may prove helpful in reducing the complications, improving the prognosis and promoting long-term survival.</p>