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OBJECTIVE@#To investigate whether ginsenoside-Rb1 (Gs-Rb1) improves the CoCl-induced autophagy of cardiomyocytes via upregulation of adenosine 5'-monophosphate-activated protein kinase (AMPK) pathway.@*METHODS@#Ventricles from 1- to 3-day-old Wistar rats were sequentially digested, separated and incubated in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum for 3 days followed by synchronization. Neonatal rat cardiomyocytes were randomly divided into 7 groups: control group (normal level oxygen), hypoxia group (500 μmol/L CoCl), Gs-Rb1 group (200 μmol/L Gs-Rb1 + 500 μmol/L CoCl), Ara A group (500 μmol/L Ara A + 500 μmol/L CoCl), Ara A+ Gs-Rb1 group (500 μmol/L Ara A + 200 μmol/L Gs-Rb1 + 500 μmol/L CoCl), AICAR group [1 mmol/L 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) + 500 μmol/L CoCl], and AICAR+Gs-Rb1 group (1 mmol/L AICAR + 200 μmol/L Gs-Rb1 + 500 μmol/L CoCl). Cells were treated for 12 h and cell viability was determined by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and cardiac troponin I (cTnI) levels were detected by enzyme-linked immunosorbent assay (ELISA). AMPK activity was assessed by 2',7'-dichlorofluorescein diacetate (DCFH-DA) ELISA assay. The protein expressions of Atg4B, Atg5, Atg6, Atg7, microtubule-associated protein 1A/1B-light chain 3 (LC3), P62, and active-cathepsin B were measured by Western blot.@*RESULTS@#Gs-Rb1 significantly improved the cell viability of hypoxia cardiomyocytes (P0.05). Gs-Rb1 significantly down-regulated P62 levels of hypoxic cardiomyocytes (P<0.05). The P62 levels of hypoxic cardiomyocytes were inhibited by Ara A (P<0.05) and were not affected by AICAR (P=0.871).@*CONCLUSION@#Gs-Rb1 may improve the viability of hypoxia cardiomyocytes by ameliorating cell autophagy via the upregulation of AMPK pathway.
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<p><b>OBJECTIVE</b>To investigate the prognostic value of acute heart block (AHB) after percutaneous transluminal septal myocardial ablation (PTSMA) in patients with hypertrophic obstructive cardiomyopathy (HOCM).</p><p><b>METHODS</b>Ninety-four HOCM patients underwent PTSMA were included in this study. Twelve-lead electrocardiograms were obtained during and post PTSMA. Association between clinic events and incidence of post-PTSMA AHB was analyzed.</p><p><b>RESULTS</b>AHB was induced in 26 patients by PTSMA and disappeared in 11 patients shortly post PTSMA, subacute intraventricular conduction disturbances was seen in 11 (42.3%), subacute I degrees AVB in 2 (7.7%) and subacute III degrees AVB in another 2 (7.7%) patients. Among 68 patients without AHB during PTSMA, intraventricular conduction disturbances was evidenced in 14 patients (20.6%), I degrees AVB in 2 (2.9%) and III degrees AVB in 1 patient (1.5%) after PTSMA. AHB patients with subacute heart block were associated with poor prognosis (conduction block duration was 42.00 h) while patients without AHB was associated with benign prognosis even with new onset of subacute heart block (conduction block duration was 7.33 h, P < 0.01).</p><p><b>CONCLUSION</b>Patients with AHB during PTSMA are at higher risk for subacute heart block, especially intraventricular conduction disturbances. AHB patients with subacute heart block were associated with poor prognosis and longer recovery time of conducting system.</p>