Pathologic changes of the cardiac conduction system in 12 patients with abnormal ECG / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the relationship between abnormal ECG and pathologic changes in the cardiac conduction system (CCS).</p><p><b>METHOD</b>Pathological changes of the CCS in 12 cases with abnormal ECG out of 16 pre-death ECG were observed.</p><p><b>RESULTS</b>(1) Among 7 cases of sudden cardiac death, ECG monitoring recorded bradyarrhythmia in 6 cases, tachyarrhythmia 6 cases, bradycardia-tachycardia syndrome 2 cases, conduction block 6 cases, atrial premature beats 6 cases, ventricular premature beats 6 cases, and ST-T changes 4 cases. (2) The histopathological findings in the CCS were noted in all cases. Of these 12 cases, three had signs of fatty infiltration, and/or fibrous 4 cases, three of amyloidosis, one of chronic inflammatory changes, two of acute inflammatory changes, two of developmental anomalies, two of hemorrhages and one of LAD stenosis. (3) Acute inflammation changes in the CCS corresponded to tachyarrhythmia and multiple ventricular premature beats, whereas chronic inflammation and degenerative changes in the CCS were often related to bradyarrhythmia, bradycardia-tachycardia syndrome and conduction block. (4) The CCS changes alone could lead to ST-T changes in ECG.</p><p><b>CONCLUSION</b>The pathological changes in the CCS are related to ECG changes, and attributed to the pathological bases of arrhythmia.</p>

Ischemic postconditioning attenuates ischemia/reperfusion injury in isolated hypertrophied rat heart / 中华心血管病杂志

<p><b>OBJECTIVE</b>To explore the effects of ischemic postconditioning on ischemia/reperfusion injury in isolated hypertrophied rat heart and investigate the signal transduction pathway changes induced by ischemia postconditioning.</p><p><b>METHODS</b>Cardiac hypertrophy was induced in rats by abdominal aortic banding, and isolated hypertrophied rat heart ischemia/reperfusion model was made by Langendorff technique to evaluate the effects of ischemia postconditioning on left ventricular systole pressure, coronary artery flow, creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) release, myocardial infarction size, and the level of myocardial phospho-protein kinase B/Akt (Ser473), phospho-glycogen synthase kinase-3beta (Ser9). Following groups were studied (n = 12 each group): IR, 30 min ischemia (I)/60 min Reperfusion (R); Post: 30 min ischemia, 6 circles of 10 s I/10 s R followed by 60 min R; Post Wort: 30 min ischemia, 6 circles of 10 s I/10 s R, wortmannin (10(-7) mol/L) followed by 60 min R; Wort: 30 min ischemia, wortmannin (10(-7) mol/L) followed by 60 min R.</p><p><b>RESULTS</b>Left ventricular systolic pressure and coronary artery flow were significantly increased, myocardial infarction size and the release of CPK, LDH significantly reduced in Post group compared to that in IR group. Phospho-protein kinase B/Akt (Ser473) and phospho-glycogen synthase kinase-3beta (Ser9) levels were also significantly higher in Post group than that in IR group. Phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin prevented the increase of phospho-protein kinase B/Akt (Ser473) and phospho-glycogen synthase kinase-3beta (Ser9) induced by ischemic postconditioning, but only partly abolished the cardioprotection of ischemic postconditioning.</p><p><b>CONCLUSION</b>Ischemic postconditioning attenuates ischemia/reperfusion injury in isolated hypertrophied rat heart. The cardioprotective effects of ischemic postconditioning were partly mediated through PI3K/Akt/GSK-3beta signaling pathway.</p>