1/4. Reperfusion-related polymorphic ventricular tachycardia as a possible mechanism of sudden death in patients with anomalous coronary arteries.We describe a patient with anomalous origin of the left coronary artery in whom polymorphic ventricular tachycardia developed immediately after an episode of chest pain with ST segment elevation. This is the first report providing direct evidence that reperfusion arrhythmias may be the cause of sudden death in individuals with anomalous coronary arteries.- - - - - - - - - - ranking = 1keywords = sudden death, death (Clic here for more details about this article) |
2/4. Clinicopathological study of myocardial infarction with normal or nearly normal extracardiac coronary arteries. Quantitative analysis of contraction band necrosis, coagulation necrosis, hemorrhage, and infarct size.In order to clarify the pathogenesis of acute myocardial infarction (MI) in hearts with normal coronary arteries, infarct size, and the extent of contraction band necrosis (CBN), coagulation necrosis, and hemorrhage were quantitatively examined using an image analyzer in 5 autopsy cases of MI with normal or nearly normal extracardiac coronary arteries. One patient died 40 h after acute MI. A second patient with acute MI due to severe spasm of segment 6, confirmed by cineangiography, died three days later. The third patient had already suffered a subarachnoid hemorrhage, and died 10 h after the onset of acute MI. The fourth patient had aortic stenosis and regurgitation. She developed acute MI due to total occlusion of segment 6, confirmed by cineangiography 4 h after the onset, and died 61 days later. autopsy revealed old anteroseptal MI with normal coronary arteries and valvular thrombi. The fifth patient had a malignancy, and died one day after the onset of acute MI. autopsy revealed multiple occlusive thrombi in the small intramural coronary arteries of the left ventricular wall supplied by segment 14, without any stenosis in the feeding vessel. Most infarcts were localized in the territory supplied by 1 or 2 of the 3 epicardial coronary arteries, and coincided with the clinically diagnosed infarct site. The infarct size ranged from 3%-26% of the left ventricular wall, and infarcts were generally localized to the inner third of the wall (67 /- 20%). Histological examination of the four patients with acute MI revealed diffuse CBN (86 /- 14% of the infarcted area) and/or hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)- - - - - - - - - - ranking = 0.21219096280321keywords = cardiac (Clic here for more details about this article) |
3/4. Termination of reperfusion arrhythmia by coronary artery occlusion.Reperfusion arrhythmias may be a cause of sudden death in acute myocardial infarction. A patient underwent successful coronary artery recanalisation by primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction. In this patient an idioventricular rhythm with a severe haemodynamic effect developed within one minute of deflation of the PTCA balloon. Sinus rhythm was immediately restored by reinflating the balloon and thus reinterrupting the supply of oxygenated blood. This suggests that reperfusion with consequent reoxygenation is a primary factor in arrhythmogenesis.- - - - - - - - - - ranking = 0.2keywords = sudden death, death (Clic here for more details about this article) |
4/4. Rescue therapy with C1-esterase inhibitor concentrate after emergency coronary surgery for failed PTCA.Administration of C1-esterase inhibitor (C1-INH) attenuates myocardial necrosis and sustains normal cardiac performance after myocardial ischemia and reperfusion in animal experiments. We report on our first experience of C1-INH application as rescue therapy in patients undergoing emergency surgical revascularization after failed percutaneous transluminal coronary angioplasty. Three patients were treated, because post-operative hemodynamic stabilization could not be achieved despite prolonged reperfusion periods, high-dose inotropic support, inodilators and aortic counterpulsation. As there was no surgical or medical option remaining, C1-INH was administered starting with a 2000 unit bolus, followed by 1000 U 12 and 24 h after surgery. C1-INH therapy resulted in rapid hemodynamic stabilization of all patients; weaning from aortic counterpulsation and epinephrine support was possible within 1 day. All patients survived and were discharged from hospital. In this group of patients suffering from severe reperfusion injury after coronary surgery, C1-INH seemed to be an effective adjuvant therapy to restore myocardial function by blocking the complement cascade. These results should encourage the performance of controlled studies on the effects of prophylactic C1-INH substitution therapy in patients undergoing coronary surgery at high risk conditions.- - - - - - - - - - ranking = 0.042438192560641keywords = cardiac (Clic here for more details about this article) |