Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytochrome C used at the postischemic period causes a rapid reestablishment of coronary circulation, hemodynamic parameters, prevents activation of lipid peroxidation in reoxygenation of the heart after prolonged total myocardial ischemia in patients with acute bacterial endocarditis in whom the prostheses of heart valves had been fulfilled. Parallel with the positive inotropic effect, Cytochrome C reduces the postloading and, as a result, transfers the cardiac muscle to a more profitable regimen. At the end of the myocardial ischemia period Cytochrome C provides rapid and effective recovery of the bioelectrical function of the heart, improves its pumping function, thus allowing the dose and duration of inotropic stimulation of the myocardium at the postischemic period to be reduced, lowers pulmonary resistance and finally leads to less postoperative intrahospital lethality from acute heart failure.
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PMID:[Use of cytochrome C in the prevention of myocardial reperfusion injury during heart valve prosthesis implantation under conditions of extracorporeal circulation]. 1125 17

Three cases are reported to demonstrate the range of possible lesions and wide variation in lethal mechanisms that may be found in cases of unexpected death subsequently shown to be due to bacterial endocarditis. Case 1: A 36-year-old man was found dead on his bedroom floor surrounded by drug paraphernalia. At autopsy, acute myocardial ischemia was present caused by coronary artery ostial occlusion complicating acute bacterial endocarditis of the aortic valve. Case 2: A 54-year-old man with chronic renal failure was found dead in bed at home. At autopsy, a left middle cerebral artery territory cerebral infarct was present due to septic embolization from bacterial endocarditis involving the aortic valve. Case 3: A 23-year-old man was found collapsed in a pool of blood. At autopsy, upper airway hemorrhage from an arteriobronchial fistula was present caused by septic pulmonary infarction from previous endocarditis of a congenital ventricular septal defect. This report demonstrates that bacterial endocarditis may still be a cause of sudden and unexpected death presenting to forensic mortuaries and that the underlying mechanisms may involve complex sequences of pathological changes that compromise vascular function.
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PMID:Sudden death as a complication of bacterial endocarditis. 2151 91