Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the relative frequency of the causes of death in the acute (less than 24 hours), early (24 hours to 3 weeks), and chronic (greater than 3 weeks) phases of myocardial infarction, data from all autopsies performed at a university hospital during a 56-month period were reviewed. Autopsies were performed in 56% of in-hospital deaths and 27% of patients dead on arrival in the emergency room (out-of-hospital deaths). In 271 cases of suspected cardiac death, a myocardial infarction of any age was identified. Death had occurred in the acute phase of a first infarction in 19 patients and was most frequently due to pump failure (37%) followed by cardiac rupture (26%) and arrhythmias (21%). Death had occurred 24 hours to 3 weeks after a first infarction in 80 patients and was most frequently due to pump failure (44%), rupture (27%), and arrhythmias (16%). Recurrent acute infarction was found in 32% of patients whose deaths were due to arrhythmias or pump failure and in 19% of those whose deaths were due to rupture. Death had occurred greater than 3 weeks after a first infarction in 172 patients. In 132 (77%) of these patients death was due to a complication of a new acute or recent infarction. Myocardial rupture was a less frequent cause of death in patients with recurrent infarction (8%) than in those dying in the acute or early phase after their first infarction (27%, p = 0.0009). A primary arrhythmia in the absence of recurrent infarction or ischemia accounted for only 14% of out-of-hospital deaths late after an infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The spectrum of death after myocardial infarction: a necropsy study. 258 58

Macroscopic hemorrhagic infarction was studied in 14 autopsied hearts with selective coronary thrombolysis (SCT) after acute myocardial infarction (AMI). In all patients urokinase, 240,000 - 720,000 units, had been selectively injected into ischemia-related coronary artery at 2 - 7 hours after the onset of AMI. The degree of stenosis after SCT was 90 - 99% in 13 patients and 100% in one patient. According to the duration of illness at death, the 14 patients were classified into 3 stages; stage I: 4 - 9 hours; stage II: 15 hours to 11 days; stage III: 19 days to 12 months. Three hearts in stage I had no macroscopic hemorrhage. In stage II, marked and diffuse hemorrhage in the infarct area was macroscopically evident in 6 of 7 hearts. In a stage II patient, extravasation of contrast medium into the myocardium was found at 3 hours after the onset of AMI. In stage III, 4 hearts had massive fibrosis or granulation in the left ventricular wall without macroscopic hemorrhage. Cardiac rupture was seen in 4 of 10 patients from stages I and II. It is concluded that macroscopic bleeding appears in most patients with AMI treated with coronary thrombolysis. In the majority of cases, the hemorrhage increases gradually after SCT and becomes macroscopically definite approximately 15 hours after the onset of AMI. Rarely, massive bleeding appears earlier. Hemorrhagic infarction is replaced by massive fibrosis after approximately 2 weeks.
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PMID:Macroscopic hemorrhagic infarction following selective coronary thrombolysis in acute myocardial infarction. 403 86

Cardiac rupture is a fatal complication of acute myocardial infarction lacking treatment. Here, acute myocardial infarction resulted in rupture in wild-type mice and in mice lacking tissue-type plasminogen activator, urokinase receptor, matrix metalloproteinase stromelysin-1 or metalloelastase. Instead, deficiency of urokinase-type plasminogen activator (u-PA-/-) completely protected against rupture, whereas lack of gelatinase-B partially protected against rupture. However, u-PA-/- mice showed impaired scar formation and infarct revascularization, even after treatment with vascular endothelial growth factor, and died of cardiac failure due to depressed contractility, arrhythmias and ischemia. Temporary administration of PA inhibitor-1 or the matrix metalloproteinase-inhibitor TIMP-1 completely protected wild-type mice against rupture but did not abort infarct healing, thus constituting a new approach to prevent cardiac rupture after acute myocardial infarction.
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PMID:Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. 1050 7