Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of ischemia on the canine myocardial (Na+ + K+)-ATPase complex were examined in terms of alterations in cardiac glycoside binding and enzymatic activity. Ability of the myocardial cell to bind tritiated ouabain in vivo was assessed after 1, 2, and 6 h of coronary occlusion followed by 45 min of reperfusion, and correlated with measurements of in vitro (Na+ + K+)-ATPase activity and in vitro [3H]ouabain binding after similar periods of ischemia. Regional blood flow alterations during occlusion and reperfusion were simultaneously determined utilizing 15 mum radioactive microspheres to determine the degree to which altered binding of ouabain might be flow related. Anterior wall infarction was produced in 34 dogs by snaring of confluent branches of the left coronary system. Epicardial electrograms delineated ischemic and border zone areas. Coronary reperfusion after 2 and 6 h of occlusion was associated with impaired reflow of blood and markedly impaired uptake of [3H]ouabain in ischemic myocardium. In both groups, in vivo [3H]ouabain binding by ischemic tissue was reduced out of proportion to the reduction in flow. Despite near-complete restoration of flow in seven dogs occluded for 1 h and reperfused, [3H]ouabain remained significantly reduced to 58 +/- 9% of nonischemic uptake in subendocardial layers of the central zone of ischemia. Thus, when coronary flow was restored to areas of myocardium rendered acutely ischemia for 1 or more hours, ischemic zones demonstrated progressively diminished ability to bind ouabain. To determine whether ischemia-induced alteration in myocardial (Na+ + K+)-ATPase might underlie these changes, (Na+ + K+)-ATPase activity and [3H]ouabain binding were measured in microsomal fractions from ischemic myocardium after 1, 2, and 6 h of coronary occlusion. In animals occluded for 6 h, (Na+ + K+)-ATPase activity was significantly reduced by 40% in epicardial and by 35% in endocardial layers compared with nonischemic myocardium. Comparable reductions in in vitro [3H]ouabain binding were also demonstrated. Reperfusion for 45 min after occlusion for 6 h resulted in no significant restoration of enzyme activity when compared to the nonreperfused animals. In six animals occluded for 2 h, a time at which myocardial creatine phosphokinase activity remains unchanged, (Na+ + K+)-ATPase activity was reduced by 25% compared with nonischemic enzyme activity. In five dogs occluded for 1 h, (Na+ + K+)-ATPase activity in ischemic myocardium was unchanged from control levels. We conclude that reduced regional myocardial blood flow, local alterations in cellular milieu, and altered glycoside-binding properties of (Na+ + K+)-ATPase all participate in the reduction of cardiac glycoside binding observed after reperfusion of ischemic myocardium. In addition, after 2 or more hours of severe ischemia, myocardial (Na+ + K+)-ATPase catalytic activity is significantly reduced despite incubation in the presence of optimal substrate concentrations.
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PMID:Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding. 13 Mar 83

To evaluate the significance of "reciprocal" ST segment depression resulting from coronary occlusion, 27 patients with single vessel coronary disease were studied with intravenous digital subtraction left ventriculography before and during angioplasty of the left anterior descending coronary artery. During balloon inflation, 13 patients developed inferior lead ST depression in addition to anterior lead ST elevation (Group 1), whereas the remaining 14 patients did not (Group 2). The degree of anterior lead ST elevation in Group 1 (5 mm) was greater than that in Group 2 (1.5 mm, p less than 0.001) as was the reduction in left ventricular ejection fraction (24% versus 13%, respectively; p less than 0.02). Anterior and apical regional shortening decreased in both groups similarly, but an additional decrease in anterobasal shortening was confined to Group 1 (from 38% to 21%; p less than 0.002). Despite the presence of inferior lead ST depression in Group 1, inferior regional shortening did not change and inferobasal contraction was enhanced (from 4% to 29%; p less than 0.01). Inferior lead ST segment depression during anterior descending coronary angioplasty reflects a greater degree of anterior wall ischemia. The concurrent preservation of inferior wall contraction and the augmentation of infero-basal shortening confirm that this electrocardiographic feature is a "reciprocal" phenomenon rather than a manifestation of remote ischemia.
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PMID:Significance of "reciprocal" ST segment depression: left ventriculographic observations during left anterior descending coronary angioplasty. 252 57

Cardiac angiography was reviewed in 91 patients with post-infarction ventricular septal rupture. The results were compared with those of 123 stable survivors who had a positive submaximal exercise test early after infarction. Anterior infarction and occlusion of the infarct vessel were more common in those with ventricular septal rupture than in the comparison group. In the group with ventricular septal rupture there was more left ventricular damage, with aneurysm formation in two thirds, and coronary angiography showed more single than triple vessel disease. In the comparison group there was more triple vessel disease than single vessel disease. Angiographically demonstrable collaterals to the infarct territory were not seen or only very faintly seen in 82% of those with septal rupture. Well developed collaterals were seen in two thirds of the comparison group. These patterns of coronary disease suggest that ventricular septal rupture is more likely in patients with coronary occlusion and little or no collateral support to the infarct territory.
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PMID:Patterns of coronary artery disease in post-infarction ventricular septal rupture. 280 72

The goal of surgical reperfusion during the first hours of acute evolving myocardial infarction is to limit the extent of the infarction. This should be reflected by improved ventricular function and low mortality. Over the past 10 years, 440 patients with transmural myocardial infarction and 261 patients with nontransmural myocardial infarction underwent coronary artery bypass graft surgery within 24 hours of peak symptoms. The in-hospital mortality was 5.2% in the transmural group and 3% in the non-transmural group. In a 10-year study period, the mortality in the transmural group rose to 12.5%, while the mortality in the nontransmural group, followed for an 8-year period, rose to a total of 6.5%. The transmural myocardial infarctions in patients revascularized within 6 hours, showed a significantly improved in-hospital mortality of 3.8% compared to an in-hospital mortality of 12% for reperfusion after 6 hours. Anterior transmural areas of myocardial infarctions were reperfused within 6 hours of symptom onset, and demonstrated improved global ejection fraction and regional wall motion. Little improvement was seen if revascularization was instituted later than 6 hours from symptoms except in patients with adequate collateral perfusion of non-total left anterior descending coronary occlusion. Long-term follow-up of patients revascularized for acute myocardial infarction shows a low rate of subsequent reinfarction, incapacitating angina and sudden death. Left ventricular function at the time of cardiac catheterization correlates well with subsequent long-term mortality.
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PMID:Surgical intervention in acute myocardial infarction. 1522 94