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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

William Heberden (1710--1801), in 1768, described angina pectoris, the classic symptom of ischemic heart disease, 150 years after the discovery of the coronary circulation by William Harvey (1578-1657). Another 110 years had elapsed before the first antemortem diagnosis (confirmed at autopsy) of coronary thrombosis was reported by Adam Hammer in 1878. The patient was a 34 year old man who died some 19 hours after a sudden collapse. Although the patient's clinical features were atypical (such as the absence of angina and the presence of complete heart block) and the autopsy showed vegetative aortic endocarditis that appeared to be causally related to the thrombotic coronary occlusion, Hammer's astute and carefully reasoned bedside diagnosis was history-making and deserves to be so recognized.
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PMID:Centenary of the first correct antemortem diagnosis of coronary thrombosis by Adam Hammer (1818--1878): English translation of the original report. 36 Aug 11

Changes in the ECG of a rhesus monkey during a classical aversive conditioning trial conducted 10 minutes after occlusion of the marginal branch of the left circumflex coronary artery have been observed. This appears to reflect an instance where myocardial ischemia following coronary occlusion was exacerbated by presentation of a conditional stimulus.
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PMID:A note on ECG changes observed during Pavlovian conditioning in a rhesus monkey following coronary arterial occlusion. 41 87

We have recently detected accumulation of lysophosphoglycerides, catabolites of phospholipids, in ischemic myocardium early after coronary occlusion. In the present study we delineated effects of selected concentrations of albumin-bound lysophosphatidyl choline (LPC) comparable to those accompanying ischemia in vivo on action potentials of isolated canine Purkinje fibers. Lysophosphoglycerides induced concentration-dependent (0.75-3.0 mM) decreases in resting membrane potential, overshoot of phase 0, maximal velocity of upstroke (Vmax) of phase 0, and action potential duration. The highest concentrations (2.0-3.0 mM) induced fractionation of the action potential into several components, unresponsiveness to external stimulation, and enhanced automaticity at normal and reduced membrane potentials. LPC induced a rightward shift in the membrane response curve, a 40-fold prolongation of conduction time, and an increase in the ratio of effective refractory period to action potential duration such that the effective refractory period persisted beyond action potential duration, resulting in postrepolarization refractoriness. These electrophysiological alterations were entirely reversible after 70 minutes of perfusion without LPC, with the exception of a persistent depression in the Vmax of phase 0. Lysophosphatidyl ethanolamine (LPE) elicited alterations in action potentials indentical to those elicited by LPC. Furthermore, LPC (3.0 mM) induced comparable alterations in action potentials recorded from isolated rabbit papillary muscles. Since lysophospholipids accumulate early after myocardial ischemia, and since concentrations equivalent to those occurring in vivo induce electrophysiological alterations resembling those seen in ischemic myocardium in vivo, lysophosphoglycerides may be of major importance as biochemical mediators of malignant dysrhythmia induced by ischemia.
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PMID:Potential arrhythmogenic electrophysiological derangements in canine Purkinje fibers induced by lysophosphoglycerides. 42 75

The present study was done to quantitate the evolution of myocardial ischemic cell death within the framework of (1) the anatomical boundaries of the ischemic bed at risk and (2) the magnitude and transmural distribution of collateral blood flow. Myocardial ischemia was produced by proximal circumflex (LCC) occlusions in open chest dogs. Infarcts reperfused at 40 minutes, 3 hours, or 6 hours were compared with permanent infarcts. All dogs were sacrificed at 4 days. Regional myocardial blood flow was measured with 9-micrometer tracer microspheres before, and 20 minutes after, LCC occlusion. The location and size of the ischemic LCC bed at risk was determined by a dye injection technique. Infarct size was quantitated from multiple histologic sections. Necrosis involved 28 per cent, 70 per cent, and 72 per cent of the ischemic bed at risk in infarcts reperfused at 40 minutes, 3 hours, and 6 hours versus 79 per cent following permanent LCC ligation. Viable and potentially salvageable subepicardial muscle persisted for at least 3 hours after the onset of ischemia. Most of the salvageable myocardium was in the subepicardial region. In all groups, the lateral margins of necrosis were sharp in the subendocardial zone and were determined by the anatomical boundaries of the ischemic LCC bed at risk. LCC bed size ranged from 29 to 48 per cent of the left ventricle and thus contributed to variation in infarct size. However, infarct size, as a percentage of bed size, was determined by the transmural extent of necrosis within that bed (r = -0.97). This transmural extent of necrosis was related to subepicardial collateral flow after 3 hours (r = 0.92) and 6 or 96 hours (r = -0.85) but not after 40 minutes (r = -0.26) of ischemia. Thus, irreversible injury of ischemic myocardium developed as a transmural wavefront, occurring first in the subendocardial myocardium but ultimately becoming nearly transmural. Eventual transmural necrosis, and therefore over-all infarct size was determined by, and can be predicted from flow measurements obtained shortly after coronary occlusion.
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PMID:The "wavefront phenomenon" of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. 44 73

We have investigated the rate of rise of myocardial PCO2 (PmCO2) after coronary artery occlusion using a new method for this measurement. Previous studies of PmCO2 have been limited by the slow response of the only available method, and no increase in MmCO2 prior to 3 minutes after occlusion has been found. We have implanted a miniature PCO2 electrode, with a 63% response time of 14 seconds, into the left ventricle of 14 open-chest dogs. After abrupt coronary occlusion, PmCO2 began to rise in 13.6 +/- 1.1 seconds in heparinized dogs and in 7.5 +/- 0.7 seconds in unheparinized dogs. The subsequent magnitude of the increase in PmCO2 was 24, 88, 171, and 222 mm Hg at 2, 5, 10, and 15 minutes after occlusion. The rate of rise of PmCO2 was essentially linear from 1 minute to 10 minutes at a rate of 18.3 mm Hg/min. The rate of rise was slower during the first 30 seconds after occlusion (6.1 mm Hg/min) and also from 30 seconds to 1 minute (9.7 mm Hg/min). This rate of rise is much greater than that previously observed and reflects the severe myocardial acidosis developing during ischemia. A rise in PmCO2 is one of the earliest metabolic changes that has been observed during myocardial ischemia.
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PMID:Rate of rise of myocardial PCO2 during early myocardial ischemia in the dog. 45 97

In order to correlate the antiarrhythmic and electrophysiological effects of disopyramide phosphate during acute myocardial ischemia, we performed experiments in 17 mongrel dogs. Refractory periods obtained by the extrastimulus method and conduction times recorded from local electrograms were determined in potentially ischemic and nonischemic areas prior to, after left anterior descending coronary occlusion, and following intravenous administration of disopyramide phosphate 3 mg./Kg. Control refractory periods were similar in both nonischemic and ischemic areas. Following coronary ligation, a disparity of refractoriness of 28 msec. was induced between these two areas. After disopyramide administration, this disparity was reduced from 28 msec. to 5 msec. (p less than 0.001) after 5 to 15 minutes, and to 15 msec. (p less than 0.01) after 15 to 30 minutes. Coronary ligation prolonged conduction times by 8 msec. (p less than 0.005) in ischemic areas and disopyramide further prolonged conduction in these areas by an additional 9 msec. (p less than 0.001). A minimal and transient prolongation of conduction was present in nonischemic areas. We conclude that the differential effects exerted by disopyramide phosphate in ischemic areas may explain its suppressant action of arrhythmias of ventricular origin.
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PMID:Electrophysiological effects of disopyramide phosphate during experimental myocardial ischemia. 47 80

Ibuprofen, a nonsteriodal anti-inflammatory agent, was studied in the early stages of myocardial ischemia in order to determine whether it helps preserve myocardial integrity. Ibuprofen was administered intravenously at a dose of 12.5 mg/kg at the time of coronary artery occlusion and again 2.5 h later. Ibuprofen significantly prevented the loss of myocardial creatine phosphokinase (CPK) release in ischemic cardiac tissue. In addition, this drug significantly returned S-T segment elevation toward normal values, and significantly prevented the myocardial loss of compounds having free amino nitrogen groups, an index of proteolysis. Although ibuprofen moderated the increased plasma CPK activity, plasma CPK values 5 h after coronary occlusion were above control values. Thus, ibuprofen significantly prevented alterations in three of the four indices used to assess myocardial ischemic damage. The protective mechanism of ibuprofen may be via stabilization of cellular membranes (i.e., lysosomal membranes) and to a lesser extent on reduction in myocardial oxygen demand.
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PMID:Beneficial effects of ibuprofen in acute myocardial ischemia. 47 33

The risk of instantaneous death due to ventricular fibrillation was compared in resting and exercised dogs. Three weeks before testing, all dogs had bipolar left ventricular stimulating electrodes implanted and a reversible snare was placed around the anterior descending coronary artery. The dogs were randomly assigned to either an exercise (13 dogs) or a control (12 dogs) group. We measured ventricular fibrillation thresholds (VFTs) in all dogs before and after inducing ischemia by tightening the snare while the dogs stood at rest. The next day, nonischemic and ischemic VFTs were redetermined for control dogs at rest and for the exercise group during a treadmill run. No statistically significant changes were noted within and between groups in nonischemic or in ischemic VFTs at rest. In five exercise dogs, spontaneous ventricular fibrillation occurred during the first 8 minutes of the ischemic run, For the eight other exercise dogs, running increased the mean drop in VFTs during coronary occlusion by 23% (p less than 0.01). These data suggest that moderate dynamic exercise may greatly enhance the risk of ventricular fibrillation and sudden death in the presence of myocardial ischemia. In the absence of ischemia, exercise does not appear to increase vulnerability to ventricular fibrillation.
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PMID:Effect of submaximal exercise on vulnerability to fibrillation in the canine ventricle. 47 84

The effect of large doses of morphine (1 mg/kg, i.v.) on experimental myocardial ischemia was evaluated in anesthetized open-chest cats. Myocardial ischemia was produced by intermittent coronary artery occlusion and assessed by measuring ST-segment elevation in multiple epicardial leads. The results obtained in the group of animals given morphine were compared with values obtained in animals given saline (control group), propranolol or nitrous oxide (reference groups). Morphine injected before coronary occlusion produced a significant increase in ST-segment elevation after left anterior descending coronary artery occlusion, whereas no significant change was noted in animals receiving normal saline or nitrous oxide. As expected, in the animals that received propranolol there was a pronounced decrease in ST-segment elevation. Our data suggest that large doses of morphine may increase myocardial ischemia when administered before coronary occlusion in the anesthetized open-chest cat.
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PMID:Effect of large doses of morphine on experimental myocardial ischemia in cats. 47 23

There have been many reports about ventricular arrhythmias during acute coronary occlusion. Nevertheless, it is only recently that interest has been taken in the occurrence of ventricular arrhythmia after reperfusion following coronary occlusion. To investigate the mechanism of the latter kind of arrhythmia, we studied the effect of changing the duration of occlusion time on the recovery time courses of the VMRT (Ventricular Multiple Response Threshold), and of the A-V differences in the serum K+ concentration across the heart. The time course of delta K+ recovered soon after reperfusion, while changes in VMRT needed more time for recovery to the initial state. Concerning heart rate, blood pH, and the levels of Na+, Cl-, and Ca++, no significant changes were detected. There was no relation between the time courses of VMRT and those of the A-V differences in serum K+. Consequently, time courses in VMRT were dependent upon the duration of coronary occlusion time. A possible explanation for these results may be that the longer the duration of the preceding occlusion time, the more severe the myocardial damage due to myocardial ischemia.
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PMID:An experimental study of release arrhythmia: Occlusion time-dependent changes in ventricular fibrillation threshold. 49 23


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