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

Myocardial ischemia occurs when there is an imbalance between myocardial oxygen demand and supply, and it is usually entirely or predominantly subendocardial. Animal experiments have shown that relative subendocardial ischemia (a reduced inner:outer flow ratio) can be predicted quite accurately from the ratio of two pressure-time areas:DPTI, the area between diastolic aortic and left ventricular pressures, and SPTI, the area beneath the systolic left ventricular pressure curve. Although the importance of relating supply and demand is obvious, care is needed in applying the results of these animal experiments to man. Recent work has shown that the critical DPTI:SPTI ratio below which subendocardial ischemia occurs is about 0.4 to 0.5 rather than 0.7 to 0.8, as originally reported. On the other hand, the critical ratio may be raised to an unknown extent by myocardial edema or hypertrophy, or by thickened or narrowed coronary arteries. Furthermore, the critical ratio is not independent of absolute coronary diastolic pressure: It is much lower than 0.4 when coronary pressures are high, perhaps because intramyocardial diastolic pressures are much higher than once thought. Further work is required to allow an important physiologic concept to be used in making decisions about patients with heart disease.
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PMID:The myocardial supply:demand ratio--a critical review. 14 25

This study evaluates the tolerance to ischemia during induced cardiac arrest in patients undergoing aortic valve replacement. In all patients cardiac standstill was of 45 minutes duration. Biopsies for electron microscopic study were taken from the left ventricle before induction of arrest, at the end of the ischemic period and 20 minutes after coronary perfusion had been reestablished. Structural ischemic damage was more pronounced in patients with severe hypertrophy and structural reconstitution was delayed. Degenerative changes of the myocardial cells, although observed frequency, apparently did not influence the tolerance to ischemia. It is concluded from this study that patients with severe hypertrophy represent a high-risk group in cardiac surgery because of their reduced tolerance to induced myocardial ischemia during cardiopulmonary bypass.
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PMID:Tolerance to ischemia of hypertrophied human hearts during valve replacement. 14 87

To assess the potential benefit of pulsatile perfusion inthe hypertrophied heart during fibrillation, 10 dogs with left ventricular hypertrophy, produced by previous supravalvular aortic banding, were used to compare linear and pulsatile perfusion in the fibrillating heart during total cardiopulmonary bypass. The mass spectrometer was used to measure subendocardial PCO2 and PO2 (PmCO2 and PmO2), and radioactive microspheres were utilized to measure myocardial blood flow in the same layers. Pulsatile perfusion was established using the recently develop "bubble tubing," which produces a pulse pressure of at least 20 mm Hg and can be used in a standard roller-pump apparatus. Both linear and pulsatile flows were compared at mean aortic root pressures of 80 and 50 mm Hg, and these four combinations of aortic root pressure and type of flow were employed for periods of 30 minutes each. Myocardial ischemia developed during linear coronary perfusion at 50 mm Hg, as evidenced by an elevation of PmCO2. Ischemia was not evident during pulsatile perfusion at the same mean pressure. Reversal ischemia was a result of increased myocardial blood flow and pulsatile perfusion, and this increase was shown to occur maximally in the deeper subendocardial layer. Ischemia was not eviden during linear or pulsatile perfusion at an mean perfusion pressure 80 mm Hg. Thus, if lower perfusion pressures are to be tolerated in patients with left ventricular hypertrophy, pulsatile perfusion with the bubble tubing technique may prevent the development of subendocardial ischemia or infarction.
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PMID:Beneficial effects of pulsatile perfusion in the hypertrophied ventricle during ventricular fibrillation. 15 96

Two thousand one men with coronary heart disease (CHD) who were enrolled in the Exercise Testing Registry of the Seattle Heart Watch had symptom-limited maximal exercise tests at the initial clinical examination and follow-up surveillance of subsequent mortality for 4.1 +/- 1.6 years. When subdivided into three mutually exclusive subgroups, 636 patients did not have exertional myocardial ischemia, left ventricular dysfunction or cardiomegaly; 885 without cardiomegaly had only exertional ischemia; 480 had left ventricular dysfunction by either cardiomegaly and/or two noninvasive exertional criteria, with or without exertional myocardial ischemia. Three hundred thirty-one men had aortocoronary bypass surgery, while 1670 remained unopened for at least 4 years. Only 34% of the operated patients who had left ventricular dysfunction, as defined, showed a marked improvement in 4-year survival rates (p less than 0.01). Differences in the annual CHD mortality rates in relation to surgical treatment in the other two groups were not statistically significant. Restricting the analysis to a subset of patients who had invasive studies did not alter the conclusion. Accordingly, we suggest the use of noninvasive criteria to aid preliminary screening of patients for invasive studies and surgical treatment.
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PMID:Noninvasive screening criteria for enhanced 4-year survival after aortocoronary bypass surgery. 15 7

Although corticosteroids have been shown to stabilize lysosomal membranes and prevent release of hydrolytic enzymes, the mechanism of membrane stabilization remains obscure. The few reports regarding the use of steroids in myocardial ischemia have been conflicting. This study was undertaken to determine if a pharmacologic dose of the glucocorticoid methylprednisolone would protect the heart during ischemic cardiac arrest. A randomized double-blind study was performed in 25 dogs. Biochemical and hemodynamic parameters were assessed during and after cardiopulmonary bypass and after 30 minutes of ischemic cardiac arrest. Animals were divided into two groups. Group I served as controls and consisted of dogs injected intravenously with the vehicle of methylprednisolone 18 hours and 1 hour prior to experiment. Group II comprised dogs injected with methylprednisolone, 30 mg. per kilogram, IV, at the same time periods. Blood pH, gases, and electrolytes were measured; aortic, left atrial, and left ventricular pressures were monitored; the first derivative of the left ventricular pressure (dp/dt max.) was also determined. Arterial and coronary sinus blood samples were assayed for lactate levels and activity of the lysosomal enzyme, beta-glucuronidase. Left ventricular muscle was assayed for the nucleotides cyclic adenosine 3',5' monophosphate (AMP) and cyclic guanosine 3',5' monophosphate (GMP). Following restoration of coronary flow, mean aortic and left ventricular systolic pressures and left ventricular contractility as determined by dp/dt max. and dp/dt max./IP were depressed in both groups as expected but were significantly higher in Group II than in Group I (p less than 0.05). An increase in levels of both cyclic nucleotides occurred in each group during ischemia, but this increase in cyclic GMP was significantly greater in Group I (p less than 0.05). beta-glucuronidase activity and myocardial potassium loss as determined in coronary sinus blood were both significantly greater in Group I than in Group II (p less than 0.05). Results of this study demonstrate that pretreatment with a pharmacologic dose of methylprednisolone significantly enhances cardiac recovery after ischemia. Lysosomal membrane stability and modulation of cyclic GMP levels may be critical determinants in the mechanism of cardiac ischemia.
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PMID:Protective effect of methylprednisolone on the heart during ischemic arrest. 17 23

Myocardial ischemia results from an imbalance of energy supply and demand. Because of the essentially aerobic nature of myocardial metabolism and the high oxygen extraction from the blood, ischemia is usually equatable with limitation of blood supply. Coronary atherosclerosis is a patchy disorder, and therefore, ischemia usually occurs in segmental fashion throughout the topography of the heart. Ischemia is invariably seen earliest and most intensely in the deep or subendocardial layers of myocardium. Ischemia leads to biochemical disruption, including initiation of glycolysis, which in turn causes electrophysiological and mechanical disturbances. Myocardial ischemia can be induced naturally or experimentally in the human subject in a variety of ways, some of which have been studied in the laboratory.
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PMID:Myocardial ischemia. 18 72

After prelabeling the adenine nucleotides (ATP, ADP, AMP) of isolated perfused guinea pig hearts with either 14C-adenine or 14C-adenosine for 35 min, labeled adenosine, inosine, hypoxanthine and cyclic 3'5'-AMP (cAMP) were continuously released into the cardiac perfusate. Determination of the specific activities (SA) of the adenine nucleotides, cAMP, and their breakdown products (adenosine, inosine, hypoxanthine) in tissue and perfusate revealed: Under steady state conditions the SA of adenosine and cAMP in the perfusate were of the same order of magnitude and proved to be many times higher than the SA of the respective precursor adenine nucleotides. This difference was observed regardless whether adenine or adenosine was used as prelabeling substances. The SA of inosine and hypoxanthine in the perfusate were constantly lower than the SA of adenosine. Cardiac ischemia of 6 min, which resulted in a markedly increased formation of adenosine, led to a pronounced decrease in the SA of adenosine released from the heart. Our findings provide evidence that at least two different adenine nucleotide compartments of the heart severe as precursors for the formation of adenosine and cAMP, one characterized by a high, the other by a lower SA. Under normoxic conditions adenosine and cAMP released into the cardiac perfusate are derived mainly from a nucleotide fraction of high SA, which appears to be rather small. During ischemia a second compartment of much lower SA in addition contributes to the formation of adenosine.
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PMID:Compartmentation of cardiac adenine nucleotides and formation of adenosine. 18 85

Although acute infarction of the myocardium is known to accumulate 99mtechnetium pyrophosphate, it is not entirely clear that ischemia alone without necrosis does not result in abnormal uptake of 99mtechnetium pyrophosphate. The present study investigates whether transient myocardial ischemia is associated with localization of 99mtechnetium pyrophosphate by evaluating images obtained with the scintillation camera at rest and after exercise in 15 patients with unequivocal myocardial ischemia. All patients had angina pectoris, multivessel coronary artery stenoses by selective arteriographic studies, and electrocardiographic ischemic responses on treadmill exercise. Eleven of the 15 patients also underwent radionuclide imaging with 81rubidium at rest and after exercise; the results demonstrated scintigraphic ischemia. The scintiscans with 99mtechnetium pyrophosphate revealed no evidence of increased myocardial radioactivity after exercise compared to rest in 14 of the 15 patients. In contrast, myocardial activity was observed with 99mtechnetium pyrophosphate after treadmill exertion in the remaining patient, in whom a small subendocardial infarction appeared to have occurred with the exercise. It is concluded from these results that transient myocardial ischemia does not cause localization of 99mtechnetium pyrophosphate. These findings support the specificity of abnormal localization of 99mtechnetium pyrophosphate for acute myocardial infarction.
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PMID:Evaluation of myocardial uptake of 99mtechnetium pyrophosphate in clinical exercise-induced ventricular ischemia. 18 75

Primary prevention of death from ischemic heart disease requires further understanding of the pathogenesis of this disorder. Cellular defects of cholesterol metabolism may be more significant markers that serum lipid levels for the identification and treatment of atherosclerotic risk. Coronary spasm has been shown to be an important cause of ischemia in the presence and absence of atherosclerotic lesions. Careful manipulation of physiologic variables with vasodilator agents during cardiopulmonary bypass can substantially alter the myocardial oxygen supply-demand relation, thereby minimizing ischemic injury. The cellular basis for loss of mechanical function during ischemia and the factors that determine irreversible injury are yet unknown.
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PMID:Pathophysiology of myocardial infarction. 19 8

Continuously recorded bipolar electrograms were obtained simultaneously from epi-, endo-, and mid-myocardial regions of the ischemic and normal zones of cat left ventricle in vivo after coronary occlusion, analyzed by computer, and compared to regional cyclic AMP levels. Regional cyclic AMP content was used as an index of the combined local effects of: (a) efferent sympathetic nerve discharge; (b) release of myocardial catecholamines due to ischemia; and (c) circulating catecholamines. Ischemia resulted in a progressive increase in pulse width and rise time and a decrease in rate of rise of voltage (dV/dt) of the local electrograms from ischemic zones reaching a maximum within 2.4+/-0.3 min (mean+/-SE) at the time of onset of severe ventricular dysrhythmias, all of which returned toward control before the cessation of the dysrhythmia (33.5+/-1.5 min after coronary occlusion). Increases in cyclic AMP in ischemic zones preceded corresponding increases in the frequency of premature ventricular complexes (PVCs). Propranolol inhibited the increases in cyclic AMP and reduced the frequency of PVCs in animals without ventricular fibrillation. In animals with ventricular fibrillation, cyclic AMP was significantly elevated in normal and ischemic zones compared to animals with PVCs only. Electrical induction of PVCs or ventricular fibrillation in ischemic and nonischemic hearts failed to increase cyclic AMP. The results suggest that the changes in regional adrenergic stimulation of the heart may contribute to perpetuation of ventricular dysrhythmia and the genesis of ventricular fibrillation early after the onset of myocardial ischemia.
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PMID:Mechanisms contributing to malignant dysrhythmias induced by ischemia in the cat. 20 67


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