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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 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

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

beta-Adrenoceptor agonists increase myocardial ischemic injury, mainly by elevating myocardial oxygen consumption. Moreover, it has been shown that isoprenaline may "steal" regional myocardial blood flow (RMBF) from ischemic to non ischemic areas and from epicardium to endocardium. The mechanisms of these two isoprenaline-induced redistributions of RMBF have been investigated by the use of radioactive microspheres in an experimental model of canine myocardial ischemia with simultaneous measurement of ST-segment elevation. Isoprenaline increased RMBF in both epi- and endocardial non ischemic areas and in epicardial ischemic areas, leading to a significant decrease in the endo/epi ratio. After atenolol, isoprenaline still increased RMBF but to a lesser extent and the endo/epi ratio was still decreased. Salbutamol, in doses inducing no significant changes in cardiac parameters or myocardial oxygen consumption, produced effects similar to those of isoprenaline. These results indicate a non-homogeneous beta2-stimulation-induced vasodilation in endo- and epicardium, which might be due either to the higher epicardial coronary vasocilatory reserve or to a heterogeneous distribution of transmural beta2-adrenoceptors. Isoprenaline also decreased the ischemic/non ischemic total blood flow ratio (I/NI) and caused further increases in ST-segment elevation. These effects were abolished by atenolol pretreatment, indicating the deleterious effects of isoprenaline-induced tachycardia in this I/NI decrease and in the ischemic injury.
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PMID:The role of beta-adrenoceptors in coronary blood flow distribution in normal and ischemic canine myocardium. 21 19

Reduction in pH is known to decrease O2 affinity (Bohr effect) and increase the rate of O2 release from blood. It provides a potential mechanism for increasing O2 transport to the myocardium. Fifteen patients with refractory, chronic angina were studied by treadmill exercise tolerance tests and whole blood-oxygen release rate measurements before and 4 days after beginning treatment with oral acetazolamide (10 to 20 mg/kg body weight). Positive treadmill exercise test or myocardial necrosis was present in each case. There was a correlation between an increased O2 release rate from blood and relief of symptoms. The major side effect in 2 patients with pathologic fatigue believed to result from acidosis. Of the 7 patients who obtained relief from angina, in each there was a 27% increase in the rate of release of O2 from their whole blood. Seven patients did not obtain relief; they showed no change in the rate of release. In the 4 patients who became worse the rate of deoxygenation decreased by 22%. All changes in deoxygenation rate coincided with the clinical findings. The treatment of ischemic heart disease with acetazolamide or other acidifying agents should not, however, be attempted until further investigation establishes their clinical value.
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PMID:Effect of acidosis on patients with myocardial ischemia. 24 34

Hyperosmotic mannitol produces salutary hemodynamic and histologic effects during experimental myocardial ischemia. However, the administration of hyperosmotic mannitol is associated with a positive inotropic influence. Positive inotropic interventions, which increase myocardial oxygen consumption (MVO2), also tend to increase the extent of ischemic myocardial injury. Thus, the purpose of this study was to determine the effect of mannitol on MVO2. Anesthetized dogs on right-heart bypass under conditions of controlled hemodynamics were studied. Both coronary arteries were perfused; mannitol was infused via the coronary perfusion cannulas to produce a 35 mosmol increase in osmolality. Heart rate was maintained constant. Cardiac output was held constant or deliberately increased so that left ventricular end-diastolic pressure and tension-time index, two other hemodynamic correlates of MVO2, remained constant or increased. MVO2 significantly decreased under conditions of decreased myocardial perfusion (P less than 0.025). This was in spite of a significant increase (P less than 0.001) in the peak rate of rise of left ventricular pressure (LV dP/dt), a hemodynamic correlate of MVO2. Thus, hyperosmotic mannitol under conditions of reduced coronary perfusion increases myocardial efficiency.
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PMID:Effect of hyperosmotic mannitol on myocardial oxygen consumption. 30 55

To assess the effects of moderate potassium cardioplegia (37 mEq/l KCl) on the severity of myocardial ischemia during arrest and on post arrest ventricular function, 32 isolated, isovolumic feline hearts were studied before, during and 1 hour after ischemic arrest. Normothermia (37 degrees C) was maintained in the remaining 16 hearts, eight without KCl and eight with KCl. Hypothermia (27 degrees C) was maintained in the remaining 16 hearts, eight with KCl and eight without KCl. Myocardial oxygen (PmO2) and carbon dioxide tensions (PmCO2) were measured by mass spectrometry. Maximum developed intraventricular pressure (max DP) and max dP/dt were used as indices of performance. Compared with normothermic or hypothermic arrest alone, the addition of potassium cardioplegia resulted in a significant reduction in the peak PmCO2 measured during the arrest period. Hypothermia alone resulted in morphologic evidence of improved myocardial preservation and a significant reduction in peak PmCO2 compared with normothermia. Post arrest ventricular function was best with the combination of hypothermic arrest and potassium cardioplegia (max DP = 96 +/- 6% of control and max dP/dt = 99 +/- 5% of control). These data suggest that the beneficial effects of postassium cardioplegia and 27 degrees hypothermia are additive, and that reduction in myocardial ischemia as evidenced by a reduction in peak PmCO2 correlated with improvement in ventricular performance in the post arrest period and with preservation of myocardial structure.
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PMID:Effect of potassium cardioplegia on myocardial ischemia and post arrest ventricular function. 30 60

Between 1964 and 1978, aortocoronary bypass graft procedures were performed in more than 300,000 patients, and the number seems to increase every year. Nevertheless, the procedure itself can result in perioperative myocardial infarction leading to death. Greater understanding of and constant attention to the myocardial oxygen (O2) supply and demand may reduce the incidence of perioperative myocardial infarction. Some of the factors influencing supply and demand can be controlled pharmacologically. Drugs such as nitroglycerin, nitroprusside, and propranolol can reduce the myocardial O2 demand. Unfortunately, there are few data to elucidate the relationship between myocardial O2 demand and supply as influenced by anesthetic drugs, especially in patients with myocardial ischemia. However, enthusiasm for aortocoronary bypass graft operations has given enormous impetus to laboratory and clinical studies of this subject. Recent developments in anesthetic management afford better means for protection of the ischemic myocardium during and after operation.
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PMID:Anesthetic considerations for aortocoronary bypass graft surgery. 31 94

The authors analyze the results of 220 applications of internal cold cardioplegia in 136 patients with ischaemic heart disease, treated surgically by aortocoronary bypass. The operation was performed under neuroleptanalgesia and artificial circulation with hypothermia (27.9 +/- 0.2 degrees C) and haemodilution (24.9 +/- 0.3%). On the basis of clinical examination, electron microscopy of the myocardial ultrastructure, and investigation of the myocardial metabolism (contents of glucose, lactate, pyruvate, free fatty acids, catecholamines, and oxygen in arterial and venous blood flowing out of the myocardium), they come to the conclusion that internal cold cardioplegia efficiently protects the myocardium during aortocoronary bypass and secures favourable conditions for the development of anastomoses between coronary arteries and venous shunts.
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PMID:Myocardial protection during aortocoronary bypass. 31 79

The challenge of the high-risk cardiac patient undergoing general surgery will be met only when an aggressive approach is taken to avoid an unfavourable balance between the oxygen supply and demand of the myocardium. In the past this challenge has been accepted in the operating room but postoperative care has been less than adequate. The intelligent use of potent, effective pharmacologic agents and intensive monitoring of myocardial performance intra- and postoperatively have greatly reduced morbidity and mortality in patients with ischemic heart disease undergoing aortocoronary bypass procedures; they can achieve similar results in such patients who must undergo general surgery.
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PMID:The high-risk cardiac patient undergoing general surgery. 36 43

To study the mechanisms by which acute beta-adrenergic blockade may change the activity of the sympathetic nervous system we have measured haemodynamic responses including splanchnic blood flow in twenty-three patients with ischaemic heart disease at rest and during supine exercise before and after i.v. injection of 0.039 mmol (10 mg) dl-propranolol. After propranolol both at rest and on exercise blood pressure, cardiac output and heart rate decreased, while splanchnic vascular resistance increased; mixed venous oxygen saturation decreased whilst arterial oxygen saturation and oxygen uptake were unchanged. Plasma noradrenaline increased after propranolol, values correlating with mixed venous oxygen saturation and splanchnic vascular resistance, both at rest and during exercise before and after propranolol, only at rest was there any correlation with arterial blood pressure. The increase in sympathetic nervous activity after propranolol may be due to a reduction in cardiac output and thereby alteration of the metabolic state (oxygen or related factors) in tissues. Afferent neural signals from the tissues may play a significant role in the regulation of sympathetic nervous activity.
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PMID:Enhanced sympathetic nervous activity after intravenous propranolol in ischaemic heart disease: plasma noradrenaline splanchnic blood flow and mixed venous oxygen saturation at rest and during exercise. 41 29


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