Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biochemical, pharmacological, and molecular biological data provide evidence for the presence of a cardiac renin-angiotensin system. Tissue angiotensins were demonstrated in all regions of the mammalian heart. Reduction of cardiac angiotensin II formation after oral administration of converting enzyme (CE) inhibitors in nephrectomized animals points to local generation of these peptides. Functional studies in isolated working rat hearts subjected to transient regional ischemia and reperfusion showed that there is aggravation of arrhythmias as well as exhaustion of energy status by angiotensins. This was prevented by CE inhibition and/or perfusion with bradykinin (BK), which in turn could be competitively antagonized with a BK antagonist. Intracoronary infusion of low-dose bradykinin attenuated ischemia-reperfusion injuries and reduced enzyme and lactate release in anesthetized dogs. Oral pretreatment with the CE inhibitor ramipril in rats, in doses that did not affect the elevation of blood pressure caused by aortic constriction, could prevent induction of as well as cause regression of established cardiac hypertrophy. In contrast, pure vasodilation was without effect on cardiac enlargement despite lowering blood pressure, pointing to a possible trophic influence of angiotensin II. Thus, apart from afterload reduction and euvolumia produced by CE inhibition, the outstanding efficacy of this therapeutic approach in congestive heart failure and cardiac hypertrophy and its potential usefulness in myocardial ischemia may also be explained by intracardiac suppression of angiotensin II generation and bradykinin degradation.
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PMID:Pharmacological interference with the cardiac renin-angiotensin system. 248 22

Catecholamine activation enhances the inotropy of the heart by increasing the sarcolemmal influx of Ca2+. This increased influx is counteracted by an increased sarcolemmal efflux and sarcoplasmic reticulum uptake of Ca2+. Thus the intracellular milieu is protected against a gradual rise in Ca2+ concentration. However, under conditions of continuous, excessive catecholamine release, the heart's potential to remove Ca2+ from the cytosol might become exhausted. This might be caused by a Ca2+-dependent exhaustion of high-energy phosphates. As a result of this, Ca2+ overload of the myocytes and eventually a decrease in the pump function of the heart might occur. This paradox has implications for the clinical management of ischaemic heart disease.
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PMID:[Catecholamines--therapeutic and adverse effects on the heart]. 254 1

Adaptation to intermittent hypoxia had a pronounced antiarrhythmic effect in acute myocardial ischemia in conscious animals. This effect was less pronounced in anesthesia and was absent in isolated heart. In reperfusion, the prophylactic effect of adaptation was equally pronounced in all cases. Adaptation prevented stress-induced exhaustion of brain beta-endorphine presumably by its accumulation in adrenal glands and resulted in the accumulation of dopamine, 5-hydroxytryptamine and 5-hydroxyindolacetic acid in brain structures. These data naturally lead to the assumption that central mechanisms play the main role in the antiarrhythmic effect of adaptation to intermittent hypoxia on ischemic arrhythmias, while mechanisms occurring at the level of heart play the main role in the protective effect of the same adaptation against reperfusion arrhythmias.
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PMID:Prevention of cardiac arrhythmias by adaptation to hypoxia: regulatory mechanisms and cardiotropic effect. 256 60

A study was carried out on 36 geriatric diabetic females (above 60 years). Marked exhaustion and significant loss of weight were common presenting complaints (60%) besides usual symptomatology. Only 25% patients were asymptomatic for diabetes. Generalised itching (20%) and pruritus vulvae (33.3%) were other common presenting complaints. Neuropathy was found to be the commonest complication being present in 77.7% patients, followed by retinopathy (50%) and nephropathy (27.7%). Hypertension was found to be associated in 44% patients and evidence of ischaemic heart disease was found in 42%. Development of nephropathy, retinopathy, neuropathy, and hypertension showed direct correlation with duration of illness ie, longer the history of diabetes higher was the incidence of complications.
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PMID:Diabetes mellitus in geriatric females. 258 30

In order to assess the incidence of silent myocardial ischaemia, 190 consecutive patients with cerebral ischaemia and without symptoms or electrocardiographic signs of ischaemic heart disease, underwent a maximal exercise treadmill test. Patients with a positive exercise test were submitted to exercise thallium myocardial scintigraphy. Results were compared with those obtained in a control group of 113 healthy subjects submitted to the same study protocol. An adequate exercise test was obtained in 140 patients with cerebral ischaemia. The exercise test was positive in 36 cases (26%). The end points were exhaustion in 24 patients, ST segment depression greater than or equal to 3 mm in seven and systolic blood pressure greater than or equal to 240 mmHg in five. The exercise thallium myocardial scintigraphy was normal in three and abnormal in 33: reversible perfusion defects were detected in 26 cases and fixed defects in seven. In the control group, matched for age and sex, the exercise test was positive in only seven cases (6%; P less than 0.01); the exercise myocardial scintigraphy was normal in five and abnormal in two subjects. In conclusion, in a remarkable proportion of middle-aged patients with cerebral ischaemia, silent myocardial ischaemia can be detected by means of noninvasive cardiologic investigations.
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PMID:Incidence of silent myocardial ischaemia in patients with cerebral ischaemia. 326 46

To investigate the presence, mechanism, and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 50 patients underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared to patients without hypertrophic cardiomyopathy, their basal coronary flow, myocardial oxygen consumption, and left ventricular end-diastolic pressure were significantly higher. Further, the 23 patients with basal obstruction to left ventricular outflow had a significantly higher basal great cardiac vein flow and oxygen consumption than the 27 patients without basal obstruction. During pacing to heart rates of 100 and 130 bpm (the anginal threshold for 41 of 50 patients), those with basal obstruction still demonstrated significantly higher coronary flow and oxygen consumption. Most patients, regardless of the presence or absence of obstruction, had metabolic evidence of ischemia, often severe. At a heart rate of 150, most patients with basal obstruction demonstrated an actual decline in coronary flow, which correlated with an increase in left ventricular filling pressures and more severe metabolic evidence of ischemia. In those without obstruction, ischemia occurred at a lower coronary flow, suggesting more impaired coronary flow delivery than those with obstruction. Abnormalities in oxygen extraction were noted in both groups. Thus, obstruction to left ventricular outflow results in higher basal and stress-induced coronary flow and oxygen requirements, related to elevated left ventricular systolic pressures, resulting in rapid exhaustion of coronary flow reserve during stress. Patients without obstruction, with lower left ventricular systolic pressures, may have greater impairment of flow delivery during stress as a cause of myocardial ischemia.
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PMID:Myocardial ischemia in hypertrophic cardiomyopathy. 343 62

In patients with cerebral transient ischemic attacks or stroke myocardial infarction is the leading long-term cause of death. Despite the importance of coronary artery disease, patients with cerebrovascular insufficiency are seldom evaluated for the detection of ischemic heart disease and usually the cardiological evaluation is limited to the patients with angina or previous myocardial infarction. In order to identify asymptomatic coronary artery disease 74 consecutive patients with cerebral ischemia, and without symptoms or electrocardiographic signs of ischemic heart disease, underwent a maximal exercise treadmill test according to the Bruce protocol. An exercise Thallium myocardial scintigraphy was performed in patients with positive exercise test. A control group of 74 asymptomatic subjects underwent the same study protocol. The study population (Group I) included 57 men and 17 women; the age ranged from 22 to 72 years (mean age 54 years). An adequate exercise test was obtained in 67 patients. Exercise test was positive (ST-segment depression greater than or equal to 1.5 mm) in 19 cases (28%). The end points were exhaustion in 15 patients, ST-segment depression greater than 3 mm in 2 and systolic blood pressure greater than 240 mmHg in 2. The exercise Thallium myocardial scintigraphy was normal in 2 and abnormal in 17: reversible perfusion defects were detected in 12 cases and fixed defects in 5. In the control group (Group II), comparable for age and sex, exercise test was positive in 4 cases (5%; p less than 0.01 percentage of positive exercise tests in Group I vs Group II); the exercise myocardial scintigraphy was normal in 1 and abnormal in 3 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Early identification of ischemic cardiopathy in patients with cerebrovascular insufficiency.A prospective study with exertion test and perfusion myocardial scintigraphy]. 373 22

In order to perform intracardiac repair safely during aortic cross clamping, we designed this study to evaluate the protective effect of coenzyme Q10 (CoQ10) on hypertrophied ischemic myocardium from the aspect of energy metabolism. Six to nine months preceding the study, aortic bandings were carried out on 14 puppies to produce left ventricular hypertrophy (LVH). These dogs with LVH were then subjected to total cardiopulmonary bypass and were evenly divided into control and CoQ10-treated groups (10 mg/kg of intravenous administration plus 1 mg/kg per hr of intracoronary injection). Myocardial ischemia was induced by aortic cross clamping for 2 hr under moderate systemic hypothermia. The results indicated that the administration of CoQ10 had a protective effect on hypertrophied ischemic myocardium, since depletion of high-energy phosphate (HEP) was uniformly prevented, and accumulation of lactate was simultaneously decreased during the 2 hr of aortic cross clamping. On the other hand, there were marked exhaustion of HEP and rapid increase in lactate following the 2 hr of ischemia in the control group, these being much more predominant in the subendocardial layer.
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PMID:Effect of coenzyme Q10 on hypertrophied ischemic myocardium during aortic cross clamping for 2 hr, from the aspect of energy metabolism. 622 44

Platelet aggregates play an important role in rheology of the blood flow in microcirculation. The formation of platelet aggregates markedly raise the threshold diameter of the vessel at which the inversion of Fahraeus-Lindquist effect takes place. In different diseases (ischemic heart disease, diabetes) thromboxane A2 production by platelets is increased and, as a consequence, platelet aggregate formation is facilitated. Platelet aggregation is modulated by several mechanisms, among which thromboxane A2 and thrombin increase and prostacyclin decrease formation of platelet aggregates. Prostacyclin is able also to increase blood red cells deformability thus it appears one of the most important factors for the control of blood flow rheology in microcirculation. However, prostacyclin production is limited in time, and repeated and close periods of venous stasis induce exhaustion of prostacyclin production and increase the formation of platelet aggregates.
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PMID:Pathophysiological aspects of platelet aggregation in relation to blood flow rheology in microcirculation. 676 41

Swimming is frequently recommended for cardiac rehabilitation, but little is known of its physiologic consequences in ischemic heart disease. Eight males who had had a myocardial infarction 8-17 months before the study were exercised to exhaustion or angina with 10 W/min-1 ramp on a cycle ergometer in sitting and supine positions. Oxygen uptake (VO2) was continuously measured to monitor the physiologic power requirement. All eight patients were taking beta blockers and four were taking digoxin. During sitting cycling, angina occurred in four and ST depression in five; during supine cycling, angina occurred in five and ST depression in six. VO2 was then measured while they swam at their own comfortable speed (mean 0.43 m/sec-1) in a swimming flume at water temperatures of 25.5 degrees C and 18 degrees C. In six, the water speed was gradually increased until they were limited by symptoms. Comfortable swimming at 25.5 degrees C was 87% (1.28 1/min-1) and at 18 degrees C 89% (1.30 1/min-1) of sitting peak VO2, while heart rates were 92% and 91% respectively. The mean peak VO2 and heart rate did not differ significantly between bicycle and swim tests (peak VO2 sitting 1.49 +/- 0.23, supine 1.42 +/- 0.24, 25.5 degrees C 1.60 +/- 0.17, 18 degrees C 1.52 +/- 0.19 1/min-1). Only two patients reported angina while swimming in warm water and one in cold water, although ST depression occurred in six in both swims. The subjective comfort and large muscle groups involved make swimming a good exercise, but the high relative energy cost and failure to identify ischemic symptoms indicate caution in cardiac patients, especially if their swimming skills are poor.
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PMID:The effect of swimming on patients with ischemic heart disease. 747 81


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