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

Since the seventies, and in particular the eighties of this century, findings on pathogenetic mechanisms of ischaemic heart disease are expanding markedly and are becoming more accurate. This makes it possible to know and understand better factors which influence the genesis and development of myocardial ischaemia including the most serious clinical forms (unstable angina pectoris, acute myocardial infarction and sudden cardiac death). Diminution of the cardiac flow and/or increased oxygen demands of the heart muscle are not the only determinants of myocardial ischaemia which is influenced markedly also by neurohumoral, metabolic, prothrombotic (proaggregation and procoagulation) factors as well as antithrombotic and haemodynamic factors. Acute coronary syndromes have as a rule, in particular in patients with out severe atherosclerotic stenosis of the coronary arteries, a common pathophysiological mechanism of fissuration of the atherosclerotic plaque followed by different grades of dynamic coronary occlusion depending on vasoconstriction--spasm of the coronary arteries and thrombus formation. The coronary arteries, usually affected with atherosclerosis, may be due to the comprehensive action of various factors temporarily, intermittently or permanently occluded. In case of the development of acute coronary syndromes thrombosis plays a key role. Better knowledge of pathogenetic mechanism of IHD markedly changes views on treatment and management of patients with IHD in particular patients with acute coronary syndromes. The authors emphasize strategies focused (also preventively) on preventing progression of the disease with the aim to improve survival and the short-term and long-term prognosis.
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PMID:[Pathogenesis of myocardial ischemia and acute coronary syndromes]. 129 43

Data obtained from a cross-sectional population study of men aged 20-54 years and results of a morphological epidemiological examination of the aorta and coronary arteries of 507 men aged 20-59 years, deceased from various causes in the city of Tallinn, were analysed to find whether there is a relationship between the prevalence of ischaemic heart disease (IHD), its risk factors and morphological features of atherosclerosis. An association has been found between the development of clinical IHD manifestations with age, extent of morphological signs of atherosclerosis in the abdominal aorta and coronary arteries, and occurrence of hypercholesterolaemia. Estonian men showed more marked changes in lipid indicators and greater extent of morphological signs of atherosclerosis than men of other nationalities; this corresponds to the more atherogenic character of the former's diet. However, Estonian men did not differ from other nationalities in the occurrence of IHD and expected death risk--a finding the authors explain by the lower percentage of smokers among Estonians.
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PMID:Ischaemic heart disease in men of productive age: comparison of epidemiological and morphological data. 130 16

Forty-five hospitalized elderly patients with coronary heart disease who died suddenly within 6 hours after the onset of symptoms were analyzed clinically and pathologically and summarized as following. (1) All the cases showed abnormal ST segments or T waves on ECG. (2) Various degrees of cardiac dysfunction were found clinically in all the patients. (3) Pathological examination of 31 cases revealed serious coronary atherosclerosis. New myocardial necrosis and/or multiple myocardial scars existed in about two-thirds of the patients. Based on these findings and characteristics, it is speculated that sudden coronary death in the elderly patients is caused by imbalance between oxygen supply and demand in the myocardium or deterioration of the cardiac function, which may result in fatal ventricular arrhythmia. Therefore, the prevention of sudden coronary death in the elderly patients should be focusing on reduction of myocardial ischemia, improvement of myocardial metabolism and protection of cardiac function.
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PMID:[Clinical and pathological analysis of sudden coronary death in hospitalized elderly patients]. 130 72

Elevated levels of lipoprotein(a) [Lp(a)] have been associated with an increased risk of ischemic heart disease (IHD), and higher levels of Lp(a) are associated with lesions of significantly greater severity. We have examined Lp(a), total cholesterol (TC) and high density lipoprotein-cholesterol (HDL-C) levels in patients with IHD including those with normal coronary arteries with vasospastic angina. The study population consisted of 206 patients (166 males and 40 females) who underwent diagnostic coronary angiography for known IHD. Twenty-eight patients had effort angina, 36 rest angina, 8 unstable angina and 134 old myocardial infarction. IHD patients were categorized as zero vessel disease (0VD), single vessel disease (SVD) and multi-vessel disease (MVD). To investigate the relationship between atherosclerosis and IHD, these patients were further divided into 3 groups based on angiographic findings. Eighteen patients had entirely normal coronary arteries (normal group), 24 discretely diseased coronary arteries (discrete group) and 80 diffusely diseased coronaries (diffuse group). The results were compared with those obtained from 50 healthy individuals. Lp(a) levels for IHD patients (12.4 mg/dl) were significantly higher than those of controls (7.1 mg/dl, p < 0.05). However, there were no statistical differences between 0VD (13.1 mg/dl) and MVD (12.8 mg/dl). Similarly, no statistical differences of Lp(a) values were found among the normal group (13.3 mg/dl), discrete group (12.0 mg/dl) and diffuse group (12.9 mg/dl). Mean levels of HDL-C in 0VD (51.3 +/- 13.5 mg/dl) were significantly higher than those of SVD (42.9 +/- 11.5 mg/dl, p < 0.05). However, no significant differences were observed between controls (59.5 +/- 15.3 mg/dl) and 0VD (51.3 +/- 13.5 mg/dl).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Importance of lipoprotein(a) in patients with ischemic heart disease]. 133 90

Recent epidemiologic studies found that there is a strong association of hemostatic factors with ischemic heart disease. The Atherosclerosis Risk in Communities (ARIC) Intraindividual Variability (IIV) Study was conducted to estimate the various components of variation in hemostasis factors measured in the ARIC Study and to estimate the measures of repeatability of these factors. A total of 39 subjects (16 men, 23 women) were studied. Each had blood collected three times, with a 1- to 2-week interval between each visit. The contributions of between-person variability, within-person (biologic) variability, and processing and assay variability were estimated. Then the reliability coefficient R was estimated as the proportion of total variance accounted for by between-person variance. The reliability coefficient can be interpreted as the correlation between measures made at repeat visits. Among the various analytes, the reliability coefficients were quite high for activated partial thromboplastin time and plasma factor VIII (R = 0.92, 0.86, respectively). Low repeatability was obtained for antithrombin III activity and protein C (R = 0.42, 0.56, respectively). The lack of repeatability for these variables derives mostly from the processing (field center and laboratory) variation. Other analytes--fibrinogen, plasma factor VII, and von Willebrand factor--were intermediate in repeatability. In comparing the analyte-specific high-level to low-level groups, no substantial difference of within-person plus method coefficient of variation between the two groups was found for any analyte except for factor VIII, whereas the corresponding variance components for most analytes were higher for the higher analyte level. Reliability coefficients from this ARIC IIV study are generally higher than those found in other studies, and this is related to the relative variations in populations studied and to the time between measurements.
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PMID:Short-term intraindividual variability in hemostasis factors. The ARIC Study. Atherosclerosis Risk in Communities Intraindividual Variability Study. 134 24

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

Calcium is a ubiquitous cation involved in a wide variety of physiological processes. Normally, cytosolic calcium is maintained within narrow limits but under certain conditions the levels rise--either because of excess calcium entry, internal release, or failure of the extrusion mechanisms. Such conditions include hypertension and myocardial ischemia. Calcium ions are also involved in the formation of atherosclerotic lesions. Hypertension, ischemic heart disease, and atherosclerosis are all amenable to calcium antagonist therapy. The efficacy of this class of drugs in the management of such a wide spectrum of disorders is in accord with the central role played by calcium in the etiology of these disorders. To some extent, however, the disorders are interrelated, with hypertension being a major risk factors for ischemic heart disease and atherosclerosis.
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PMID:Calcium, calcium antagonism, atherosclerosis, and ischemia. 137 99

Calcium antagonists are useful for the management of patients with ischaemic heart disease, particularly when used prophylactically. At the cellular level, these drugs act primarily by limiting calcium ion (Ca++) entry through the voltage-sensitive Ca(++)-selective channels, an effect that contributes markedly to their 'energy sparing' properties. However, the long term use of these drugs has additional advantages, particularly with respect to their ability to slow Ca(++)-dependent processes involved in the formation of atherogenic lesions, partially antagonise the effects of the raised levels of circulating endothelin-1 encountered during ischaemia-induced heart failure and hypertension, and trap and immobilise oxyradicals. Prolonged episodes of ischaemia result in an irreversible loss of homeostasis with respect to Ca++. However, the increase in myocardial cytosolic Ca++ caused by relatively short periods of ischaemia is small, reversible, and markedly attenuated by the prophylactic use of calcium antagonists. In the isolated, perfused rat heart, verapamil pretreatment produces statistically significant inhibition of the increase in cytosolic Ca++ during 20-minute global ischaemia. This stereospecific effect is associated with a decrease in the rise in total tissue Ca++ during reperfusion and amelioration of the adenosine triphosphate depletion caused by ischaemia. In general, discussion relating to the molecular basis of the use of calcium antagonists in the management of patients with ischaemic heart disease needs to take into account the duration of the ischaemic event, the workload on the myocardium, the need for prophylactic therapy, and the presence of exacerbating factors such as atherosclerosis and tobacco smoking. The early rise in cytosolic Ca++, the source of which remains uncertain, appears to be an important focus for anti-ischaemic drug therapy.
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PMID:The molecular basis for the use of calcium antagonists in ischaemic heart disease. 137 84

The authors investigated selected indicators of the lipid metabolism in 31 children with insulin-dependent diabetes for a period of 3 to 14 years. They divided the patients into two groups those with a glycosylated haemoglobin below or above 9 mumol/1 g haemoglobin. They compared the assembled results of the two groups and also with the results obtained in a control group. The total cholesterol was in both diabetic groups higher than in healthy subjects and was higher than the value which is considered from the aspect of the genesis and development of atherosclerosis as a risk value. Children with poorly compensated diabetes, i. e. with a glycosylated Hb level above 9 mumol had a higher cholesterol level as compared with well compensated diabetic children. The pre-beta fraction of lipoprotein increased in both groups of patients, however, more in those where the disease was not well compensated. There was a parallel decrease of the alpha fraction and the lipoprotein profile had a markedly atherogenic character. The apolipoprotein B concentration was in patients with well compensated diabetes lower, as compared with controls but in patients with poorly compensated diabetes after 4-5 years treatment is was significantly higher. Poor compensation of diabetes led after 4-5 years duration to a significant rise of the serum triglyceride level. As the blood lipid levels are influenced in a significantly way by diet, compensation of the disease and a low-fat diet are essential with regard to the results assembled in this investigation for prevention of ischaemic heart disease in diabetic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Variations in lipid metabolism in long-term monitoring of children treated for diabetes mellitus]. 139 53

Anomalous origin of the left or right coronary artery from the contralateral sinus of Valsalva with coursing between the aorta and the pulmonary trunk way cause angina, myocardial infarction or sudden death. This anomaly should be suspected especially when ischemic symptoms occur in young patients without risk factor for atherosclerosis. We believe that surgical operation after demonstration of myocardial ischemia is indicated to prevent severe myocardial ischemia or sudden death.
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PMID:[Birth anomalies of coronary arteries. Responsibility in myocardial ischemia]. 140 67


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