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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis and insufficiency of the coronary arteries and their sequelae are summarized in the term "coronary heart disease". For the evaluation of the coronary arteries the knowledge of malformations, variants and supply areas is of importance. Extension and severity of atherosclerosis of the coronary arteries and their insufficiency is being influenced by hyperlipidemia, hypertension and diabetes mellitus. The process of atherosclerosis as a cause of the proliferation of vascular smooth muscle cells in complicated by ulceration, parietal and obliterative thrombosis as well by intramural hemorrhages. Relative ischemia leeds to disseminated cell necrosis; total ischemia causes large myocardial tissue necrosis, called infarction. Localization and extension of infarction and the later scars correspond to the caliber of the obliterated coronary artery and to the significance of the collaterals. Postmortem coronary angiography can detect cause and extension of the damaged cardiac area. Functional significance of chronic coronary heart disease is related to the "critical connective tissue content" of the heart. After surgical treatment qualitative and quantitative morphology may help to explain postoperative cardiac failure.
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PMID:[Morphology of coronary heart disease (author's transl)]. 126 48

Coronary heart disease is the most frequent cause of death in Western, industrialized countries. Coronary risk factors are prevalent in such countries and sometimes combine to constitute the so-called syndrome X--hypertension, central obesity, serum lipid and clotting disturbances, and insulin resistance. beta-Blockers, unlike calcium antagonists, have proved highly effective in secondary prevention of myocardial infarction. If present at the time of the myocardial infarction, beta-blockers (unlike calcium antagonists and diuretics) probably decrease mortality 1 month later. Early intervention (within 12 h) of chest pain with intravenous beta-blockers results in a 15% reduction in cardiovascular mortality at 1 week. Later intervention (3-28 days) with oral non-ISA beta-blockers results in a 30% reduction in mortality after 1 year; ISA-containing beta-blockers are probably less effective (less decrease in heart rate). Hydrophilicity/lipophilicity of beta-blockers is unimportant in terms of decreased mortality. Primary prevention of myocardial infarction, unlike stroke, in hypertensive patients has been disappointing, possibly due to treatment-induced biochemical/lipid changes or inappropriate lowering of diastolic blood pressure in high-risk subjects (J-curve effect). beta-Blockers should be first-line therapy for hypertensive patients up to the age of 65 years, particularly men (and nonsmokers) as Q-wave myocardial infarction is significantly decreased by beta-blockers and significantly increased by diuretics. However, in elderly hypertensive subjects, beta-blockers have not significantly decreased myocardial infarction (unlike stroke), whereas diuretics have. The effects of beta-blockers and diuretics on heart size (and thus coronary flow reserve) in the elderly may be important. Thus, beta-blockers should be second-line therapy for the elderly hypertensive individual but first-line if overt ischemia (e.g., angina or recent myocardial infarction) also is present. In patients with angina but normal blood pressure, beta-blockers tend to decrease and calcium antagonists increase cardiovascular events. Thus, beta-blockers are highly effective agents in the secondary prevention of myocardial infarction and are moderately effective in primary prevention of myocardial infarction in hypertensive patients (particularly men) under the age of 65 years.
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PMID:Beta-blockers: primary and secondary prevention. 128 45

Diabetes mellitus (DM)-linked metabolic alterations and hypertension concomitantly accelerate or precipitate cerebrovascular and coronary heart disease, nephropathy, retinopathy and widespread macroangiopathy, thereby conferring to diabetic patients a very high risk of morbidity, disability and early death. Therefore, the long-term care for diabetic patients should be aimed at concomitant metabolic and blood pressure (BP) control. Dietary measures are indispensable; a high fibre, low fat, low salt diet is recommended, complemented with caloric restriction and physical exercise when body weight is above the ideal. Antidiabetic pharmacotherapy involves an unresolved dilemma. The desired achievement of euglycemia necessitates effective levels of insulin, but hyperinsulinemia (due to parenteral [over]treatment in insulin-dependent DM) is suspected to promote atherogenesis and represents a coronary risk factor and perhaps even facilitates hypertension. Considering antihypertensive pharmacotherapy, thiazide-type or loop diuretics are problematic drugs in DM because they can aggravate metabolic alterations. These agents also seem to exert only a limited preventive or regressive effect on left ventricular hypertrophy (LVH); beta-blockers are also not considered ideal, since they decrease the awareness of hypoglycemia and tend to promote glucose intolerance. Unselective beta-blockers in particular promote peripheral ischemia and insulin-induced hypoglycemia, while beta-blockers without intrinsic sympathomimetic activity lower serum HDL-cholesterol. Calcium antagonists and ACE inhibitors have equivalent antihypertensive efficacy, do not impair carbohydrate and lipid homeostasis or peripheral perfusion and can effectively improve LVH. Certain ACE inhibitors may even slightly ameliorate abnormal insulin sensitivity and plasma glucose levels. While alpha-blockers share most of these desirable properties, these agents are more prone to precipitate orthostatic hypotension in the diabetic patient. The non-thiazide diuretic indapamide and the serotonin2-antagonist ketanserin also combine antihypertensive efficacy with metabolic neutrality. The ultimate goal of therapy is to improve life prognosis. In essential hypertension, conventional drug treatment based on diuretics in high dosage satisfactorily reduced cerebrovascular but not coronary complications or sudden death. In diabetic patients, the influence of antihypertensive therapy on prognosis has not been assessed prospectively. Based on retrospective analyses, Warram et al reported a 3.8 times higher mortality in diabetics treated with diuretics alone, than in diabetics with untreated hypertension (Arch Intern Med. 1991;151:1350). H. H. Parving calculated that effective BP control in patients with diabetic nephropathy might reduce 10 year-mortality from about 65 to 20 percent (J Hypertension. 1990; 8[Suppl 7]:187).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antihypertensive therapy in diabetic patients. 128 10

The myocardial ischemic threshold (heart rate at the onset of ischemia) was assessed in 92 patients with coronary heart disease. The highest myocardial ischemic threshold (HMIT) ranged from 83 to 163 (122 +/- 18) beats/min usually happened during activities at the daytime. The lowest myocardial ischemic threshold (LMIT) ranged from 45 to 115 (82 +/- 17) beats/min usually happened when awaken early morning or asleep at night. The differences were statistically significant (P < 0.01). The mean variability of myocardial ischemic threshold (VMIT) was 30.22% (range from 8.2 to 51.2%). The variability was correlated positively with the number of ischemic episodes, negatively with LMIT, and larger in senior-aged group than in middle-aged group (P < 0.001). The authors suggest that LMIT and VMIT may be related to the severity of coronary lesions, coronary tonus, and the patients' prognosis, etc.
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PMID:[The clinical relevant factors of the myocardial ischemic threshold]. 130 74

Sudden death accounts for about 15-20% of all natural fatalities in the industrially developed world. Most of the victims have a substrate of extensive myocardial injury caused by coronary heart disease, cardiomyopathy and hypertensive heart disease. In most cases, the immediate cause of death is triggered by ventricular tachycardia which degenerates into ventricular fibrillation. Changes in myocardial electrical properties may be critically modified by ischemia, imbalance in the autonomic nervous system, electrolytic disorders, and haemodynamic factors. We review the causes of sudden cardiac death, giving special attention to the effect of beta-adrenoceptor blockade as a preventive measure.
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PMID:[Sudden cardiac death. Significance of beta blockaders]. 135 74

The relationship between coronary heart disease, postischemic work recovery and tissue ATP levels as well as mitochondrial respiration rates were studied. Respiration of mitochondria was assessed without their isolation by using a novel method applying skinned fibers in physiological saline. The maximal mitochondrial respiration rates were unchanged during 35 min of normothermic ischemia in St. Thomas Hospital cardioplegic solution in the subsequent 30 min aerobic reperfusion period. A reversible increase in the basal respiration and a decrease in creatine-stimulated oxygen uptake were observed. Thus, the combined determination of mitochondrial respiration in situ in skinned cardiac fibers and tissue ATP may be a useful approach to studies of the pathogenesis of cardiac diseases.
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PMID:[Quantitative relationship between ischemic heart disease and parameters of energy metabolism]. 138 53

Lipid peroxidation initiated by oxygen free radicals played an important role in the pathogenesis of coronary heart disease. The purpose of this study was to explore the effects of Tian-Ma (Gastrodia elata Bl.) injection on myocardial infarct size and lipid peroxidation by observing serum malondialdehyde (MDA) levels. Twenty-six New Zealand rabbits were divided into control group (n = 6), ischemic group (n = 10), and Tian-Ma treated group (n = 10). Left ventricular branch (LVB) of coronary artery was ligated at its middle third in ischemic and treated groups. LVB was not ligated in control group. Tian-Ma injection was given intravenously (1 mg/kg) every 8 hours after ligation in treated group for 48 hours. Precordial 12-lead ECG mapping was recorded before operation and at 3, 24 and 48 hours after occlusion. Hemodynamic changes (HR, LVP) were monitored before and 0.5, 3 and 48 hours after ligation. Serum MDA levels were determined by thiobarbituric acid spectrophotometry before operation, and 0.5, 3, 9, 24, and 48 hours after ligation. Dual staining technique was used 48 hours after ligation to determine the area at risk and infarct size. The results showed that Tian-Ma injection did not decrease sigma ST elevation (P greater than 0.05), but NQ was significantly lower during ischemia in treated group (P less than 0.01), Tian-Ma injection reduced the area at risk by 23.5% (P less than 0.05) and infarct size by 34.5% (P less than 0.01). Tian-Ma injection significantly decreased the levels of serum MDA 24 and 48 hours after occlusion (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of tian-ma injection on myocardial ischemia and lipid peroxidation in rabbits]. 139 26

Left ventricular blood filling was performed in 72 patients by using pulsed Doppler echocardiography at rest and in postpacing ischemia. In 10 patients, non-invasive examination findings were compared with the values of a left ventricular pressure curve which had been obtained in frequent atrial pacing. No changes in transmitral blood flow were found in patients without coronary heart disease, whereas 2 types of abnormal transmitral blood flow were detected in those with coronary heart disease in the postpacing period. The patients with Type I abnormal transmitral blood flow exhibited prolonged isovolumetric relaxation and slightly elevated left ventricular end-diastolic pressure in the postpacing period when catheterization was conducted. Those with Type I ("pseudonormal") transmitral blood flow displayed more prolonged relaxation and significantly (greater than 20 mm Hg) elevated end-diastolic pressure. The pattern of changes in transmitral blood flow was not pathognomonic to any definite myocardial abnormality, but reflected the hemodynamics.
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PMID:[Study of left ventricular blood filling during post-pacing ischemia: comparison of Doppler echocardiography and heart catheterization]. 140 28

Since the mid eighties of our century the clinical importance of silent myocardial ischemia, concerning definition, prevalence and pathophysiology is well established. The implication of silent myocardial ischemia, or its combination with other parameters of coronary heart disease on the outcome of ischemic heart disease concerning the endpoints myocardial infarction, myocardial insufficiency or death is still not clear. In consequence therapeutic guidelines at the moment can not be given for the entire spectrum of silent ischemia, whereas some details are becoming more and more evident.
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PMID:[Is it necessary to treat silent myocardial ischemia?]. 141 65

In untreated essential hypertension cardiovascular structural changes will develop after some time. In arteries and arterioles, thickening and reduced compliance of the vascular wall is noted and in the left ventricle, myocardial hypertrophy. Both types of changes will enhance the risk of ischemia and of developing cardiac complications, i.e. coronary heart disease, myocardial infarction and heart failure. Methods for measurement of vascular and cardiac hypertrophy are reviewed and the value of echo-cardiographic evaluation of the hypertensive patient is stressed.
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PMID:[Cardiovascular changes in arterial hypertension]. 146 23


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