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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of some blood hormones was determined by radioimmune analysis in 58 patients with chronic ischemic heart disease (CIHD), 60 patients with myocardial infarction (MI) and in 24 practically healthy individuals. Increased activity of pituitary hormones (ACTH and TTH) with simultaneous increase in the blood STH content in the absence of essential changes in the FSH and LH content was established. These shifts in the production of pituitary hormones are evidently due both to disorders in the hypothalamo-hypophyseal area and to changes in the activity of systems coordinated to the pituitary gland in patients with CIHD. In patients with MI the activity of these hormones in blood does not differ from that in the control group. In patients with CIHD, the activity of the thyroid is diminished due to a decrease in its thyroxin-producing ability against the background of high activity of the pituitary thyreotropic function. The discussed shifts in the activity of some hormones in CIND and MI are conducive to the advancement of atherosclerosis and changes in myocardial metabolism.
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PMID:[Blood hormones in chronic ischemic heart disease and acute myocardial infarct]. 51 79

In 30 patients with stage I and III coronary atherosclerosis the interrelationship between K and Na content in blood and erythrocytes, daily urine excretion of aldosterone and blood level of cholesterol was studied. It was established that in patients with chronic ischaemic heart disease the electrolyte balance disorders manifested themselves on the early stages of the disease in increased plasma Na concentrations. The hypernatremia in such cases was traced against the background of an elevated mineral-corticoid activity of the adrenal glands during exacerbations of coronary insufficiency. A positive correlation was revealed between the blood levels of Na and cholesterol.
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PMID:[Disorders of electrolyte balance in patients with coronary atherosclerosis]. 114 20

The concentrations of individual phospholipids and of cholesterol have been determined in plasma samples taken from 77 apparently healthy individuals, and from 76 male patients presenting with atherosclerotic diseases. Significant differences in the relative and absolute concentrations of lysolecithin were found between different populations. In healthy individuals the plasma levels of lysolecithin were lower in women than in men and lower in the younger age groups studied. The relative and absolute concentrations of plasma lysolecithin were lower in men suffering from chronic ischaemic heart disease and peripheral arterial disease when compared with age-matched healthy male subjects. The lowest levels of plasma lysolecthin were, however, associated with patients suffering from acute myocardial infarction or acute myocardial ischaemia studied within 48 hr of the onset of chest pain. In a further study, significantly decreased relative concentrations of lysolecithin were found in blood platelets and erythrocytes as well as in plasma of patients suffering from chronic ischaemic heart disease. The results are discussed in terms of a possible thrombo-protective role for plasma lysolecithin in man.
Atherosclerosis
PMID:Plasma concentrations of lysolecithin and other phospholipids in the healthy population and in men suffering from atherosclerotic diseases. 115 68

Nitroglycerin and the long-acting nitrates are widely used in all of the anginal syndromes and have proven effectiveness in relieving or preventing myocardial ischemia. Recent developments into nitrate mechanisms of action provide new insights as to the many anti-ischemic effects of these agents. Important concepts relating to coronary arterial endothelial function are germane to nitrate therapy. Endothelial-derived relaxing factor (EDRF) is presently believed to be nitric oxide (NO), which exerts vasodilatory and/or antiplatelet actions by increasing intracellular cyclic guanosine monophosphate as a result of activation of the enzyme guanylate cyclase. In the setting of coronary atherosclerosis, or even hyperlipidemia without histologic vascular disease, endothelial dysfunction may be present, promoting a vasoconstrictor/proplatelet aggregatory milieu. Nitroglycerin and the organic nitrates are NO donors; NO is the final product of nitrate metabolism, and in the vascular smooth muscle NO induces relaxation, resulting in vasodilation of arteries and veins. In the presence of inadequate EDRF production and/or release, it appears that nitroglycerin may partially replenish EDRF-like activity. Nitrates have long been known to have major peripheral circulatory actions resulting in a marked decrease in cardiac work. Venodilation and arterial relaxation result in a decrease in intracardiac chamber size and pressures, with a resultant decrease in myocardial oxygen consumption. In addition, a variety of direct coronary circulatory actions of the nitrates have been documented. These include not only epicardial coronary artery dilation, but the prevention of coronary vasoconstriction, enhanced collateral flow, and coronary stenosis enlargement. Recent work suggests that the nitrates may also act by preventing distal coronary artery or collateral vasoconstriction, which can reduce blood flow downstream from a total coronary obstruction. Thus, there are many anti-ischemic mechanisms of action by which nitroglycerin and the organic nitrates may be beneficial in both acute and chronic ischemic heart disease syndromes. The unique salutory effects of the nitrates in subjects with left ventricular dysfunction or congestive heart failure make these drugs particularly attractive for patients with abnormal systolic function and intermittent myocardial ischemia. Finally, the emergent role of intravenous nitroglycerin in acute myocardial infarction offers new prospects that nitrate therapy may prove to be beneficial in acute myocardial infarction as well as postmyocardial infarction for the reduction of left ventricular remodeling.
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PMID:Mechanisms of action of the organic nitrates in the treatment of myocardial ischemia. 152 24

Laboratory studies have shown that saturated fats in the diet increase vulnerability to ventricular fibrillation and other cardiac arrhythmias while polyunsaturates, especially the n-3 fatty acids of fish oils, are antiarrhythmic. Similarly, dietary saturated fat has been implicated in the development of coronary atherosclerosis while polyunsaturated fatty acids are reported to provide protection. In the present study, dietary fat supplements known to influence arrhythmic vulnerability after long term feeding in the rat were tested for their propensity to induce or prevent changes in the aorta or coronary vasculature. It was found that dietary supplementation for 15 months with saturated fat (from sheep fat) or n-6 (sunflower seed oil) or n-3 (fish oil) polyunsaturated fatty acids made no difference to the development of vascular changes in coronary arteries or aorta of the rat despite some significant differences in plasma triglyceride and cholesterol levels. The vascular lesions observed were minimal even in non-supplemented age-matched reference animals. They consisted of focal intimal thickening and slight mucopolysaccharide accumulation with no evidence of progression to fibrotic lesions or calcium accumulation and there were no fatty deposits observed. It is concluded that significant atherosclerosis-induced chronic myocardial ischaemia in no way contributes to dietary lipid modulation of arrhythmic vulnerability in the rat.
Atherosclerosis 1990 May
PMID:Absence of coronary or aortic atherosclerosis in rats having dietary lipid modified vulnerability to cardiac arrhythmias. 169 27

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. A positive correlation was also found between leukocyte count and severity of coronary artery disease. Rabbit derived antiserum dependent-reduction of circulating PMNs in the dog or using monoclonal antibody anti-CD11b/CD18 of PMNs resulted in smaller myocardial infarcts. Granulocytes can release a variety of mediators tissue injury and synergize with these different mediators and other cells resulting in amplification of neutrophil stimulation and rising to additional products with enhanced endothelial injury. This paper reviews "in vivo" studies that have been instrumental in demonstrating this role of granulocytes as a mediator of myocardial ischemia. Experience in humans shows the modification of PMNs function in angina and during myocardial ischemia, and data from our group demonstrated that their aggregability is increased in the coronary sinus of patients with angiographically documented coronary disease. Upon re-perfusion PMNs accumulate and produce an inflammatory response resulting in endothelial injury. Free radicals formed during ischemia or re-perfusion produce deleterious effects on cell membranes, endothelial cell and myocardium. On the other hand the PMNs activation occurring during coronary angioplasty (PTCA) by the release of proteolytic enzymes and the generation of oxygen-free radicals, may aggravate the endothelial damage induced by PTCA and further stimulate platelets having potential implications in subsequent development of restenosis. An other aspect of PMNs function is related to leukotriene C4 release; the vasoconstrictor effect of this leukotriene on coronary arteries is synergistic with that induced by platelet-released thromboxane A2, as well as the decrease in coronary flow produced by the combination of both substances is greater than the sum of changes caused by the two eicosanoids separately administered. The potential role of leukocytes, oxygen radicals, leukotrienes and granulocyte enzymes in pathophysiology of myocardial injury due to a regional ischemia and reperfusion is an area of intense investigation. Experimental and clinical studies to elucidate these events should not only provide insights into acute and chronic pathologic tissue damage, but may also lead to the identification of important new targets of pharmacologic intervention.
Atherosclerosis 1991 Nov
PMID:Role of granulocytes in endothelial injury in coronary heart disease in humans. 181 45

Morphogenesis of the chronic disturbance of lymph effluence from the heart was studied in the course of experimental alimentary atherosclerosis and in combination of atherosclerotic dyslipoproteinemia with recurrent coronary failure. Stereoangioscopic analysis, semithin sections and electron microscopy of different areas of the heart lymphatic network injected with fine corpuscular substances were used. Type and dynamics of the development of main pathologic and adaptive changes in the heart lymphatic bed are established. Systemically repeating coronary crises aggravate the pathologic restructuring of the lymphatic bed limiting the efficiency of the compensatory adaptive processes. The results indicate that the chronic lymphostasis and lymphogenic cardiosclerosis stimulated by atherogenic dyslipoproteinemia and coronary failure represent an essential factor in the progression of a chronic ischemic heart disease.
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PMID:[The morphogenesis of chronic failure of the lymph outflow from the heart in dyslipoproteinemia and recurrent myocardial ischemia]. 239 12

The effect of hypertension, hyperlipidemia, and the combination of both on acute and chronic myocardial ischemia were evaluated in a total of 30 male rabbits. After preliminary hypertension and/or hyperlipidemic load by loading of the abdominal aorta and/or cholesterol feeding, acute ischemia was produced by clipping of the left coronary artery. The banding produced elevation of carotid arterial pressure and left ventricular hypertrophy. Cholesterol feeding resulted in severe atheromatous changes in all sizes of coronary arteries. The intimal thickening was due to foam cell accumulation in all arteries examined. Animals pretreated with the combination of hypertension and hyperlipidemia displayed the most severe cardiolmegaly with advanced coronary atherosclerosis and chronic ischemic lesions of the myocardium, i.e., perivascular patchy fibrosis in the subendocardial area. Furthermore, electron microscopic detection of ultrastructural myocardial damage, involving glycogen depletion, sarcoplasmic edema, mitochondrial swelling, and contractile abnormalities, was also most frequent in this group. These changes were quantitated using the ischemic score. These results confirm the hypothesis that fatal ischemic injuries may occur clinically in human hearts with coronary insufficiency due to coexistence of hypertensive cardiomegaly and severe coronary atherosclerosis. They offer a model for further study of these combined effects.
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PMID:An ultrastructural study on ischemic lesions in rabbits' hearts with pressure overload and hyperlipidemia. 315 60

The contractile apparatus of cardiomyocytes was examined at the ultrastructural level in 20 heart biopsy specimens obtained during operations for aortocoronary bypass in patients with chronic ischemic heart disease (IHD). Myofilaments were found to have sustained compensatory-adaptive and destructive changes as well as changes indicative of impaired intracellular regenerations under conditions of chronic hypoxia and energy deficiency experienced by the muscle cells, with the result that myocardial contractility was substantially reduced. Together, these processes led to progressive restructuring of both the contractile apparatus of the cardiomyocytes and the cytoarchitectonics in general. This combined with signs of increasing hyperfunction of the contractile myocardium, which made the energy deficit worse and thus interfered with plastic processes in, and diminished the structural and functional capabilities of, the myocardium. On the other hand, distinct changes were noted in the cardiomyocytes that reflected their adaptation to the adverse conditions created by progressing coronary atherosclerosis. It is concluded that therapy for patients with chronic IHD should include measures aimed at promoting such adaptive changes.
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PMID:[Characteristics of the restructuring of the cardiomyocyte contractile apparatus in chronic ischemic heart disease]. 366 47

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of coronary artery spasm in ischemic heart disease. Therapeutic implications. 633 45


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