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

Patients with coronary atherosclerosis present with angina, myocardial infarction and sudden death, most often caused by atherosclerotic stenosis complicated by spasm and/or occlusive thrombosis. All of these events have been shown to exhibit similar diurnal rhythms, with a peak incidence in the morning after waking and rising. Other cardiovascular parameters also show a similar diurnal rhythm associated with increased sympathetic outflow and circulating catecholamines, producing increases in heart rate, blood pressure, myocardial contractility and oxygen demand soon after waking and rising. Experimental and clinical research has recently pointed to several possible mechanisms that might be responsible for these events. In patients with atherosclerosis, dysfunction of the endothelium in the epicardial coronary arteries results in a failure to limit the constrictor response to catecholamines. Catecholamines can also alter the procoagulant nature of vascular surfaces. We speculate that the interaction between increased sympathetic activity and the procoagulant and vasoconstrictor states of atherosclerotic coronary stenoses may lead to a lower threshold to ischaemia in the waking hours, with a corresponding increase in angina, myocardial infarction and sudden death. These factors may be important considerations for the selection of suitable therapies and for future research.
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PMID:Diurnal rhythms and clinical events in coronary artery disease. 180 40

Most ischemic heart disease in associated with severe coronary atherosclerosis. A small subset of patients, however, had angina pectoris despite angiographically normal coronary arteries and absence of inducible coronary spasm. Coronary microcirculation (i.e. arteries too small to be visualized by current angiographic techniques) has been identified as the weak point of these patients. Small coronary vessel involvement may be due to organic conditions (such as diabetes, vasculitis, systemic collagen-vascular diseases, infectious processes) that act through coronary thrombosis or embolism and related alteration in coronary vasomotion; alternatively, the vascular abnormality appears to be entirely functional (no ultrastructural myocardial changes) such as the case of hypertension, hypertrophic cardiomyopathy and syndrome X. Whatever the cause(s) and mechanism(s) of the small coronary artery involvement, this leads to myocardial ischemia and to the related complications as in classic atherosclerotic heart disease. Syndrome X is characterized by effort-induced angina pectoris, ST-segment changes during exercise testing, negative ergonovine test and reduced coronary reserve. A pre-arteriolar hypersensitivity to vasoconstrictor influences (elicited by cold pressor test or ergonovine) and a reduced vasodilator capacity (unmasked by metabolic and pharmacological studies) have been proposed as potential pathogenetic substrate. This dynamic alteration in vasomotion would answer for both symptoms and signs of myocardial ischemia, that, however, appear to be contemporarily elicitable in a minority of patients. Treatment with beta-blockers and calcium-antagonists has been found to be effective. The long-term follow-up shows favorable outcome with a high survival rate and a low incidence of cardiovascular events.
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PMID:[Angina due to microvascular pathology]. 184 63

Acute myocardial infarction is a potentially fatal complication of SLE. Reported mechanisms include atherosclerosis, arteritis and coronary arterial spasm. The following case report presents a fourth possible cause; intracoronary thrombus with angiographically normal coronary arteries in a patient with active lupus and AMI.
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PMID:Myocardial infarction due to intracoronary thrombi without significant coronary artery disease in systemic lupus erythematosus. 186 45

Severe and often fatal cardiac complications have been reported in cocaine users with narrowed coronary arteries caused by atherosclerosis as well as in young adults with normal coronaries. We have found that in normal dogs cocaine induces severe temporary hypoperfusion of the left ventricle as indicated by a significantly lower 201Tl concentration compared to the baseline state. The most significant decrease in uptake occurred 5 min after injection and was more pronounced in the septal and apical segments. Following intravenous administration of cocaine, instead of gradual disappearance of 201Tl from the left ventricle, there was continuous increase in 201Tl concentration in the left ventricle. These imaging experiments indicate that the deleterious effects of cocaine on the heart are probably due to spasm of the coronaries and decreased myocardial perfusion. Since spasm of the large subpericardial vessels does not seem to explain the magnitude of the increased coronary resistance and decreased coronary flow after cocaine as described in the literature, it is suggested that microvascular spasm of smaller vessels plays a major role in the temporary decrease in perfusion. The data may also suggest that severe temporary myocardial ischemia is probably the initiating factor for the cardiac complications induced by cocaine.
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PMID:Imaging of cocaine-induced global and regional myocardial ischemia. 186 81

Pathogenesis of the so-called "heart attack" still remains to be elucidated. The links between stable effort angina and unstable or acute myocardial infarction, and between asymptomatic and spontaneous angina are all missing. In medicine presently, pathophysiology of ischemic heart disease is considered a consequence of i) the progression of atherosclerotic narrowing of the coronary artery, and ii) dynamic and transient obstruction (coronary spasm), but these mechanisms are traditionally believed to be unrelated. This article demonstrates various experimental evidence indicating that these two mechanisms are related. And, this review article describes how to produce experimental coronary spasm in the presence of atherosclerosis, similar to that seen in patients with variant angina, and that coronary spasm can produce sudden progression of coronary atherosclerotic obstruction due to intramural hemorrhage. Establishment of various animal models to elucidate mechanisms related to various stages of ischemic heart disease are needed.
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PMID:Experimental induction of spasm, sudden progression of organic stenosis and intramural hemorrhage in the epicardial coronary arteries. 195 7

It has been suggested that histamine is involved in the pathogenesis of coronary spasm but its exact role remains unclear. H1 receptor stimulation of the coronary artery was performed with a selective intracoronary infusion of histamine (2 micrograms/min) in 21 patients with variant angina after blockade of the H2 receptor with cimetidine (25 mg/kg) and its effect on the coronary artery diameter was examined. Intracoronary injection of acetylcholine was also performed in 19 of the 21 patients. Ergonovine (0.2 mg) was intravenously administered in one patient. The coronary artery diameter was measured with cinevideodensitometric analysis. A mean plasma histamine concentration in the coronary sinus increased from 4 x 10(-9) to 7 x 10(-8) M 5 min after histamine infusion into the left coronary artery (n = 18). Coronary spasm was induced in 6 patients (29%) with histamine, in 18 (95%) with acetylcholine and in 1 with ergonovine. The effect of histamine on the luminal diameter was analyzed at the site of spasm in the 26 coronary arteries in which spasm was induced by acetylcholine or ergonovine. Of the 20 coronary arteries with a normal arteriogram or a fixed stenosis less than or equal to 50% of luminal diameter, histamine decreased the diameter in 4, increased it in 14 (70%) and caused no change in 2; of the 6 coronary arteries with a fixed stenosis greater than or equal to 75%, histamine decreased the diameter in 5 and increased it in 1. In the coronary arteries in which spasm was not induced by either acetylcholine or ergonovine, histamine increased the diameter, especially in those without advanced atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of H1 receptor stimulation on coronary artery diameter in patients with variant angina: comparison with effect of acetylcholine. 167 98

Several new concepts are reviewed concerning structural and functional changes in atherosclerotic and hypertensive blood vessels. First, in regard to modulation of vascular changes, atherosclerosis appears to progress more slowly during hypotension than during normotension. This finding may have implications for the optimal level of blood pressure. Second, structural "remodeling" of the vessel wall occurs in both atherosclerosis and hypertension. Remodeling helps to preserve the arterial lumen despite intimal proliferation in atherosclerosis. In contrast, remodeling (which differs from vascular hypertrophy) reduces the vascular lumen in chronic hypertension. Third, functional changes impair active vasodilator responses in both atherosclerotic and hypertensive vessels, in part by endothelium-dependent mechanisms. Finally, we propose that leukocytes as well as platelets may be important cellular mediators of spasm in atherosclerotic arteries.
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PMID:Hemodynamic determinants of vascular changes in hypertension and atherosclerosis. 201 97

The endothelium releases a powerful vasodilating and anti-aggregant substance, the EDRF, both under basal conditions and after stimulation by a large number of hormones and endogenic factors. Endothelial lesions or dysfunction may play important roles in causing coronary spasm although other changes related to atherosclerosis must also be taken into consideration. One possible stimulus is aggregating platelets as they are an important source of vasoconstricting substances. The endothelium also secretes other vasoactive substances, EDHF and/or EDCF, the physiopathological role of which has not yet been established.
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PMID:[Relaxing factors of endothelial origin and coronary spasm]. 211 82

Within the last 2-3 decades neuropsychological factors have assumed a role of importance in atherogenesis implicating a contribution from the CNS to the development of arterial lesions. Despite extensive documentation in clinical studies, little work has been performed with experimental animals which could elucidate underlying mechanisms. Employing hypothalamic stimulation (HS) to model the role of the CNS, experiments in the author's laboratory have shown that atherosclerotic lesions develop in time. Evidence is presented that the underlying mechanism is due to vasospasm associated with proliferation of intimal arterial smooth muscle cells (ASMC). Both, the vasospastic and proliferative responses may originate with the same hypothalamic signal. The vasospastic response compromises perfusion, but by injuring the vessel produces pathology which increases the resistance of the artery to further spasm. The proliferation of ASMC which provides the elements for this 'stiffening' process also helps restore the vascular tone necessary to maintain the important function of perfusion. Atherosclerosis, therefore, may represent an adaptive response to excessive spasm which in many instances has advanced too far.
Atherosclerosis 1990 May
PMID:The central nervous system and atherogenesis: role of the arterial smooth muscle cell. 219 38

Male rats of the JCR:LA-corpulent strain spontaneously develop atherosclerosis and myocardial lesions if corpulent. The corpulent rats exhibit a marked very low density hyperlipidemia and insulin resistance. The incidence of both vascular and myocardial lesions correlates strongly with the hyperinsulinemia, but not with the hyperlipidemia. Corpulent male rats were chronically treated with nifedipine or acetylsalicylic acid to explore the roles of smooth muscle spasm and platelet activity in induction of the myocardial lesions. Acetylsalicylic acid treatment was associated with no significant changes in fasting glucose, insulin, or lipid concentrations. Nifedipine caused no significant changes in glucose concentration but was associated with mildly increased insulin levels. Treatment with nifedipine resulted in significant decreases in serum triglyceride concentrations. The decreases were confined to longer-chain triacylglycerol molecular species with no change in the concentration of molecular species with 48 or 50 acyl carbon atoms. There was no effect on myocardial lesion frequency with acetylsalicylic acid treatment. In contrast, nifedipine prevented the development of old organized scarred lesions. This effect is similar to that seen with treatments that markedly reduce the insulin resistance. These findings suggest that platelet-initiated thrombus formation is not an important factor in lesion formation in the JCR:LA-cp rat, but that smooth muscle spasm is probably important.
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PMID:Prevention of myocardial lesions in JCR:LA-corpulent rats by nifedipine. 219 41


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