Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Large-scale clinical trials of the use of aspirin in post-myocardial infarction patients were based on the assumption that inhibition of platelet activity would reduce thromboembolism associated with atherosclerosis, and that thromboembolism is a major cause of the clinical complications of atherosclerosis. However, spasm and occlusive thrombi may also contribute to this picture, and thus thromboembolism is probably only one of the mechanisms that cause the clinical complications. Aspirin inhibits thrombosis only if thromboxane A2 formation by platelets plays a major part in the growth of thrombi; aspirin has little effect on thrombosis when thrombin generation and fibrin formation are dominant factors. Nevertheless, analysis of the combined data from the six clinical trials indicates a highly significant (21 percent) reduction in reinfarction rate and a 16 percent reduction in cardiovascular mortality rate in patients treated with aspirin. Aspirin may be most useful in treating an as-yet-unidentified subgroup of patients.
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PMID:Aspirin in the treatment of cardiovascular disease: a review. 640 10

Effort angina is the result of acute myocardial ischemia on exercise due to an imbalance between myocardial oxygen demand and supply. During exercise, ischemia is provoked by an increase in myocardial oxygen needs (tachycardia, increased blood pressure, etc.) which cannot be met by increased coronary blood flow. The commonest cause of insufficient flow is coronary atherosclerosis. Coronary spasm does, however, play a role, whether it occurs during exercise on normal or atheromatous coronary vessels. Classical anti-anginal therapy is directed towards a reduction in the intense adrenergic activity associated with exercise, and to the limitation of myocardial oxygen consumption. Calcium inhibitors which cause peripheral vasodilation, decrease ventricular wall tension and coronary resistance, are usually reserved for unstable or resistant angina. We studied 10 patients with stable effort angina for over 2 years with significant (greater than 70 per cent) atheromatous lesions on coronary angiography unsuitable for surgical treatment. The patients underwent a randomised double blind trial to compare the effects of propranolol, diltiazem and placebo. Exercise ECG was performed after a treatment period of one week, 3 hours after drug administration. The results showed a significant improvement of work capacity with propranolol and diltiazem as compared to placebo. Propranolol (160 mg/day) was more effective than diltiazem (180 mg/day) in 6 patients. In 4 cases, the improvement with diltiazem and propranolol was the same. The association of the two drugs in one open study in 5 patients was even more effective in 3 patients. The small number of patients studied makes it impossible to draw any firm conclusions. Although calcium inhibitors are the treatment of choice in coronary spasm and betablockers in effort angina, diltiazem exerts an anti-anginal effect by reduction of myocardial oxygen consumption without depression of myocardial contractility, as other workers have shown.
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PMID:[Are calcium inhibitors useful in the treatment of effort angina pectoris]. 640 53

A series of 40 myocardial infarctions, occurring in patients under 36 years of age was studied retrospectively (Group I: mean age 31.3 years). The medium term results of coronary angiography in this group were compared with those of 60 myocardial infarctions after 50 years of age (Group II: mean age 56.6 years). Group I had a clear male predominance (92.5%), a high incidence of smoking (69%), hypercholesterolaemia (69%); myocardial infarction was the first manifestation of their disease in 54% and it was often extensive (42%). A comparative angiographic study between the two groups showed: 1) Less widespread lesions in Group I, as assessed by the number of main arteries stenosed (p less than 0.001), the coronary index (p less than 0.01) and the mean coronary score using Friesinger's method (p less than 0.01). 2) A higher incidence of subnormal coronary angiogrammes in Group I (absence of 50% stenosis) (15%) and of single vessel disease (40%): compared with Group II in which multivessel disease was observed in 86.5% of cases. 3) Collateral circulation was less common in Group I (p less than 0.01). On the other hand, a comparative study of regional and global left ventricular function showed no difference between the two groups. Two subgroups were distinguished in Group I: in one subgroup, multiple lesions similar to those found in Group II, suggestive of premature coronary atherosclerosis (52.5%); the other group (47.5%) presented unilocular lesions i.e. focal mono-arterial lesions compatible with other causes of infarction (thrombosis and/or spasm). These patients were younger (p less than 0.05) and had significantly fewer cardiovascular risk factors (p less than 0.01). Despite the fact that the coronary lesions were limited, the myocardial damage was comparable with the other groups as the collateral circulation was much less developed (p less than 0.02). These appearances were only observed in 3.5% of patients in Group II. The study of the angiographic outcomes of these two types of lesions should show a difference and could contribute to the understanding of their mechanisms.
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PMID:[Myocardial infarction in the young subject: a medium-term clinical and coronary angiographic study in 40 patients under 36 years of age. Comparison with coronary angiographic data of myocardial infarction in patients after 50 years of age]. 642 91

Two cases of the spontaneous dissecting aneurysm (SDA) of the cervical carotid artery (ICA) were reported. Case 1: A 36 years old man was admitted with a sudden onset of right hemiparesis, aphasia and a one-week history of headache and neck pain. Serological examinations were normal. Angiography showed a severe stenosis with two intimal flaps of the left cervical ICA. Four weeks later, left STA-MCA anastomosis was performed. After six weeks from the onset, re-angiography showed the resolution of the left cervical ICA stenosis. Case 2: A 26 years old man experienced the transient monoocular blindness a week before admission. He was admitted with a sudden onset of right hemiparesis and aphasia. Serological examinations were normal. Angiography showed a postsinus tapering occlusion of the left cervical ICA. Four weeks later, left STA-MCA anastmosis was performed. After the operation, left hemiparesis improved remarkably. After two weeks from the operation, re-angiography showed the complete resolution of the left cervical ICA stenosis. As the differential diagnoses, spasm, arteritis, embolism and thrombosis with atherosclerosis were listed. But from the reason reported, we diagnosed the two cases as the resolution of the SDA of the ICA. From the previous literature, 129 cases of SDA of the ICA were reviewed and discussed about the symptom, angiographic findings and treatment. Some specific findings (high frequency of resolution, 87%, etc.) were found. SDA of the ICA occurs in the non-atherosclerotic age and causes the ischemic brain damage. SDA of the ICA should be paid more attention and will probably be identified more frequently.
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PMID:[Spontaneous dissecting aneurysm of the cervical internal carotid artery. Report of 2 cases and review of literature]. 652 29

Cross-compression of cranial nerves at the brain stem by an arterial loop appears to be responsible for several dysfunction syndromes like trigeminal neuralgia and hemifacial spasm. The pathogenesis of these syndromes still remains obscure; some authors call atherosclerosis of the cross-compressing vessel a local pathogenetic factor. Histological examination of the lower cerebellar arteries, obtained at autopsies of humans without cranial nerve dysfunction, was carried out. There was no evidence of significant atherosclerotic changes of distant cerebellar arteries even in places predisposing to intimal thickening by haemodynamic reasons. The adventitia and arachnoidea contributed 30% to the vessel wall and may be the substrate of the reported local vessel thickening in neurovascular compression syndromes.
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PMID:[Intimal fibrosis of cerebellar arteries--a contribution to the pathogenesis of neurovascular syndromes]. 665 24

Anesthetized rats were sterotaxically implanted with electrodes and electrically stimulated in the lateral hypothalamus. During elevation of the S-T segment on simultaneous precordial electrocardiograms, the heart was perfused with glutaraldehyde-paraformaldehyde fixative and the major coronary arteries prepared for morphometry of luminal dimensions. A similar procedure was performed in a second group receiving intravenous arginine vasopressin (AVP) in place of hypothalamic stimulation. Elevation of the S-T segment was present in these animals as well. Control animals were implanted, not stimulated and otherwise treated in the same way. Morphometry showed that reductions of mean luminal diameter and cross-sectional area of statistical significance occurred in the two experimental groups compared to controls, suggesting that coronary spasm was the cause of the elevated S-T segments. Pooled plasma from separate groups of implanted control and hypothalamically-stimulated animals revealed substantial elevation of AVP levels in the latter raising the possibility that the neuroendocrine was involved in eliciting coronary artery spasm.
Atherosclerosis 1984 Apr
PMID:Coronary artery spasm in the rat induced by hypothalamic stimulation. 672 1

Abundant experimental evidence indicates that damage to vascular endothelium decreases intimal fibrinolytic activity, causes mural platelet and fibrin deposition, encourages proliferation of the exposed subintimal fibrocytes and smooth muscle cells, and increases endothelial permeability. These processes lead to thrombosis, subendothelial hyperplasia, or accelerated atherosclerosis. We have demonstrated in monkeys that distention of veins at high pressures (700 mm Hg), as commonly done clinically in preparation for coronary bypass, causes severe damage to the endothelium (as seen by scanning electron microscopy), and increased lipid uptake by the vein wall. The endothelium of veins distended at lower pressures (300-400 mm Hg) was not significantly different from that of undistended veins. Because of the potential late consequences of early endothelial damage to vein grafts, distention of veins before grafting to overcome spasm and to identify leaks must be done at controlled pressures. A convenient balloon device has been developed which limits the maximum pressure that can be applied when the vein is dilated.
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PMID:Prevention of endothelial damage during preparation of saphenous veins for bypass grafting. 676 34

With the arteriographic demonstration of coronary arterial spasm, fundamental questions have been raised concerning the role of spasm in myocardial ischemia and infarction. It is now clear that coronary arterial spasm is the cause of Prinzmetal's variant angina pectoris in patients with and without coronary atherosclerosis. In most patients with coronary heart disease, major ischemic events frequently result from increased myocardial oxygen demand or coronary thrombosis. However, recent evidence suggests that coronary arterial spasm may initiate or contribute to the development of unstable angina pectoris, acute myocardial infarction, and sudden death in these patients. Thus, episodes of myocardial ischemia and infarction are induced by factors, acting singly or in combination, that augment myocardial oxygen demand or diminish myocardial oxygen supply, and the latter alteration can result from thrombotic coronary occlusion or a dynamic increase in coronary arterial tone (that is, coronary arterial spasm).
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PMID:The role of coronary arterial spasm in ischemic heart disease. 689 63

This study explores the relation between coronary arterial spasm and the development of coronary atherosclerosis. The clinical history and coronary angiographic and electrocardiographic data in 212 consecutive patients with ischemic heart disease were correlated. These patients were classified into four groups: Group 1, patients without angiographic evidence of atherosclerosis; Group 2, patients with single vessel disease; Group 3, patients with double vessel disease; and Group 4, patients with significant narrowing of major coronary arteries. Although spontaneous angina occurred in all four groups, it was more common (55 percent) in the patients in Group 1, who were predominantly female and young. Spontaneous angina was confirmed in Group 1 with several techniques, including thallium-201 scintigraphy, ergonovine administration and electrocardiography during attacks of pain. Prior myocardial infarction was present with similar frequency in all four groups. A patient is discussed whose spontaneously occurring coronary arterial spasm later progressed to fixed arteriosclerotic narrowing requiring coronary bypass surgery. These observations and a review of the literature lend support to the hypothesis that coronary arterial spasm can be a possible antecedent leading to the later development of fixed atherosclerotic coronary arterial obstruction.
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PMID:Some clinical considerations regarding the relation of coronary vasospasm to coronary atherosclerosis: a hypothetical pathogenesis. 698 58

A lack in prostacyclin (PGI2) production due to atherosclerosis may play a role in the pathophysiology of some of the clinical manifestations of ischemic heart disease and in particular, of coronary vasospasm. We therefore evaluated the effects of i.v. PGI2 in nine patients with variant angina and six normal volunteers. In normal subjects, PGI2 (2.5, 5, 10 and 20 micrograms/kg/min) had significant antiplatelet effects, caused a dose-dependent decrease in both systolic and diastolic arterial pressure and a decrease in pulmonary resistance. Heart rate increased in a dose-dependent manner, but no consistent effects on myocardial contractility (evaluated by ultrasound) were observed. Side effects were negligible and readily reversible. Although producing obvious antiplatelet and vasodilatory effects, PGI2 did not affect the number, severity and duration of spontaneous ischemic episodes due to coronary vasospasm in five patients and ergonovine-induced spasm in three. However, the number of ischemic episodes was consistently reduced in one patient during four consecutive periods of PGI2 infusion alternated with placebo. a severe, prolonged ischemic episode with ST elevation and pain was consistently observed in this patient every time PGI2 was discontinued. In the appropriate environment, PGI2 can be administered safely to patients with ischemic heart disease. Occasionally, PGI2 may result in a complete disappearance of ischemic episodes due to coronary vasospasm, but usually it is ineffective. These conflicting results could be related to different etiologies of coronary spasm.
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PMID:Effects of intravenous prostacyclin in variant angina. 703 90


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