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)

Arterial hypertension is a major risk factor for the clinical syndrome of angina pectoris, in which the ECG is abnormal but the coronary arteries are normal. Structural and functional abnormalities in coronary circulation as well as extravascular factors (eg, left-ventricular hypertrophy, fibrosis with diastolic dysfunction) compromise the adequate ratio of coronary blood flow to oxygen demand causing angina, dyspnea, and major cardiac events. Recent studies stress the importance to functional disturbances of coronary microvasculature leading to profound morphologic changes associated with impaired coronary conductance. In patients without epicardial coronary stenosis hypertensive microvascular disease can be qualitatively assessed by noninvasive diagnostic approaches based on new Doppler echocardiography techniques and may also be monitored by widely available stress tests. For ultimate quantitative assessment, invasive procedures are still required. Beyond guidelines to control blood pressure in hypertensive individuals, restoration of functional and structural integrity of the coronary microvasculature represents the ultimate therapeutic goal in hypertensive patients with coronary insufficiency and without angiographic evidence of atherosclerosis. Concomitant factors reducing coronary conductance such as left-ventricular hypertrophy and diastolic dysfunction should be reversed in parallel. Currently, therapeutic intervention in the renin-aldosterone-angiotensin-II-system using ACE inhibitors, angiotensin receptor blockers, and low doses of aldosterone antagonists represent the most promising strategy to achieve these goals. Using the knowledge of these recent results we should refine the overall management of our hypertensive patients with coronary insufficiency but without atherosclerosis.
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PMID:Management of the hypertensive patient with coronary insufficiency but without atherosclerosis. 1285 22

Ergometrine usually depresses the S-T segment as in coronary insufficiency, when injected intravenously in rabbits with experimental coronary atherosclerosis and in patients with effort angina, but not in normal animals and man. To explain this difference, we carried out Langendorff perfusion studies in 32 normal and 29 atherosclerotic isolated rabbit hearts. Preliminary tests with ergometrine were done to ensure that advanced coronary atherosclerosis had developed in the rabbits fed a cholesterol diet; pathological examination of the heart after perfusion confirmed the result of the final test with ergometrine. Before drugs were perfused, the basal rate of coronary flow was greater, the heart rate was slower and the contractile amplitude was smaller in the atherosclerotic than in the normal hearts; nitroglycerin markedly increased flow in both normal and atherosclerotic groups. Ergometrine consistently caused a reduction in contractile amplitude with negligible changes in heart rate in both normal and atherosclerotic hearts. On coronary flow, however, the effects of ergometrine differed significantly in these groups; in doses of between 0.2 and 0.4 mg., the average decrease in flow was 8% in normal and 22% in atherosclerotic hearts. The effect was more variable in normal hearts and an increase in flow sometimes occurred. The difference in the response of normal and atherosclerotic hearts was particularly striking when ergometrine was given during recovery from a reduction of coronary flow which had been induced by vasopressin. Ergometrine then uniformly increased flow in the normal, but usually had the opposite effect in the atherosclerotic heart. In normal and atherosclerotic hearts, cardiac effects of vasopressin were similar. Tachyphylaxis to vasopressin, but not to ergometrine, was observed.
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PMID:Effects of ergometrine (ergonovine) on the isolated atherosclerotic heart of the cholsterol-fed rabbit. 1440 56

Hypertriglyceridemia is a cardiovascular risk factor in type-2 diabetes. However, this abnormality may be caused by several mechanisms. In familial hypertriglyceridemia, a hyperlipidemia associated with type-2 diabetes, plasma accumulation of non atherogenic particles explains the presence of hypertriglyceridemia. Our objective was to compare the prevalence of coronary insufficiency and carotid artery stenosis in patients with type-2 diabetes with or without familial hypertriglyceridemia. Controls were paired against cases based on age, gender, diabetes duration, treatment and other cardiovascular risk factors. Controls had either a normal lipid profile (n=48) or hyperlipidemia (n=15). The intima-media thickness of the carotid arteries was significantly lower in cases compared to controls (0.55 +/- 0.12 vs 0.63 +/- 0.22 in normolipidemic controls and 0.66 +/- 0.18 mm in hyperlipidemic subjects (p=0.02)). Exercise treadmill testing was abnormal in a similar proportion of cases and controls (4.8 vs 6.2%). Incidence of cardiovascular complications was not different between groups. We therefore conclude that severe hypertriglyceridemia due to familial hypertriglyceridemia is not associated with an increased prevalence of symptomatic atherosclerosis in patients with type-2 diabetes.
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PMID:[Familial hypertriglyceridemia and diabetes mellitus type 2]. 1602 85

The management of children with hypercholesterolemia (HC) depends on the level of premature atherosclerosis - associated risk. Inherited autosomal-dominant forms of HC (Family HC, Familial deficiency of apolipoprotein B, Family combined dyslipidemia) are at high risk of premature cardiovascular disease. These inherited forms of HC need to be systematically screened during childhood in case of family history and require a long term follow-up in order to prevent adult coronary insufficiency. The first recommended therapy consists in dietary intervention. When necessary, treatment with statin can be used from 8 years old. Before this age, acid-binding resins remain the first step treatment. Plant sterol-esters enriched spreads could be an additional useful treatment.
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PMID:[Management of children with hypercholesterolemia]. 1625 93

The purpose of the study was to determine the conditions under which hyperinsulinemia (HI) is manifested in patients with coronary heart disease (CHD). Such factors as clinical manifestations of CHD, coronary atherosclerosis severity, and myocardial dysfunction severity, were taken into account. The subjects were 201 men aged 47.3 +/- 1.5 years, suffering from CHD. The condition of coronary and intracardial hemodynamics, as well as insulin and glucose blood levels were compared, and correlations between these parameters and the stage, severity, and type of coronary insufficiency (CI) were studied. Two clinical groups were formed. Group I consisted of 74 CHD patients with no myocardial infarction (MI) background; group II consisted of 127 patients with postinfarction myocardial dysfunction (PIMD). Subgroups of patients with acute coronary syndrome (ACS), including subjects with newly developed stenocardia (NDS) and subjects with progressive stenocardia (PS), were formed. In all cases of ACS the basal insulin levels were increased: by 197.4% in patients with NDS, by 167% in patients with PS and no MI background, and by 114,3% in PIMD subgroup (p < 0.05). Some of the ACS patients developed a short-term moderate hyperglycemia (up to 7 mmol/l), that was coped with after 1 to 3 days of antischemic therapy and protective therapeutic regimen. The extent of HI correlated with the severity of coronary atherosclerosis as well as the degree of intracardial and coronary hemodynamic disturbances, and myocardial dysfunction. The results show that HI in CHD patients manifests itself under the condition of CI progression and may be used as a diagnostic marker of residual myocardial ischemia; the degree of HI at different stages of the disease is determined by the severity of CI and myocardial insufficiency, as well as, probably, by the organism's compensatory capacity.
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PMID:[The clinical conditions of the manifestation of hyperinsulinemia in patients with coronary heart disease]. 1675 49

It is not surprising that cardiovascular diseases such as congestive heart failure and coronary insufficiency can give rise to varying degrees of sleep impairment; it is less readily appreciated that certain physiologic events occurring during sleep-as well as long-term unsatisfactory sleep-may cause or increase the risk of cardiovascular conditions such as hypertension, atherosclerosis, stroke, and cardiac arrythmias. Heart rate abnormalities during sleep in normotensive subjects predict later cardiovascular disease, and their early identification alerts the physician to undertake preventive measures. Maneuvers, such as induction of hypoxia, can elicit abnormal blood pressure responses during sleep, and such responses have been used to identify impending cardiovascular problems that could become therapeutic targets. The spontaneously hypertensive rat has been used to examine the effect of sympathetic nervous system (SNS) activity on the heart under a variety of experimental conditions, including quiet and paradoxical sleep. The results have disclosed significant differences between the responses of spontaneously hypertensive rats and normal rats to SNS stimulation. Exploration of other pathophysiologic pathways affected by exposure to light and dark, including those responsive to the cyclic production of melatonin, will improve our understanding of the effect of disruptions of the circadian cycle on cardiovascular function. There is growing evidence that melatonin can influence important processes such as fluid, nitrogen, and acid-base balance. Human subjects whose nocturnal arterial blood pressure fails to show the "normal" decrement during sleep ("nondippers") are also prone to sleep poorly, exhibit increased SNS activity during sleep, and have an increased risk of total and cardiovascular disease mortality. Chronic sleep deficit is now known to be a risk factor for obesity and may contribute to the visceral form of obesity that underlies the metabolic syndrome. The rising prevalence of obstructive sleep apnea and central sleep apnea is linked to the modern-day epidemic of obesity. Obstructive sleep apnea is associated with an enhanced risk of having a new stroke or a transient ischemic attack.
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PMID:Sleep and vascular disorders. 1697 27

This study was designed to assess the diagnostic value of dynamic patterns of anti-inflammatory cytokines (IL-1b, IL-6, TNF-alpha) in patients with ischemic heart disease (IHD) and restenosis of coronary stents 14 months after their implantation for long-term prophylaxis of dyslipoproteinemia. A total of 40 patients with IHD of advanced functional classes (FC) were examined. Blood cytokine levels were measured before, 1 day, and 12-18 months after coronary stenting. Two groups of 23 and 17 patients included cases with recurrent angina and without it respectively. The main parameters measured in the study were in-stent restenosis rate, incidence of' acute myocardial infarction (AMI), mortality rate, frequency of hospitalization for unstable angina, and the levels of proinflammatory cytokines. Considerable activation of cytokines in patients with post-infarction cardiac dysfunction who rarely resorted to therapy with statins (16.7%) was associated with the high rate of recurrent coronary insufficiency related to in-stent occlusion (8.7%), progressive atherosclerosis (65.2%), impaired myocardial perfusion, and restenosis of coronary stents (26.1%). Patients lacking apparent expression of serum cytokines after revascularization while receiving efficacious secondary prophylaxis of dyslipidemia (13.8 and 17% decrease of triglycerides (TG) and low density lipoproteins (LDL) cholesterol respectively, p = 0.04) had left ventricular ejection fraction (LVEF) improved by 12.5% (p = 0.03%), left ventricular end diastolic pressure (LVEDP) decreased by 15.8% (p = 0.03), and frequency of ischemic perfusion defect (PD) reduced by 45.3% (p = 0.01). Moreover, they showed low incidence of progressive coronary atherosclerosis (17.6%) in the absence of in-stent restenosis. It is concluded that the frequency of restenosis of coronary stents after endovascular myocardial revascularization depends on the preprocedural rise in IL-1b content (R = 0.62, p = 0.0023). It is concluded that long-term secondary prophylaxis of dyslipoproteinemia in patients with ischemic dysfunction at risk of coronary restenosis effectively (more than thrice) decreases the occurrence of coronary stent restenosis after endovascular revasularization.
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PMID:[The role of cytokines in restenosing coronary stents and the efficiency of its secondary prophylaxis with statins]. 1881 44

Purpose. This study was undertaken to examine adverse changes in coronary hemodynamics associated with hypertension, aging, and excessive salt intake. To dissociate from the possible effects of atherosclerosis, the study was done in rats because they do not develop atherosclerosis. Moreover, this strain of spontaneously hypertensive rats (SHR) develops hypertension similar to essential hypertension in man.Methods. Systemic and coronary hemodynamics, left ventricular mass, and collagen content in normotensive and SHR of various ages and given different treatments were determined.Results. Compared with normotensive Wistar-Kyoto rats, coronary blood flow reserve was lower and minimal coronary vascular resistance was higher in SHR of all ages; an age-related decrease in flow reserve and an increase in minimal vascular resistance were observed for both strains of rats. In very old rats with isolated systolic hypertension, an increase in left ventricular collagen was associated with coronary insufficiency; antihypertensive therapy nearly normalized both measures. In SHR excessive salt intake increased pressure, increased collagen deposition in myocardial interstitium and perivascularly, and impaired coronary circulation; angiotensin II receptor blocker therapy prevented fibrosis and improved coronary hemodynamics.Conclusion. In conclusion, these data indicate that considerable coronary insufficiency associated with hypertension, aging, and salt overload exists in the absence of atherosclerotic coronary changes. Perivascular fibrosis within myocardium may significantly contribute to the coronary vascular impairment.
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PMID:Coronary circulation in hypertension and aging: an experimental study. 2160 50

A rise in the incidence of latent and late forms of neuro- and visceral syphilis significantly complicates diagnostics of the disease in patients admitted to emergency medicine clinics. Syphilis is believed to be a cause of roughly 0.5% of all cardiopathies. Late syphilitic lesions of the cardiovascular system (cardiovascular syphilis) occur in 0.25-0.96% patients in need of therapeutic treatment, 93.4% of them present with mesaortitis but its life-time diagnosis is possible only in 10% of the cases. Syphilitic lesions in the aorta are especially well apparent at the points of its branching into coronary arteries of the heart and aortic arch. One of the main consequences of syphilitic aortitis is the narrowing of coronary arteries frequently complicated by atherosclerosis, coronary thrombosis, and the resulting myocardial infarction. Another severe complication of syphilitic aortitis is progressive aortic valve insufficiency (in 25-50% of the patients) related to dilatation of the valve ring affected by inflammation. Some patients develop bacterial endocarditis of the aortic valve. Close localization of the coronary artery junction and the aortic valve account for a combination of aortic valve insufficiency and coronary insufficiency in patients with syphilitic process in the initial part of aorta. A case report is presented.
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PMID:[Syphilitic mesaortitis]. 2256 47

Clinical syndromes induced by high intensity radiofrequency electromagnetic field chronic exposure are described. Persons injured by occupational exposure have been observed central nervous system changes in diencephalic syndrome form, cardio-vascular system changes revealed in atherosclerosis, isch(a)emic heart disease and coronary insufficiency rapid progressive expansion. General public living in territory of radar station exposure zone different functional disorders have been identified: vegetative dystonia (asthenovegetative syndrome), thrombocytopenia, decrease of blood coagulation index, and thyroid gland function changes. Observed diseases clinical variability may be determined by electromagnetic exposure characteristics.
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PMID:[Clinical monitoring in areas of exposure to radiofrequency electromagnetic fields]. 2378 12


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