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)

Systemic lupus erythematosus (SLE) is associated with premature atherothrombotic complications. Hyperhomocysteinemia is considered a cardiovascular risk factor. Increased vascular stiffness may increase cardiovascular mortality. Pulse wave velocity (PWV) is a noninvasive method of analyzing vascular stiffness in the assessment of atherosclerosis. The objective of this study was to identify the relationship between plasma homocysteine levels and brachial-ankle pulse wave velocity (baPWV) measurement in SLE. Plasma homocysteine, baPWV, ankle-brachial index, blood pressure, C3, C4, anticardiolipin antibody (aCL), and anti-double-stranded DNA antibodies were determined in a total of 58 female patients with SLE. The control group comprised 32 age-matched healthy females. In addition, all patients were further classified into subgroups according to the presence of aCL (SLE/aCL+, n=27 vs SLE/aCL-, n=31) to determine the effect of aCL on the tested variables. The mean values for plasma homocysteine and baPWV were 13.19 mumol/l and 1,482 cm/s, respectively. Plasma homocysteine levels were significantly elevated in SLE patients when compared with the healthy controls. SLE patients with aCL had a significantly higher plasma homocysteine level than those without aCL. A significant positive correlation between plasma homocysteine and baPWV was found in patients with SLE (r=0.335, P=0.028, n=58). Plasma homocysteine also significantly correlated with right baPWV in all SLE patients (r=0.371, P=0.014, n=58) and in the SLE/aCL+ group (r=0.523, P=0.031, n=27). These findings indicate a possible link between plasma homocysteine and baPWV in SLE. In conclusion, SLE patients had an increased level of plasma homocysteine, and this phenomenon appeared to be related to vascular stiffness.
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PMID:A positive correlation between homocysteine and brachial-ankle pulse wave velocity in patients with systemic lupus erythematosus. 1642 35

Evidence has accumulated that asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of nitric oxide (NO) synthase. ADMA inhibits vascular NO production at concentrations found in pathophysiological conditions; it also causes local vasoconstriction when infused intra-arterially. ADMA is increased in the plasma of humans with hypercholesterolemia, atherosclerosis, hypertension, chronic renal failure, chronic heart failure, and other clinical conditions. Increased ADMA levels are associated with reduced NO synthesis as assessed by impaired endothelium-dependent vasodilation or reduced NO metabolite levels. In several prospective and cross-sectional studies, ADMA has evolved as a marker of cardiovascular risk. Moreover, prospective clinical studies have suggested that it may play a role as a novel cardiovascular risk factor. Zoccali and coworkers were the first to show that elevated ADMA is associated with a three-fold increased risk of future severe cardiovascular events and mortality in patients undergoing hemodialysis. Valkonen and coworkers demonstrated in a nested case-control study that elevated ADMA was associated with a four-fold increased risk for acute coronary events in clinically healthy, nonsmoking men. In patients with stable angina pectoris, preinterventional ADMA indicates the risk of developing restenosis or severe clinical events after coronary intervention. Furthermore, in humans with no underlying cardiovascular disease who are undergoing intensive care unit treatment, ADMA is a marker of the mortality risk. A number of additional prospective clinical trials are currently under way in diverse patient populations, among them individuals with congestive heart failure, cardiac transplantation patients, and patients with pulmonary hypertension. In summary, an increasing number of prospective clinical trials have shown that the association between elevated ADMA levels and major cardiovascular events and total mortality is robust and extends to diverse patient populations. However, we need to define more clearly in the future who will profit from ADMA determination, in order to use this novel risk marker as a more specific diagnostic tool.
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PMID:Asymmetric dimethylarginine (ADMA) and cardiovascular disease: insights from prospective clinical trials. 1644 65

Thirty-eight studies have been published to date on the association between elevated heart rate and mortality. After adjustment for other risk factors, only two studies for all-cause mortality and four studies for cardiovascular mortality reported an absence of association between heart rate and mortality in male populations. This relationship has been found to be generally weaker among females. Most of these studies investigated samples of general populations. The four studies performed in hypertensive men found a positive association between heart rate and all-cause mortality (hazard ratios ranging from 1.9 to 2.0) or cardiovascular mortality (hazard ratios ranging from 1.3 to 1.7). In spite of this evidence, elevated heart rate remains a neglected cardiovascular risk factor in both genders. The pathogenetic mechanisms connecting high heart rate, hypertension, atherosclerosis and cardiovascular events have also been explicated in many studies. Elevated heart rate is due to an increased sympathetic and decreased parasympathetic tone. This altered balance of the autonomic nervous system tone could explain the increase in events with the increased heart rate. However, it has also been proved that blood flow changes associated with high heart rate favour both the formation of the atherosclerotic lesion and the occurrence of the cardiovascular event. Reduction of heart rate in hypertensive patients with increased heart rate could be an additional goal of antihypertensive therapy. Several trials retrospectively showed the beneficial effect of cardiac-slowing drugs, such as beta-adrenoceptor antagonists (beta-blockers) and non-dihydropyridine calcium channel antagonists, on mortality, notably in patients with coronary heart disease, but no published data are available in patients with hypertension free of coronary heart disease. Other antihypertensive drugs that have been shown to reduce the heart rate are centrally acting drugs and angiotensin II receptor antagonists, but their bradycardic effect is rather weak. The f-channel antagonist ivabradine is a selective heart rate-lowering agent with no effect on blood pressure. Although it has not been proven in existing trials, it would seem reasonable to recommend antihypertensive agents that decrease the heart rate in hypertensive patients with a heart rate higher than 80-85 beats per minute. Since the fast heart rate per se causes cardiovascular damage, all drugs that lower the heart rate have the potential of further reducing cardiovascular events in patients with elevated heart rate. Unfortunately, lowering of the heart rate is not a clinically recognised goal. Prospective trials investigating whether treatment of high heart rate can prevent cardiovascular events, notably in hypertensive patients, are warranted.
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PMID:Impact of increased heart rate on clinical outcomes in hypertension: implications for antihypertensive drug therapy. 1645 Oct 89

Erectile dysfunction (ED) has been associated with risk factors for atherosclerosis. Medications used for atherosclerosis have also been implicated in ED. The aim of this study is to investigate the relationship of erectile function to cardiovascular risk factors and specific drug therapies before and after 6 months of statin therapy. In this prospective observational study, International Index of Erectile Function (IIEF) scores were measured in 93 men attending cardiovascular risk clinics. Cardiovascular risk factors and drug therapies were assessed prior to initiation and after 6 months of statin therapy. Prior to statin therapy, the median IIEF score was 21 (range 0-25), and 57% had impairment of erectile function. After statin therapy, IIEF scores were reduced to 6.5 (range 0-25) (p < 0.001), and 22% experienced new onset ED. Before statin therapy no correlation was observed between IIEF score and any individual cardiovascular risk factor. After 6 months of statin therapy, correlations were observed between lower IIEF scores (r = 0.62; p < 0.001) and age and diabetes and weakly with smoking. Differences in dose, relative efficacy or relative lipophilicity of statin prescribed showed no correlation with change in IIEF score. This study suggests ED following statin therapy is more likely in patients with severe endothelial dysfunction due to established cardiovascular risk factors including age, smoking and diabetes.
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PMID:Erectile dysfunction and statin treatment in high cardiovascular risk patients. 1645 Dec 83

Patients with type 2 diabetes mellitus are at high risk for cardiovascular events and heart failure. The major serious complication of this disorder is large vessel atherosclerosis leading to myocardial infarction and stroke. Aggressive target setting for modifiable cardiovascular risk factors such as dyslipidemia, hypertension, and a procoagulant state, and judicious choice of efficacious therapies have been shown to produce significant reductions in cardiovascular events. The effectiveness of percutaneous coronary intervention (PCI) in diabetes is discussed, and the factors that may influence outcomes are explored. A major unresolved question is the potential role of tight glucose control for reducing macrovascular complications in patients with diabetes. With the increased attention being given to cardiovascular risk factor reduction, the opportunity exists to substantially decrease the largest causes of mortality in diabetic patients. This article reviews the current and emerging therapeutic strategies for these purposes from the cardiologists' point of view.
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PMID:[Type 2 diabetes mellitus and cardiovascular diseases: evaluation, treatment and prevention strategies]. 1650 21

Low density lipoproteins (LDL) comprise in humans two different main fractions: large, buoyant and small, dense particles. Small, dense LDL particles correlate negatively with plasma HDL levels and positively with plasma triglyceride concentrations and are associated with the metabolic syndrome and increased risk for cardiovascular disease. LDL size seems to be an important predictor of cardiovascular events and progression of coronary heart disease (CHD). In addition, several studies have suggested that therapeutic modulation of specific LDL subclasses may be of great benefit in reducing the atherosclerotic risk. Therefore, LDL size measurement may be of potential value in the clinical assessment and management of patients at high risk of CHD, a category that comprises individuals with non-coronary forms of atherosclerosis: peripheral arterial disease, carotid artery disease, abdominal aortic aneurysm. Potentially, screening for the presence of small, dense LDL in patients with those clinical forms of atherosclerosis may identify those with even higher vascular risk and may contribute in directing specific anti-atherosclerotic treatments in order to prevent new vascular events in the same or another district. However, to-date, not so many studies have investigated the LDL size in patients with non-coronary forms of atherosclerosis and we need to wait for further contributions with larger number of patients, even if available data seem to suggest an association between small, dense LDL and such diseases. The predominance of small dense LDL particles has been accepted as an emerging cardiovascular risk factor by the National Cholesterol Education Program Adult Treatment Panel III but screening for the presence of small, dense LDL particles in patients with non-coronary forms of atherosclerosis has not been so far recommended.
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PMID:The significance of low-density-lipoproteins size in vascular diseases. 1652 Jul 17

Thirty-eight articles have been published on the association between elevated heart rate and mortality. After adjustment for other risk factors, most studies found an independent association between heart rate and all-cause and/or cardiovascular mortality. This relationship has been found to be generally weaker among females. The four studies performed in hypertensive patients found a positive association between heart rate and all-cause mortality or cardiovascular mortality. In spite of this evidence, elevated heart rate remains a neglected cardiovascular risk factor in both genders. The pathogenetic mechanisms connecting high heart rate, hypertension, atherosclerosis and cardiovascular events have also been elucidated in many studies. Several trials retrospectively showed the beneficial effect of cardiac-slowing drugs, such as beta-blockers and non-dihydropyridine calcium antagonists on mortality, notably in patients with coronary heart disease, or heart failure, but no published data are available in patients with hypertension free of coronary heart disease. Although it has not been proven in existing trials, it would seem reasonable to recommend in hypertensive subjects with heart rate > 80-85 b/min, antihypertensive agents that decrease the heart rate. The f-channel blockers, selective heart rate-lowering agents with no effect on blood pressure, could also be profitably used in hypertensive subjects with fast heart rate.
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PMID:[Heart rate: a cardiovascular risk factor that can no longer be ignored]. 1675 22

In recent years the main focus of cardiovascular prevention has been to identify people without clinical evidence of coronary disease, but with a high risk of developing a clinical event. Long term follow up studies show that a young person with a high "Relative Risk" of presenting a cardiovascular event becomes an adult with a high "Absolute Risk" of suffering it. The aim of primary prevention is to avoid the appearance of cardiovascular diseases, delaying the development of atherosclerosis and its consequences. In this scenario, the first step is to increase awareness among healthy people of their own cardiovascular risk, enhancing their knowledge of their risk parameter values and generating a correct perception of the risk burden that those values mean. Literature review reveals that significant percentages of healthy individuals are unaware of their own values of blood pressure, total cholesterol and blood glucose. Furthermore, people aware of having abnormal parameters have low treatment compliance rates or evidence inconsistency between knowledge and behavior. This paper reviews educational strategies and other factors that influence this knowledge-behavior gap, such as the stages of behavior changes of the Prochaska and Diclemente Model. Evidence has shown that knowledge about cardiovascular risk factors is not enough to influence behavior and that the degree of preparation of people towards behavior changes is a strong predictor of the success of educational and counseling interventions. Local Chilean data from the RICAR project also shows that the profile of behavior change is different for each modifiable cardiovascular risk factor.
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PMID:[Cardiovascular prevention and attitude of people towards behavior changes: state of the art]. 1655 32

Environmental as well as genetic factors are involved in the pathogenesis of myocardial infarction. The disease is a frequent cause of mortality in the middle-aged male population of Estonia. The high prevalence of premature myocardial infarction (PMI) in this country is not fully understood. The association of atherogenic and thrombogenetic risk factors with lifestyle was evaluated in men who had suffered myocardial infarction at 55 years of age (n = 71) and in randomly selected corresponding controls (n = 85). Serum routine lipids, apolipoprotein (apo)A-I, apoB, apoE polymorphism, lipoprotein(a) and fibrinogen levels were determined. Behavioural risk factors, indices of obesity, blood pressure and pedigree data were registered. In 80.6 % of PMI subjects some type of hyperlipidaemia was observed (European Atherosclerosis Society Classification) and lipid-lowering drugs were taken by 13.9 % of patients. In PMI patients the most common positive determinants of atherogenic lipoprotein indices were waist-to-hip ratio and physical inactivity, and in controls, waist-to-hip ratio and apoE phenotype. The odds ratio (OR) of PMI was 8.9-fold greater in the highest tertile of apoB/apoA-I distribution compared with the lowest tertile. The OR of PMI in the highest tertile of fibrinogen distribution versus the lowest tertile was 6.2 (95 % CI 2.46-15.44), and OR of PMI in the highest Lp(a) tertile versus the lowest was 3.1 (95 % CI 1.31-7.40). Thus, atherogenic dyslipidaemia was the most serious cardiovascular risk factor among PMI patients. From two thrombogenesis-related markers, the levels of fibrinogen and Lp(a), the first one was more strongly associated with PMI status.
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PMID:Determinants of risk factors of atherosclerosis in the postinfarction period: the Tallinn MI study. 1671 48

Atherosclerosis and cardiovascular disease (CVD) are the main causes of death in the Western world, for both men and women. The onset and development of diseases of the cardiovascular and cerebrovascular system are strongly dependent on multiple risk factors that promote pathologic conditions like atherosclerosis, hypertension and thrombosis. Besides genetic factors also environmental influences such as diet composition are known to be closely related to CVD. In this context obesity has been postulated as an independent cardiovascular risk factor. Data from the Framingham Heart Study have consistently shown that increasing degrees of obesity are accompanied by greater rates of CVD. At present, obesity affects 10-35% of the European and US population and increases steadily. As obesity is a serious health problem which promotes metabolic abnormalities (insulin resistance, hyperinsulinemia and dyslipidemia) and dramatically increases the risk for CVD, this review will focus on the epidemiologic and genetic background of obesity. Furthermore, the molecular mechanisms involved in obesity development and their contribution to CVD will be discussed.
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PMID:Molecular basis of obesity and the risk for cardiovascular disease. 1677 May 55


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