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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Considerable progress has been made in our understanding of the role of high heart rate in determining cardiovascular morbidity and mortality. However, whether the association between fast heart rate and cardiovascular disease is equally strong in males and females is still a matter for debate. In most studies, the predictive value of tachycardia for all-cause mortality has been found to be weaker in women than in men, and in some studies no association between heart rate and cardiovascular mortality was observed. In particular, high heart rate appeared to be a weak predictor of death from coronary heart disease in the female gender. Multiple mechanisms by which sympathetic overactivity could cause hypertension and the metabolic syndrome of insulin resistance have been documented. Recent results obtained at the Ann Arbor laboratory from the analysis of four populations indicate that these mechanisms are operative mostly in males in whom tachycardia reflects a heightened sympathetic tone. In women, fast heart rate would merely represent the extreme of a normal distribution. However, tachycardia can also have a direct impact on the arterial wall, as demonstrated in laboratory studies, and can favour the occurrence of cardiac arrhythmias. The impact of these mechanisms may be similar in men and women and could explain why a high heart rate has been found to have a detrimental effect also in the female gender. Pharmacological reduction of high heart rate is an additional desirable goal of therapy in several clinical conditions such as hypertension, myocardial infarction and congestive heart failure. Although a greater effect is expected in men, cardiac slowing could counteract the detrimental haemodynamic effect of tachycardia also in women.
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PMID:Heart rate as a cardiovascular risk factor: do women differ from men? 1140 41

After the menopause the consequences of hypertension in women change. Their risks of myocardial infarction and stroke rise steeply, a rise that has been blamed in part on the loss of estrogen and the onset of menopausal metabolic syndrome, with endothelial dysfunction, hyperlipidemia, insulin resistance and derangement in coagulation. Hypertensive menopausal women have not had optimum treatment. They have poorer prognoses than men of the same age. Their antihypertensive management therefore merits special attention. Hormone replacement, aspirin prophylaxis and lipid-lowering drugs have their place. The antihypertensive drug chosen should not worsen the metabolic syndrome: angiotensin-II converting enzyme (ACE) inhibitors are therefore among the first-line drugs. Few drugs have been specifically aimed at menopausal hypertension and these are reviewed here.
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PMID:Hypertension in menopausal women--a special case, for special treatment? 1172 63

Prevalence of coronary heart disease (CHD), of type 2 diabetes (T2DM) and of the metabolic syndrome are in Mauritius amongst the highest in the world. As T2DM and CHD are closely associated and have both a polygenic basis, we conducted a 10 cM genome scan with 403 microsatellite markers in 99 independent families of North-Eastern Indian origin including 535 individuals. Families were ascertained through a proband with CHD before 52 years of age and additional sibs with myocardial infarction (MI) or T2DM. Model-free two-point and multipoint linkage analysis were performed using the Mapmarker-Sibs (MLS) and maximum-likelihood-binomial (MLB) programs for autosomal markers and the Aspex program for chromosome X markers. In a second step, additional markers were studied to increase the genetic map density in three regions on chromosomes 3, 8 and 16 where initial indication for linkage was found. Our data show suggestive linkage with CHD on chromosome 16p13-pter with the MLS statistics at 8.69 cM (LOD = 3.06, P = 0.00017) which partially overlaps with a high pressure (HBP) peak. At the same locus, a nominal indication for linkage with T2DM was found in 35 large T2DM Pondicherian families also having Indian origin. With respect to region 8q23, we found suggestive linkage with T2DM (LOD = 2.55, P = 0.00058) as well as with HBP. On 3q27, we replicated previous indication for linkage found in Caucasians (for the metabolic syndrome and for diabetes) according to the categorized trait for CHD and MI with the MLB statistics (LOD = 2.13, P = 0.0009). The genome scan also revealed nominal evidence of linkage with CHD on 10q23 (LOD = 2.06, P = 0.00188). Interestingly, we detected in the same region overlapping linkages with three QTLs: age of onset of CHD (LOD = 2.03), HDL cholesterol (LOD = 1.48) and LDL/HDL ratio (LOD = 1.34). Ordered-subset analysis based on family body mass index ranking replicated finding on 2q37 for T2DM (at Calpain 10 locus). These results show the first evidence for susceptibility loci that predispose to CHD, T2DM and HBP in the context of the metabolic syndrome.
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PMID:A genome-wide scan for coronary heart disease suggests in Indo-Mauritians a susceptibility locus on chromosome 16p13 and replicates linkage with the metabolic syndrome on 3q27. 1173 40

C-reactive protein (CRP) is a prototypic marker of inflammation. Numerous prospective studies in healthy volunteers have confirmed that high-sensitivity CRP (hsCRP) predicts cardiovascular events (CVEs), and hsCRP seems additive to an elevated total cholesterol level and a total/high-density lipoprotein cholesterol ratio in men and women in predicting risk. In smokers and people with metabolic syndrome, hsCRP levels are elevated; in elderly people, there seems to be a relationship between hsCRP and CVEs and mortality. Several properties of CRP make it proatherogenic; however; pending further studies, it should be considered as a risk marker. In people with acute coronary syndromes, hsCRP measurement may be valuable. Elevated levels in the highest quantile seem to predict greater mortality and poorer prognosis in patients with unstable angina and myocardial infarction (MI). While hsCRP is a strong independent predictor of risk of future MI, stroke, peripheral arterial disease, and vascular death, the validity of hsCRP as a risk marker needs to be assessed in all populations. Weight loss, statin drugs, aspirin, and high-dose alpha tocopherol therapy could affect hsCRP. It has its greatest validity as an adjunctive measure in the primary prevention of cardiovascular disease.
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PMID:Inflammation and atherosclerosis: the value of the high-sensitivity C-reactive protein assay as a risk marker. 1199 95

Seven patients with ischemic cardiomyopathy who underwent elective endoventricular circular patch plasty (EVCPP) were included in this study. The mean age of the patients at the time of surgery was 63 years old. All seven patients had anterior left ventricular aneurysms following old myocardial infarction. Two patients were graded NYHA class II, 4 patients class III, and one patient class IV. EVCPP was performed under cardiac arrest with moderate hypothermia in five patients. The two most recent patients underwent EVCPP under on-pump beating and normothermia. Coronary artery bypass grafting was conducted in all cases and the mean number of grafts was 1.8, ranging from one to three. The mitral valve was replaced in one patient. One patient died of myonephrotic metabolic syndrome caused by ischemia of the lower limb. In the follow-up of six patients, the left ventricular end-diastolic volume index (LVEDI) decreased significantly from 128 +/- 31 mL/ m2 to 108 +/- 37 mL/m2. Left ventricular end-systolic volume index (LVESI) decreased in five patients. Left ventricular end-diastolic and end-systolic diameter remained unchanged after surgery. The left ventricular ejection fraction (LVEF) increased from 0.28 +/- 0.08 to 0.321 +/- 0.1. LVESI and LVEF did not improve in one patient with a large residual dyskinetic area at the distal LV septum. A residual dyskinetic area at the distal LV septum was observed in two of four patients who underwent EVCPP under cardiac arrest. This condition, however, was not detected in two patients who underwent EVCPP under on-pump beating conditions. In the follow-up study, the grade of NYHA functional classification improved in all six patients. In conclusion, EVCPP under on-pump beating is a realistic and effective procedure with which to complete ideal LV geometry and promote good results in patients with ischemic cardiomyopathy.
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PMID:Early results and operative considerations of endoventricular circular patch plasty for ischemic cardiomyopathy. 1202 1

Coronary heart disease is a leading cause of death in industrialized nations. Hyperlipidemia with elevated serum total cholesterol, LDL cholesterol, and triglycerides is a known major cardiovascular risk factor. HDL cholesterol is considered to be protective, so low HDL cholesterol is being recognized as an independent cardiovascular risk factor that contributes to the development of atherosclerosis and related adverse cardiovascular events. The recognition of insulin resistance and metabolic syndrome is a step further in understanding these risk factors. Attempts at reducing serum cholesterol with different strategies in the past have met with limited success until the development of statins. The advent of statins has revolutionized the management of hyperlipidemia. The post-statins era has seen major clinical trials demonstrating the benefit of cholesterol reduction in the setting of both primary and secondary prevention. In general, there appears to be a 25% to 40% relative risk reduction in major adverse cardiovascular events such as death, myocardial infarction, and stroke. The recent megatrials further suggest that aggressive management of cholesterol in patients with high cardiovascular risk may be beneficial. Though the concept of the-lower-the-better may be looming, the question of "How low is good enough?" remains controversial. The results of recent megatrials such as the Heart Protection Study go a step further than the NCEP guidelines and suggest that statin therapy may benefit patients at high risk of cardiovascular disease regardless of their baseline values. We summarize the results of the available large clinical trials in our understanding of the management of dyslipidemia in a setting of primary prevention.
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PMID:Management of dyslipidemia in the primary prevention of coronary heart disease. 1235 27

The seminal studies of Brown and Goldstein (Science 1986;232:34-47) coupled with the findings of the Framingham study revolutionized our understanding of the metabolic basis for vascular disease. These studies led to the widespread use of the coronary risk lipid profile, which uses the total cholesterol/high-density lipoprotein (HDL) ratio (or low-density lipoprotein [LDL]/HDL ratio) in predicting risk for vascular disease and as a tool for therapeutic management of patients at risk for vascular disease. However, although these methods are predictive of coronary artery disease (CAD) in general, it is also well known that the extent of occlusive disease and CAD varies greatly between individuals with similar cholesterol and HDL lipid profiles. For this reason, the National Cholesterol Education Program Expert Panel revised these guidelines and now recommends monitoring LDL and HDL cholesterol in the context of coronary heart disease risk factors and "risk equivalents." In addition, more recent findings indicate that specific alterations in individual lipoprotein subclasses may account for the variations in CAD in subjects with similar lipid profiles. For example, a preponderance of small, dense LDL particles correlates with a marked increase in risk for myocardial infarction independent of LDL levels. In particular, the association of small, dense LDL with elevated triglycerides (large, less dense VLDL) and reduced HDL has been defined as the atherogenic lipoprotein profile, and the key metabolic defect driving this profile may be elevated levels of triglycerides, specifically large, less dense VLDL. In an attempt to explain the physiologic basis for lipoprotein variations, this review describes the basic metabolic scheme underlying the traditional view of lipoprotein metabolism and physiology. It then examines the identity and role of the various lipoprotein subfractions in an attempt to distill a working model of how lipoprotein abnormalities might account for vascular disease in general and the metabolic syndrome in particular.
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PMID:The physiology of lipoproteins. 1246 89

Over the past ten years it has become clear that cardiovascular disease (CVD) and atherosclerosis have a 'microinflammatory' component and are often associated with low levels of inflammatory markers that are in the upper part of the 'normal' range. In particular, diseases that predispose to CVD, such as the metabolic syndrome and type 2 diabetes, appear to have a very strong inflammatory component. While the inflammatory process is very complicated, single measures, such as C-reactive protein (CRP) or fibrinogen, have clear benefits as they summarise many different parts of the inflammatory process and are easy to apply. However, it is important to remember that the process of inflammation includes coagulation, fibrinolysis, complement activation, antioxidation, immune response and hormonal regulation through the hypothalamic-pituitary-adrenal axis. Furthermore, genetic variation, differences in exposure to environmental influences and the mass of inflammation-producing tissue (e.g. adipose tissue) can all influence responses. Thus, the relationship between atherosclerosis, the metabolic syndrome and inflammation is extraordinarily complex. Inflammatory markers such as CRP exhibit strong CVD-risk prediction that is consistent across sexes and a number of different populations. They reflect risk not only for 'vulnerable plaque' and myocardial infarction (MI) but also for other cardiovascular diseases. In fact, inflammation is associated with several, if not all, of the chronic diseases of old age, and it is now clear that there are important links between inflammation and general metabolism. For instance, visceral adiposity exerts a major influence on inflammation status. Medications that affect atherosclerosis appear to do so at least in part by influencing inflammation (for instance, the emerging pleiotropic effects of statins), and this has far-reaching ramifications for chronic diseases of old age and their treatment.
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PMID:Inflammation, the metabolic syndrome and cardiovascular risk. 1279 93

Negative emotions, such as depression and anxiety, have been associated with the development of coronary heart disease (CHD). In multivariate models, negative emotions have predicted CHD outcomes, such as nonfatal myocardial infarction and CHD mortality. Few studies, however, have investigated this relation while controlling for variables associated with the metabolic syndrome or those indicative of sympathetic nervous system activity. We prospectively examined the relation between negative emotions and incident CHD in older men (mean 60.3 +/- 7.9 years) participating in the Normative Aging Study (NAS). Four hundred ninety-eight men who completed the Minnesota Multiphasic Personality Inventory (MMPI) and who participated in a subsequent laboratory assessment were included in the study. All men were not on medication and free of diagnosed CHD and diabetes. Negative emotions were measured by the MMPI Welsh A scale, which is comprised of 39 items measuring symptoms of depression and anxiety. Negative emotion score, sociodemographic characteristics, health behaviors, components of the metabolic syndrome, and stress hormones were used to predict incident CHD over a 3-year follow-up period. During follow-up, 45 CHD events were observed. In unadjusted logistic regression analyses, negative emotions significantly predicted the incidence of CHD (odds ratio [OR] 1.06, 95% confidence interval [CI] 1.01 to 1.10, p = 0.02). After adjusting for potential covariates, negative emotions continued to predict the incidence of CHD (OR 1.06, 95% CI 1.01 to 1.12, p = 0.02) A linear, dose-response relation was observed (chi-square 10.8, degree of freedom 2, p = 0.005): participants who had the highest level of negative emotions experienced the greatest incidence of CHD.
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PMID:Effect of negative emotions on frequency of coronary heart disease (The Normative Aging Study). 1455 63

Available evidence clearly indicates a rapid progression in the prevalence of obesity worldwide. As a consequence, there has also been a marked increase in the prevalence of type 2 diabetes all over the world and this chronic metabolic disease is now considered as a coronary heart disease risk equivalent. However, even in the absence of the hyperglycaemic state which characterizes type 2 diabetic patients, non diabetic individuals with a specific form of obesity, named abdominal obesity, often show clustering metabolic abnormalities which include high triglyceride levels, increased apolipoprotein B, small dense low density lipoproteins and decreased high density lipoproteins-cholesterol levels, a hyperinsulinemic-insulin resistant state, alterations in coagulation factors as well as an inflammatory profile. This agglomeration of abnormalities has been referred to as the metabolic syndrome which can be identified by the presence of three of the five following variables: abdominal obesity, elevated triglyceride concentrations, low HDL-cholesterol levels, increased blood pressure and elevated fasting glucose. Post-mortem analyses of coronary arteries have indicated that obesity (associated with a high accumulation of abdominal fat measured at autopsy) was predictive of earlier and greater extent of large vessels atherosclerosis as well as increase of coronary fatty streaks. Metabolic syndrome linked to abdominal obesity is also predictive of recurrent coronary events both in post-myocardial infarction patients and among coronary artery disease men who underwent a revascularization procedures. It is suggested that until the epidemic progression of obesity is stopped and obesity prevented or at least properly managed, cardiologists will be confronted to an evolving contribution of risk factors where smoking, hypercholesterolemia and hypertension may be relatively less prevalent but at the expense of a much greater contribution of abdominal obesity and related features of the metabolic syndrome.
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PMID:[Obesity and cardiovascular disease]. 1461 4


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