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 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Risk of cardiovascular events was determined over 24 years of surveillance in relation to general adiposity reflected by relative weight and by regional obesity estimated by skinfolds and waist girth per inch of height. Upper quintile values of relative weight, subscapular skinfolds and waist girth were each associated with increased risks of cardiovascular disease in both sexes. Risk of total cardiovascular events increased with the degree of regional, central or abdominal obesity. Mortality from cardiovascular disease was also increased. Increased relative weight and central obesity were both associated with increased risk factors including cholesterol, blood pressure, glucose and uric acid. Changes in weight were mirrored by changes in risk factors with linear trends over a 15 lb range of weight fluctuations. Subscapular skinfold and the ratio of subscapular-to-triceps skinfold, measures of central obesity, were in either sex also associated with an increased probability of coronary attacks in particular. The subscapular skinfold contributed to CHD risk independent of body mass index (BMI). Multivariate analyses taking all the risk factors into account indicate an independent effect of abdominal obesity on stroke, cardiac failure and cardiovascular and all-cause mortality in men. In women, only the subscapular-to-triceps skinfold ratio independently contributes to CHD, cardiovascular and all cause mortality. Regional obesity appears to be an independent contributor to cardiovascular disease at a given level of general adiposity, its effect only partially mediated through promotion of other known risk factors. These data suggest that cardiovascular disease is as closely linked to abdominal as to general adiposity.
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PMID:Regional obesity and risk of cardiovascular disease; the Framingham Study. 199 75

This paper is a comprehensive and critical review of the updated information available in Spain for the elderly population on the epidemiology of cardiovascular diseases. Clinical (coronary heart disease, heart failure, and cerebrovascular disease) and subclinical (left ventricular hypertrophy, carotid stenosis) cardiovascular diseases are reviewed. Prevalence and distribution of major classical cardiovascular risk factors such as hypertension, hyperlipidemia, diabetes mellitus and smoking and information on new risk factors such as microalbuminuria or abdominal obesity are also presented. The article is also focused on the high rates of morbidity, mortality and the burden of handicap in this age group in comparison with middle-aged people. Finally we call attention to the few and inconsistent population data available for some of the mentioned topics in our country, particularly the lack of specific figures of incidence and risk rates from cohort studies of elderly people in Spain.
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PMID:[Epidemiology of cardiovascular diseases in the Spanish elderly population]. 985 8

Five decades of epidemiologic research have established that blood pressure elevation is a common and powerful contributor to all of the major cardiovascular diseases, including coronary disease, stroke, peripheral artery disease, renal disease, and heart failure. The common variety of hypertension designated benign essential hypertension was not shown to be either benign or essential. Although clinicians favor the diagnosis and treatment of hypertension in terms of diastolic blood pressure elevation and categoric cut points, epidemiologic data show a more important influence of systolic blood pressure, and a continuous, graded influence of blood pressure even within what is regarded as the normotensive range. An important revelation in epidemiologic hypertension research is that hypertension usually occurs in conjunction with other metabolically linked risk factors; therefore, less than 20% occurs in isolation. The other risk factors that tend to accompany hypertension include glucose intolerance, obesity, left ventricular hypertrophy, and dislipidemia (elevated total, LDL, and small dense LDL cholesterol levels, raised triglyceride, and reduced HDL cholesterol levels). Clusters of three or more of these additional risk factors occur at four times the rate expected by chance. This clustering is attributed to an insulin resistance syndrome promoted by abdominal obesity. The amount of risk factor clustering accompanying elevated blood pressure was observed to increase with weight gain. Based on Framingham Study data the prevalence of insulin resistance syndrome in the general population could be as high as 22% in men and 27% in women. Risk of coronary disease, the most common and most lethal sequel to hypertension, increased stepwise with the extent of risk factor clustering. Among persons with hypertension, about 40% of coronary events in men and 68% in women are attributable to the presence of two or more additional risk factors. Only 14% of coronary events in hypertensive men and 5% of those in hypertensive women occurred in the absence of additional risk factors. Other important features of risk stratification of hypertension are the presence of an elevated heart rate and left ventricular hypertrophy, and an elevated fibrinogen that often accompany hypertension. Recent population-based data reported suggest that elevated renin accompanying hypertension may independently enhance the risk of coronary events. Because clustering of other major risk factors with hypertension is the rule, the prudent physician should routinely screen for the presence of these other factors. Multivariate risk assessment profiles are now available for coronary disease, stroke, peripheral artery disease, and heart failure, to enable physicians to pool all the relevant risk factor information so as to arrive at a composite risk estimate. Hypertensive patients are more appropriately targeted for therapy by such risk stratification and the goal of the therapy should be to improve the multivariate risk profile.
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PMID:Risk stratification in hypertension: new insights from the Framingham Study. 1067 82

The Framingham Study established hypertension as a major cardiovascular risk factor and quantified its atherogenic cardiovascular disease potential. An historical perspective is presented on the epidemiological insights about hypertension derived from 50 years of Framingham Study research into the prevalence, incidence, determinants and hazards of hypertension. Existing misconceptions about the presence of critical levels of blood pressure, the impact of the systolic and diastolic components of blood pressure, the hazard 'mild' hypertension, the impact in advanced age and the hazard of left ventricular hypertrophy. The importance of isolated systolic hypertension and the pulse pressure were demonstrated. It has been demonstrated that hypertension seldom occurs in isolation of other atherogenic risk factors, with which it tends to cluster. This clustering with other metabolically linked risk factors has been shown to reflect insulin resistance promoted by weight gain and abdominal obesity. Obesity was shown to be one of the major determinants of hypertension in the general population. Left ventricular hypertrophy was shown to be an ominous harbinger of cardiovascular disease rather than an incidental compensatory phenomenon. Multivariate risk profiles for coronary disease, stroke, peripheral artery disease and heart failure have been devised to facilitate incorporation of elevated blood pressure in a global, multivariate cardiovascular risk assessment.
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PMID:Fifty years of Framingham Study contributions to understanding hypertension. 1072 12

Recent studies suggest that adipose tissue hormones ("adipokines") are involved in the pathogenesis of various complications of obesity, including hyperlipidemia, diabetes mellitus, arterial hypertension, atherosclerosis, and heart failure. Apelin and visfatin are two recently described adipokines, although they are also synthesized outside adipose tissue. Apelin exists in at least three forms, consisting of 13, 17, or 36 amino acids, all originating from a common 77-amino-acid precursor. In the cardiovascular system, apelin elicits endothelium-dependent, nitric oxide-mediated vasorelaxation and reduces arterial blood pressure. In addition, apelin demonstrates potent and long-lasting positive inotropic activity which is preserved even in injured myocardium and is not accompanied by myocardial hypertrophy. Apelin synthesis in adipocytes is stimulated by insulin, and plasma apelin level markedly increases in obesity associated with insulin resistance and hyperinsulinemia. In addition to regulating cardiovascular function, apelin inhibits water intake and vasopressin production. Visfatin, previously recognized as a pre-B cell colony-enhancing factor (PBEF), is abundantly expressed in visceral adipose tissue and is upregulated in some, but not all, animal models of obesity. Preliminary studies suggest that plasma visfatin concentration is also increased in humans with abdominal obesity and/or type 2 diabetes mellitus. Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues. Thus, apelin and visfatin are unique among adipose tissue hormones in that they are upregulated in the obese state and both exert primarily beneficial effects.
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PMID:Apelin and visfatin: unique "beneficial" adipokines upregulated in obesity? 1694 Sep 39

Diabetes mellitus (DM) is considered a major public health problem in both developed and developing countries due to its chronic complications, at the macro or microcirculation, with great impact on mortality and morbidity in all patients. The disease is considered the end of a pathophysiologic process involving peripheral and hepatic insulin resistance and reduced insulin secretion that have been started years before the clinical diagnosis. Metabolic syndrome (MS) is a disorder that results from the increasing prevalence of obesity worldwide. DM is frequently associated with clinical and laboratory features of MS, like abdominal obesity, hypertension, dyslipidemia and microalbuminuria that are also risk factors for cardiovascular disease. Populational studies have demonstrated increasing prevalence of all the features of MS from pre-diabetes to clinical DM resulting in a great risk of cardiovascular disease. The prevalence of MS in DM type 2 is estimated to be >80%. Glitazones are PPAR-gamma agonists that improve insulin sensitivity. These drugs induce the transcription of genes related to glucose and lipid metabolism, and expression of inflammatory and endothelial proteins associated with atherosclerosis process resulting in an improvement in endothelial function. However several questions need to be clarified regarding the glitazones, in special those associated with their adverse effects such as weight gain, edema and heart failure.
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PMID:[Glitazones and the metabolic syndrome: mechanism of action, pathophysiology and therapeutic indications]. 1676 93

The epidemiology of cardiovacular disease risk factors is changing rapidly with the obesity pandemic. Obesity is independently associated with the risks for coronary heart disease, atrial fibrillation, and heart failure. Intra-abdominal obesity is also unique as a cardiovascular risk state in that it contributes to or directly causes most other modifiable risk factors, namely, hypertension, dysmetabolic syndrome, and type 2 diabetes mellitus. Obesity can also exacerbate cardiovascular disease through a variety of mechanisms including systemic inflammation, hypercoagulability, and activation of the sympathetic and renin-angiotensin systems. Thus, weight reduction is a key strategy for simultaneous improvement in global cardiovascular risk, with anticipated improvements in survival and quality of life.
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PMID:Impact of obesity on cardiovascular disease. 1877 58

Endocannabinoids are endogenous bioactive lipid mediators present both in the brain and various peripheral tissues, which exert their biological effects via interaction with specific G-protein-coupled cannabinoid receptors, the CB(1) and CB(2). Pathological overactivation of the endocannabinoid system (ECS) in various forms of shock and heart failure may contribute to the underlying pathology and cardiodepressive state by the activation of the cardiovascular CB(1) receptors. Furthermore, tonic activation of CB(1) receptors by endocannabinoids has also been implicated in the development of various cardiovascular risk factors in obesity/metabolic syndrome and diabetes, such as plasma lipid alterations, abdominal obesity, hepatic steatosis, inflammation, and insulin and leptin resistance. In contrast, activation of CB(2) receptors in immune cells exerts various immunomodulatory effects, and the CB(2) receptors in endothelial and inflammatory cells appear to limit the endothelial inflammatory response, chemotaxis, and inflammatory cell adhesion and activation in atherosclerosis and reperfusion injury. Here, we will overview the cardiovascular actions of endocannabinoids and the growing body of evidence implicating the dysregulation of the ECS in a variety of cardiovascular diseases. We will also discuss the therapeutic potential of the modulation of the ECS by selective agonists/antagonists in various cardiovascular disorders associated with inflammation and tissue injury, ranging from myocardial infarction and heart failure to atherosclerosis and cardiometabolic disorders.
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PMID:The emerging role of the endocannabinoid system in cardiovascular disease. 1935 46

Obesity is an independent risk factor for recurrent events among patients with established coronary heart disease (CHD). The goal of the present study was to identify potential mechanisms underlying this association. We measured the waist-to-hip ratio and body mass index in 979 outpatients with stable CHD and followed them for a mean of 4.9 years. We used proportional hazards models to evaluate the extent to which the association of obesity with subsequent heart failure (HF) hospitalization or cardiovascular (CV) events (myocardial infarction, stroke, or CHD death) was explained by baseline co-morbidities, cardiac disease severity, inflammation, insulin resistance, neurohormones and adipokines. Of the 979 participants, 128 (13%) were hospitalized for HF and 152 (16%) developed a CV event. Each standard deviation (SD) increase in the waist-to-hip ratio was associated with a 30% increased risk of HF hospitalization (unadjusted hazard ratio [HR] 1.3, 95% confidence interval [CI] 1.1 to 1.6). This association was not attenuated after adjustment for potential mediators (HR 1.6, 95% CI 1.2 to 2.1). Likewise, each SD increase in the waist-to-hip ratio was associated with a 20% greater risk of CV events (unadjusted HR 1.2, 95% CI 1.0 to 1.4), and this remained unchanged after adjustment for potential mediators (adjusted HR 1.3, 95% CI 1.0 to 1.5). The body mass index was not associated with the risk of HF or CV events. In conclusion, abdominal obesity is an independent predictor of HF hospitalization and recurrent CV events in patients with stable CHD. This association does not appear to be mediated by co-morbid conditions, cardiac disease severity, insulin resistance, inflammation, neurohormones, or adipokines.
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PMID:Relation of obesity to heart failure hospitalization and cardiovascular events in persons with stable coronary heart disease (from the Heart and Soul Study). 1976 51

Heart failure (HF) has become a major public health problem in both developed and developing countries of the world. The individual and joint associations of physical activity and obesity on the risk of HF have been extensively studied in recent years. The results from prospective studies consistently indicate that regular physical activity reduces the risk of HF, while both general obesity and abdominal obesity increase the risk of HF. Furthermore, research related to the joint association of obesity and physical activity on HF risk indicates that lean and active individuals had the lowest risk of HF. Therefore, preventing HF by maintaining optimal weight and engaging in regular physical activity may reduce the public health burden of HF worldwide.
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PMID:Individual and joint associations of obesity and physical activity on the risk of heart failure. 2109 16


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