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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite major advances in the diagnosis and treatment of atherosclerotic cardiovascular disease (CVD) in the past century, it remains a serious clinical and public health problem. Multivariable risk factor analysis is now commonly performed to identify high-risk candidates for CVD who need preventive measures and to seek out clues to the pathogenesis of the disease. The set of risk factors used for the former is constrained by practical considerations, and the set of risk factors used for the latter is constrained by the hypothesis being tested. This report reviews the evolution and usefulness of multivariable risk functions crafted for estimating risk of clinical manifestations of atherosclerosis and for gaining insights into their pathogenesis. Decades of evaluation of CVD risk factors by the Framingham Study led to the conclusion that CVD risk evaluation is most fruitfully appraised from the multivariable risk posed by a set of established risk factors. Such assessment is essential because risk factors seldom occur in isolation, and the risk associated with each varies widely depending on the burden of associated risk factors. About half the CVD in the general population arises from the segment with multiple marginal risk factor abnormalities. Although disease-specific profiles are available, a multivariable risk formulation for coronary disease comprised of age, sex, the total/high-density lipoprotein cholesterol ratio, systolic blood pressure, glucose intolerance, cigarette smoking, and electrocardiography-left ventricular hypertrophy is also predictive of peripheral artery disease, heart failure, and stroke because of shared risk factors. Correcting risk factors for any particular CVD has the potential to protect against > or =1 of the others. Multivariable risk stratification is now recognized as essential in efficiently identifying likely candidates for CVD and quantifying the hazard.
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PMID:Concept and usefulness of cardiovascular risk profiles. 1521 87

Diabetic cardiomyopathy encompasses the spectrum from subclinical disease to the full-blown syndrome of congestive heart failure. The prevalence of type 2 diabetes mellitus is increasing at an alarming rate in the western world. and with it, the frequency of diabetes-related heart failure. There is at least early suggestion that target-driven, long-term, intensified intervention that is aimed at multiple risk factors in patients who have type 2 diabetes and microalbuminuria may reduce the risk of macrovascular (cardiovascular) and micro-vascular complications by approximately 50%. Thus, it is imperative that patients, particularly those who are at risk for the cardiovascular dysmetabolic syndrome, be screened aggressively for the presence of glucose intolerance and diabetes. When detected, all metabolic and cardio-vascular parameters should be evaluated and treated aggressively to reach currently recommended clinical targets. Such action will result in great benefit for patients by reducing morbidity and mortality and improving quality of life and will reduce the financial burden that is associated with this epidemic disease.
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PMID:Diabetes mellitus and heart failure: basic mechanisms, clinical features, and therapeutic considerations. 1550 23

Type 2 diabetes and hypertension are both insulin-resistant states that impose an excessive risk burden for future major cardiovascular events, including coronary heart disease, stroke, and heart failure. beta-adrenergic receptor antagonists are effective for the treatment of hypertension, but they are underused in diabetic patients because of possible adverse effects on carbohydrate and lipid metabolism, including insulin resistance, glucose intolerance, and dyslipidemia. Traditional beta blockers, both nonselective and selective, are vasoconstrictive due to unopposed alpha1 activity; however, vasodilating beta blockers are not associated with these negative metabolic effects. This review discusses the background of insulin resistance and its link to diabetes and hypertension, emphasizing the role of vascular control by the renin-angiotensin and sympathetic nervous systems on insulin sensitivity and glucose utilization. Clinical evidence is reviewed for the use of vasodilating beta blockers in the treatment of hypertension and in reducing cardiovascular risk in the diabetic population.
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PMID:Metabolic properties of vasodilating beta blockers: management considerations for hypertensive diabetic patients and patients with the metabolic syndrome. 1559 17

Diabetes mellitus is a worldwide epidemic. Cardiovascular disease remains the major cause of morbidity and mortality in people with diabetes. Studies have suggested that increased risk of cardiovascular disease is not restricted to type II or type I diabetes mellitus, but extends to prediabetic stages such as impaired fasting glucose, impaired glucose tolerance, metabolic syndrome, and obesity. Insulin resistance, impaired fasting glucose, impaired glucose tolerance, and diabetes mellitus form a continuous sequence of risk for cardiovascular disease. Therefore, cardiovascular disease mortality and morbidity within the diabetes epidemic grow into vast proportions. Evidence also exists that diabetic patients have a high prevalence of heart failure or impaired diastolic and systolic cardiac function subsequent to the combination of coronary artery disease, hypertension, and diabetic cardiomyopathy. In view of the proportions of this new epidemic, prevention of diabetes and its prediabetic states is likely to be the most effective strategy to prevent serious cardiovascular events.
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PMID:Epidemiology of the diabetic heart. 1634 Apr 2

Obesity is becoming a global epidemic in both children and adults. It is associated with numerous comorbidities such as cardiovascular diseases (CVD), type 2 diabetes, hypertension, certain cancers, and sleep apnea/sleep-disordered breathing. In fact, obesity is an independent risk factor for CVD, and CVD risks have also been documented in obese children. Obesity is associated with an increased risk of morbidity and mortality as well as reduced life expectancy. Health service use and medical costs associated with obesity and related diseases have risen dramatically and are expected to continue to rise. Besides an altered metabolic profile, a variety of adaptations/alterations in cardiac structure and function occur in the individual as adipose tissue accumulates in excess amounts, even in the absence of comorbidities. Hence, obesity may affect the heart through its influence on known risk factors such as dyslipidemia, hypertension, glucose intolerance, inflammatory markers, obstructive sleep apnea/hypoventilation, and the prothrombotic state, in addition to as-yet-unrecognized mechanisms. On the whole, overweight and obesity predispose to or are associated with numerous cardiac complications such as coronary heart disease, heart failure, and sudden death because of their impact on the cardiovascular system. The pathophysiology of these entities that are linked to obesity will be discussed. However, the cardiovascular clinical evaluation of obese patients may be limited because of the morphology of the individual. In this statement, we review the available evidence of the impact of obesity on CVD with emphasis on the evaluation of cardiac structure and function in obese patients and the effect of weight loss on the cardiovascular system.
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PMID:Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. 1638 May 42

Women live longer than men and develop cardiovascular disease (CVD) at an older age. The metabolic syndrome represents a major risk factor for the development of CVD, and gender differences in this syndrome may contribute to gender differences in CVD. In recent years, the metabolic syndrome has been more prevalent in men than in women. Prevalence is increasing and this increase has been steeper in women, particularly in young women, during the last decade. The contributions of the different components of the metabolic syndrome differ between genders and in different countries. In a recent survey in Germany, 40% of the adult population had been diagnosed with disturbed glucose tolerance or type 2 diabetes. Undiagnosed diabetes was more frequent in men than in women, and risk factors for undiagnosed diabetes differed between the sexes. Worldwide, in individuals with impaired glucose tolerance, impaired fasting glucose was observed more frequently in men, whereas impaired glucose tolerance occurred relatively more often in women. Lipid accumulation patterns differ between women and men. Premenopausal women more frequently develop peripheral obesity with subcutaneous fat accumulation, whereas men and postmenopausal women are more prone to central or android obesity. In particular, android obesity is associated with increased cardiovascular mortality and the development of type 2 diabetes. Visceral adipocytes differ from peripheral adipocytes in their lipolytic activity and their response to insulin, adrenergic and angiotensin stimulation and sex hormones. Visceral fat is a major source of circulating free fatty acids and cytokines, which are directly delivered via the portal vein to the liver inducing insulin resistance and an atherogenic lipid profile. Inflammation increases cardiovascular risk particularly in women. A relatively greater increase in cardiovascular risk by the appearance of diabetes in women has been reported in many studies.Thus, the presently available data suggest that the pathophysiology of the metabolic syndrome and its contribution to the relative risk of cardiovascular events and heart failure show gender differences, which might be of potential relevance for prevention, diagnostics, and therapy of the syndrome.
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PMID:Gender differences in the metabolic syndrome and their role for cardiovascular disease. 1659 26

Diabetes is frequently encountered in patients presenting with end-stage heart failure to be listed for transplantation. While diabetes used to be a contra-indication for heart transplantation, careful preoperative evaluation and individualized postoperative medication lead to long-term outcome after heart transplantation equal to non-diabetic patients. About 1/3 of transplanted patients develop a post-transplant diabetes. Several risk factors have been identified leading to this condition. Mostly, post-transplant diabetes is of temporary nature. Several studies have shown no impact of diabetes on the incidence of rejection, malignancies, and transplant vasculopathy. However, glucose intolerance must be taken into consideration when planing immunosuppressive therapy since different medications have distinct impact on glucose metabolism after transplant. A multidisciplinary team allows for closely monitoring and treating patients with diabetes after heart transplant.
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PMID:[Diabetes and heart transplantation]. 1659 48

Oral antidiabetic agents were introduced into clinical practice during the 1950s. Biguanides and sulfonylureas are still used extensively today and their safety and tolerability profiles are well defined. Developments and refinements within these classes have included the introduction of second- and third-generation sulfonylureas, the introduction of modified-release preparations, and the emergence of fixed-dose preparations with metformin and with novel drugs. The latter include the thiazolidinediones, agents with a putative genomic mechanism of action that have been under intense scrutiny since the emergence of severe hepatotoxicity with troglitazone. Recent concerns about thiazolidinediones have centred on the issue of oedema and the risk of precipitating heart failure in vulnerable patients. Only prolonged exposure will determine the long-term safety of thiazolidinediones. Rapid-acting non-sulfonylurea secretagogues appear to be effective and perhaps safer than sulfonylureas in some groups of patients with certain comorbidities (e.g., those with renal impairment). alpha-Glucosidase inhibitors have an excellent safety record and acarbose has been shown to retard the progression from impaired glucose tolerance to Type 2 diabetes. However, their use is limited by tolerability issues.
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PMID:Comparative safety of newer oral antidiabetic drugs. 1704 9

DREAM ("Diabetes Reduction Assessment with ramipril and rosiglitazone Medication") is a double-blind randomised placebo-controlled clinical trial with a 2-by-2 factorial design aiming to study the effects of an ACE inhibitor (ramipril 15 mg/day) and/or a thiazolidinedione (rosiglitazone 8 mg/day) on the development of diabetes or death (primary outcome) and on the regression to normoglycaemia (secondary outcome) in 5269 adults aged 30 years or more with impaired fasting glucose and/or impaired glucose tolerance, and no previous cardiovascular disease. There was no statistical evidence of an interaction between the ramipril and the rosiglitazone arms. After a mean follow up of 3 years, the use of ramipril does not significantly reduce the incidence of diabetes or death but does significantly increase regression to normoglycaemia. In contrast, the treatment with rosiglitazone reduces by almost 60% the incidence of type 2 diabetes and increases the likelihood (+70%) of regression to normoglycaemia. Whether it is a true prevention effect or simply a treatment effect remains to be determined when participants will be retested after a washout period. Cardiovascular event rates were rather low and much the same in all treatment groups, except a higher rate of heart failure in the rosiglitazone group. These results suggest that the routine inhibition of the renin-angiotensin system for the express purpose of preventing diabetes is not indicated in individuals not at high risk for cardiovascular disease and appear to confirm the promises of the glitazone use in the very early stage of the natural history of type 2 diabetes.
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PMID:[DREAM study: prevention of type 2 diabetes with ramipril and/or rosiglitazone in persons with dysglycaemia but no cardiovascular desease]. 1720 7

Since 1) dilated cardiomyopathy (DCM) causes chronic heart failure (CHF), and 2) augmentation of neurohumoral factors such as angiotensin II impairs glucose metabolism, we examined the rate of abnormal glucose metabolism in patients having both DCM and CHF and whether correction of the impairment of glucose metabolism would improve the pathophysiology of CHF in DCM patients. A 75-g oral glucose tolerance test (OGTT) was performed in 56 patients with DCM-induced CHF and 168 age- and sex-matched control subjects. Among the CHF patients, 26.8% and 50.0% suffered from diabetes mellitus (DM) and impaired glucose tolerance (IGT), respectively, showing that abnormal glucose tolerance was more prevalent in DCM patients than in the control subjects (7.7% and 14.3%, respectively). In the patients with DCM-induced CHF, a correlation was observed between the brain natriuretic peptide (BNP) levels and the difference between the plasma glucose levels at the time of fasting and at 2 h of OGTT. Since neither DM nor IGT are thought to cause DCM, the abnormalities of glucose metabolism may be attributed to the progression of CHF. Furthermore, we tested whether correction of the abnormal glucose tolerance using voglibose (an alpha-glucosidase inhibitor) would improve the severity of CHF in another group of 30 patients with DCM-induced CHF and IGT. The patients treated with voglibose for 24 weeks showed decreases in left ventricular dimension, NYHA functional classification values, and plasma BNP levels, and an improvement in cardiac function. In conclusion, abnormal glucose tolerance was more prevalent among patients with DCM-induced CHF than controls, and the correction of IGT improved the pathophysiology of CHF.
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PMID:Abnormal glucose tolerance contributes to the progression of chronic heart failure in patients with dilated cardiomyopathy. 1728 58


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