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Query: UMLS:C0018801 (heart failure)
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Obesity has reached epidemic proportions in the United States and worldwide. Heart failure (HF) is also a major public health problem, which, despite therapeutic advances, is associated with substantial mortality. The adverse impact of obesity on the cardiovascular system is being increasingly recognized, and includes a hyperdynamic circulation, subclinical cardiac structural and functional changes, and overt HF. At the same time, the possible protective effect of obesity in patients with established HF has been emphasized in recent studies. This article reviews evidence from epidemiologic studies evaluating the impact of overweight and obesity on the risk of HF, appraises published data on the prognostic significance of overweight and obesity after the onset of HF, describes the potential mechanisms underlying these associations,speculates on the clinical implications of current evidence, and suggests directions for future research.
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PMID:Impact of obesity on the risk of heart failure and survival after the onset of heart failure. 1533 17

Obesity alone is the cause of 11% of cases of cardiac failure in men and 14% of cases in women in the United States. The frequency of obesity continues to rise in our country, 41% of our compatriots being obese or overweight. It is expected that obesity will become an important cause of cardiac failure in the coming years. The Framingham study showed that, after correction for other risk factors, for every point increase in body mass index, the increase in risk of developing cardiac failure was 5% in men and 7% in women. There are three physiopathological mechanisms to explain the adverse effects of obesity on left ventricular function: an increase in ventricular preload secondary to increased plasma volume induced by the high fatty mass; an increase in left ventricular afterload due to the common association of hypertension generated by activation of the sympathetic nervous system by hyperinsulinism; and systolic and diastolic dysfunction due to changes in the myocardial genome and coronary artery disease induced by risk factors of atherosclerosis aggravated by obesity. The adipocyte also secretes a number of hormones which act directly or indirectly on the myocardium: angiotensin II, leptin, resistin, adrenomedulin, cytokines. These haemodynamic and hormonal changes profoundly modify the genetic expression of the myocardium in obesity, favourising hypertrophy of the myocyte and the development of interstitial fibrosis. Whether it be eccentric in the absence of hypertension or concentric when hypertension is associated with obesity, left ventricular hypertrophy, although normalising left ventricular wall stress, has adverse consequences causing abnormal relaxation and decreased left ventricular compliance. Therefore, in obese patients, two forms of cardiac failure may be observed. The more common is due to diastolic dysfunction, obesity being one of the principal causes of cardiac failure with preserved systolic function. Cardiac failure due to systolic dysfunction is less common and may be observed in cases with inappropriate left ventricular hypertrophy which does not normalise abnormal left ventricular wall stress leading to cardiomyopathy, and in cases with associated coronary artery disease. Whatever the underlying mechanism, the diagnosis of cardiac failure is made more difficult by obesity. From the prognostic point of view, in the global population of patients with cardiac failure, obesity improves survival because it counteracts the adverse effect of cachexia; however, obesity increases the risk of sudden death. In fact, obesity is associated with dynamic change in QT interval. In cases of cardiac failure secondary to obesity-related cardiomyopathy, loss of weight leads to an improved functional status and a reduction of left ventricular remodelling and an increase of the ejection fraction.
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PMID:[Obesity and cardiac failure]. 1572 18

In the general population, a high body mass index (BMI; in kg/m(2)) is associated with increased cardiovascular disease and all-cause mortality. However, the effect of overweight (BMI: 25-30) or obesity (BMI: >30) in patients with chronic kidney disease (CKD) undergoing maintenance hemodialysis (MHD) is paradoxically in the opposite direction; ie, a high BMI is associated with improved survival. Although this "reverse epidemiology" of obesity or dialysis-risk-paradox is relatively consistent in MHD patients, studies in CKD patients undergoing peritoneal dialysis have yielded mixed results. Growing confusion has developed among physicians, some of whom are no longer confident about whether to treat obesity in CKD patients. A similar reverse epidemiology of obesity has been described in geriatric populations and in patients with chronic heart failure (CHF). Possible causes of the reverse epidemiology of obesity include a more stable hemodynamic status, alterations in circulating cytokines, unique neurohormonal constellations, endotoxin-lipoprotein interaction, reverse causation, survival bias, time discrepancies among competitive risk factors, and malnutrition-inflammation complex syndrome. Reverse epidemiology may have significant clinical implications in the management of dialysis, CHF, and geriatric patients, ie, populations with extraordinarily high mortality. Exploring the causes and consequences of the reverse epidemiology of obesity in dialysis patients can enhance our insights into similar paradoxes observed for other conventional risk factors, such as blood pressure and serum cholesterol and homocysteine concentrations, and in other populations such as those with CHF, advanced age, cancer, or AIDS. Weight-gaining interventional studies in dialysis patients are urgently needed to ascertain whether they can improve survival and quality of life.
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PMID:Survival advantages of obesity in dialysis patients. 1621 Jul 24

The projection of Henry VIII in the first half of his reign, which began in 1509, is of a magnificent and accomplished 'imperial prince', the possessor of superb physical health. In 1528, when aged 37, he showed a marked change in personality due, it is here argued, to depressive illness, from which he recovered by the mid-1530s. Such ill health has not been recognized previously and it engenders a need for a reassessment of his character and actions during these years of illness. He did not suffer from syphilis and the well-known leg ulcers were less incapacitating than has been described in the past. This truly enormous and overweight man was 55 years old when he died in 1547 in chronic heart failure.
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PMID:The personality and health of King Henry VIII (1491-1547). 1605 31

Insulin-like growth factor-1 (IGF-1), which mediates most effects of growth hormone, has effects on cardiac mass and function, and plays an important role in the regulation of vascular tone. In humans, an inverse relationship between degree of heart failure (HF) and circulating IGF-1 concentrations has been found in several studies. In dogs with HF, few studies have focused on IGF-1. We examined circulating IGF-1 concentrations in dogs with mitral regurgitation (MR) caused by myxomatous mitral valve disease. Study 1 included 88 Cavalier King Charles Spaniels (CKCSs) with a broad range of asymptomatic MR (median serum IGF-1: 76.7 microg/L; 25-75 percentile, 59.8-104.9 microg/L). As expected, standard body weight and percentage under- or overweight correlated directly with IGF-1. MR (assessed in 4 different ways) did not correlate with IGF-1. In study 2, 28 dogs with severe MR and stable, treated congestive HF had similar serum IGF-1 concentrations (median, 100.8 g/L; 25-75 percentile, 74.9-156.5 microg/L) as 11 control dogs (79.6 microg/L; 25-75 percentile, 64.1-187.4 microg/L; P = .84). In study 3, the plasma IGF-1 concentration of 15 untreated CKCSs with severe MR was 16.4 +/- 24.2 microg/L lower (P = .02) at the examination when decompensated HF had developed (80.8 +/- 30.9 microg/L) than at a visit 1-12 months earlier (97.2 +/- 39.8 microg/L), possibly in part due to an altered state of nutrition. The studies document that circulating IGF-1 concentrations are not altered before development of congestive HF in dogs with naturally occurring MR, but decrease by approximately 20% with the development of untreated HE In treated HF, circulating IGF-1 concentrations apparently return to within the reference range.
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PMID:Circulating concentrations of insulin-like growth factor-1 in dogs with naturally occurring mitral regurgitation. 1609 70

(1) When single-agent therapy provides inadequate glycaemic control for patients with type 2 diabetes, most guidelines recommend metformin in combination with a glucose-lowering sulphonylurea as standard treatment, despite the lack of any proven impact on morbidity or mortality. Other options include switching to insulin or abandoning the target of strict glycaemic control. (2) Pioglitazone and rosiglitazone are approved for use in combination with a glucose-lowering sulphonylurea when metformin is poorly tolerated or contraindicated, and in combination with metformin in overweight patients. (3) A fixed-dose combination containing 1 or 2 mg of rosiglitazone plus 500 mg of metformin (hydrochloride) was launched onto the French market in October 2004. (4) The indication for rosiglitazone was extended to include its use as triple-agent therapy in combination with metformin and a glucose-lowering sulphonylurea. (5) No clinical trials assessing effects on mortality or morbidity have evaluated rosiglitazone or pioglitazone in combination with other oral antidiabetic drugs. (6) Several trials have compared the glucose-lowering effects of dual-agent therapy using rosiglitazone or pioglitazone plus a glucose-lowering sulphonylurea or metformin versus dual-agent therapy with metformin and a glucose-lowering sulphonylurea. (7) These clinical trials indicate that in terms of HbA1c level, dual-agent therapy based on rosiglitazone or pioglitazone is about as effective as combination therapy with metformin plus a glucose-lowering sulphonylurea. (8) The main known adverse effect of pioglitazone and rosiglitazone is water-sodium retention, which can provoke oedema and haemodilution anaemia, and can aggravate or reveal heart failure. (9) Pioglitazone has a positive effect on the lipid profile, whereas rosiglitazone increases the LDL-cholesterol level. (10) Dual-agent therapy with pioglitazone and a sulphonylurea causes more weight gain than metformin plus a sulphonylurea. (11) Several trials have assessed triple-agent regimens containing a glitazone. Three placebo-controlled double-blind trials have tested pioglitazone (one trial, nearly 300 patients) or rosiglitazone (two trials, about 1200 patients) for 12 to 26 weeks in patients whose glycaemia was poorly controlled by dual-agent therapy with a sulphonylurea plus metformin. The glycated haemoglobin level fell by 0.3% to 1.1% (in absolute values), depending on the trial and the dosage, but at a cost of the usual adverse effects such as weight gain, anaemia and oedema. Three unblinded trials have compared oral triple-agent regimens containing glitazone versus insulin plus metformin, alone or in combination with a glucose-lowering sulphonylurea; the treatment including glitazone was no more effective in terms of the glycated haemoglobin level, but was associated with an increase in adverse effects and dropouts. (12) Given the limited clinical data available in early 2005, pioglitazone and rosiglitazone have no place in the management of type 2 diabetes.
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PMID:Pioglitazone, rosiglitazone, and rosiglitazone + metformin: new drugs. Glitazone + oral antidiabetic combination: inadequately evaluated. 1610 95

Hypertension is predictive of a wide variety of subsequent adverse events in elderly patients, at least up to the age of 80 years. Treatment can reduce these adverse outcomes, although the benefits in the very elderly remain somewhat unclear. In the very elderly, there appears to be a reduction in cardiovascular events, but this reduction is perhaps at the expense of an increase in overall mortality. Target BPs in the elderly remain controversial. Among patients who have not had previous stroke or significant cardiovascular or renal disease, the benefits of reducing the SBP below 159 mm Hg are well documented. There is some evidence to suggest, however, that if doing so increases the day-night difference in BP by more than 20% or is associated with a decline in DBP below 65 mm Hg, then the benefits of treatment may be attenuated or lost. In addition, there is some suggestion that reducing SBP consistently below 135 mm Hg may accelerate cognitive decline. There appears to be a role for sodium restriction in those who can comply without otherwise compromising nutrient intake. Likewise, exercise may be beneficial and have benefits beyond simply lowering BP. Weight loss in those who are overweight may also help in lowering the BP. For most patients, low-dose thiazides such as hydrochlorothiazide are likely to be the appropriate first-line therapy (even in patients who have diabetes) unless they exacerbate or precipitate urinary incontinence or gout or complicate concomitant drug therapy (eg, lithium treatment of bipolar disorder). In very elderly patients, the apparent beneficial effects on strokes, major cardiovascular events, and heart failure rates may justify treating despite lack of benefit on overall mortality.
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PMID:Hypertension in the elderly. 1614 Jan 25

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

Heart failure (HF) is a major cardiovascular disorder, public health concern, and growing epidemic that affects approximately 5,000,000 people in the United States with 550,000 new cases reported annually. The clinical and economic impact of HF is associated with high hospitalization and early readmission rates. Recognizing factors that contribute to increasing the risk for HF, particularly the persistent rise in prevalence of overweight and obesity, may be imperative to reducing the burdens of this poorly prognostic disease process. Overweight and obesity have been associated with increased morbidity and mortality, and have incited extensive interest in therapeutic interventions. However, within the last decade, studies have illustrated the positive effects of overweight and obesity on survival after the onset of HF, which has prompted a variance of opinion within the healthcare community. This article reviews data supporting both the negative and positive effects of overweight and obesity in relationship to HF with implications for future research, and describes recommendations for practice as it relates to lifestyle modification through diet, exercise, and cognitive-behavioral therapy.
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PMID:Overweight and obesity in the context of heart failure: implications for practice and future research. 1640 34

Exercise is an important behavior for long-term weight control in overweight and obese patients. However, little evidence exists confirming such findings in patients with advanced heart failure (HF). Using a prospective, experimental design, the effects of 24 weeks of a low-level, home-based walking program on weight loss were studied in overweight and obese (body mass index > or =27 kg/m(2)) patients with advanced HF who were randomized to exercise (n = 48) and control (n = 51) groups. Weight changes between the 2 groups at baseline and 6 months were compared using repeated-measures analysis of variance. Patients were on average aged 53.3 +/- 10.1 years and predominantly male (75%), Caucasian (57%), and married (55%). Most patients were in New York Heart Association class III or IV (67%), with a mean ejection fraction of 25%. Patients in the exercise group showed significant weight reduction from baseline to 6 months compared with those in the control group (-6.37 +/- 11.7 vs -0.33 +/- 9.3 kg, p = 0.002). No significant differences were noted between the 2 groups in 6-minute walk distance or depression, although the changes were in the anticipated direction. Modest weight losses of >5% were associated with cardiopulmonary exercise test-documented workload levels at 6 months (r = 0.331, p = 0.006), as well as decreased depression (r = -0.315, p = 0.01) and hostility (r = -0.355, p = 0.005). The number of hospital admissions was significantly smaller for patients in the exercise group compared with those in the control group (0.63 +/- 0.94 vs 1.07 +/- 0.95, p <0.05). In conclusion, the findings demonstrate the beneficial effects of a low-level, home-based walking program on weight loss in overweight and obese patients with advanced HF.
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PMID:Usefulness of a home-based exercise program for overweight and obese patients with advanced heart failure. 1651 95

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