Body mass indices and outcome in patients with chronic heart failure.
ABSTRACT There is an inverse relation between body mass and mortality in large populations of patients with chronic heart failure with a broad range of disease severity. The best measure of body size to describe the relation is not clear.
Patients with chronic heart failure (n = 2271, age 71.9 ± 11.3 years; 74.6% male) due to left ventricular systolic dysfunction were followed for a median of 1785 days (inter-quartile range, 874-2311 days) in survivors. We measured body mass index (BMI: weight/height²), ponderal index (PI: weight/height³), and body surface area (BSA). In a subset of 1025 patients, we also calculated the 'Charles index' [weight/(waist² × height)] together with bioimpedance data. During follow-up, 912 patients died. Measures of body mass were strong univariable predictors of outcome, and BSA (χ² = 71.3) was the strongest predictor followed by height (χ² = 68.6), weight (χ² = 57.4), then BMI (χ² = 15.2). The larger the patient's size, the lower the risk of mortality. Body surface area was the single strongest predictor of outcome in a multivariable model including 14 variables. In the subset with bioimpedance data, basal metabolic rate, BSA, weight, BMI, percentage body fat, fat mass, PI, and fat-free mass were all univariable predictors of outcome.
Measures of body size are strongly related to outcome in patients with chronic heart failure. Body surface area is a stronger predictor of mortality than other measures of body habitus, irrespective of height correction. The greater the overall bulk of the body, the better the survival.
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ABSTRACT: Glucagon-like peptide-1 (GLP-1) is an incretin hormone that enhances glucose-stimulated insulin secretion and exerts direct and indirect actions on the cardiovascular system. GLP-1 and its related incretin hormone, glucose-dependent insulinotropic polypeptide, are rapidly inactivated by the enzyme dipeptidyl peptidase 4 (DPP-4), a key determinant of incretin bioactivity. Two classes of medications that enhance incretin action, GLP-1 receptor (GLP-1R) agonists and DPP-4 inhibitors, are used for the treatment of type 2 diabetes mellitus. We review herein the cardiovascular biology of GLP-1R agonists and DPP-4 inhibitors, including direct and indirect effects on cardiomyocytes, blood vessels, adipocytes, the control of blood pressure, and postprandial lipoprotein secretion. Both GLP-1R activation and DPP-4 inhibition exert multiple cardioprotective actions in preclinical models of cardiovascular dysfunction, and short-term studies in human subjects appear to demonstrate modest yet beneficial actions on cardiac function in subjects with ischemic heart disease. Incretin-based agents control body weight, improve glycemic control with a low risk of hypoglycemia, decrease blood pressure, inhibit the secretion of intestinal chylomicrons, and reduce inflammation in preclinical studies. Nevertheless, there is limited information on the cardiovascular actions of these agents in patients with diabetes and established cardiovascular disease. Hence, a more complete understanding of the cardiovascular risk to benefit ratio of incretin-based therapies will require completion of long-term cardiovascular outcome studies currently underway in patients with type 2 diabetes mellitus.Endocrine reviews 02/2012; 33(2):187-215. · 19.76 Impact Factor
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ABSTRACT: The goal of the study was to examine whether resting or post-exercise metabolic substrate levels are associated with differential exercise performance and long-term outcome in control subjects or heart failure (HF) patients with or without type 2 diabetes mellitus (DM). Twenty five healthy controls matched with 97 patients with stable advanced HF were prospectively enrolled. Exercise capacity, age, gender, and HF aetiology were balanced between HFDM- and HFDM+ groups. Subjects underwent maximal bicycle spiroergometry with blood sampling to measure metabolites and neurohormones before and immediately after the exercise. HFDM+ patients had increased free fatty acids, glucose, and β-hydroxybutyrate compared with controls. HFDM+ patients had higher baseline copeptin (24 ± 16 vs. 17 ± 13 pmol/L, P < 0.05) but otherwise showed similar neurohumoral activation and exercise response to HFDM- patients. Peak oxygen consumption (VO(2)) was unrelated to post-exercise free fatty acids, glucose, lactate, or glycerol, but strongly correlated with post-exercise pyruvate (in all: r = 0.62, P < 0.001). During the next 17 ± 10 months, 36% of HF patients experienced an adverse event (death, urgent transplantation, or assist device insertion). From metabolic factors, only post-exercise glucose [hazard ratio (HR) 1.28, P = 0.04), total body fat (HR 0.58, P < 0.001), and the presence of DM (HR 1.98, P = 0.04) were predictive of the outcome. With the exception of pyruvate, acute changes of metabolic substrates are not related to cardiac performance in HF, regardless of diabetic status. Inhibition of body fat depletion, attenuation of stress-related hyperglycaemia, or increasing dynamics of plasma pyruvate may represent therapeutic targets in advanced HF.European Journal of Heart Failure 06/2012; 14(7):754-63. · 5.25 Impact Factor