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Abstract: Total caloric expenditure is the sum of resting energy expenditure (REE) and caloric expenditure during physical activity. In this study, we examined total caloric expenditure in 25 morbidly obese patients (body mass index≥35 kg/m2) using dual energy X-ray absorptiometry (DXA) scanning and cardiorespiratory exercise testing. Our results show average REE for all individuals was 2027±276 kcal/d and mean net caloric expenditure during 30 min of exercise was 115±16 kcals. Assuming the mean of all input values, a strict 1500 kcal/d diet combined with 150 min per wk of structured physical activity, the projected weight change was −7% (8.8±6.2 kg) for 6 mo. We conclude that morbidly obese individuals should be able to achieve only a modest weight loss by following minimal national guidelines. These data suggest that more aggressive energy expenditure and caloric restriction targets for long periods of time are needed to result in significant weight loss in this population. [Copyright &y& Elsevier]

We sought to examine the relationship of body mass index (BMI) at age 18 years with the degree and rate of rise in body weight during adulthood among the morbidly obese. We evaluated 196 patients with a standard medical history form and a structured interview with questions regarding weight at age 18 years. The study included 40 (20.4%) men and 156 (79.6%) women. The mean BMI was 50.2 ± 8.0 kg/m² , range 37.0 .80.0 kg/m². Based on self-reported weight, 133 (67.9%) were overweight/obese (BMI >25 kg/m²) and 68 (34.7%) were obese (BMI ≥ 30 kg/m² ) at age 18 years. The distribution of cumulative weight gain was normal with a mean of 60.8 ± 23.7 kg. There was a positive relationship (r=0.36,p <0.0001) between BMI at age 18 years and BMI in adulthood at a mean of 44 ± 10.6 years. Independent predictors for cumulative adult weight gain were BMI at age 18 years (p <0.0001); women (p <0.0001); African Americans (p=0.05). These data suggest that modestly overweight young adults can have excessive weight gains during adult life, resulting in morbid obesity and high rates of obesity-related comorbidities. [ABSTRACT FROM AUTHOR]

We sought to describe a large heart failure (HF) population with respect to systolic and diastolic abnormalities in terms of demographics, echocardiographic parameters, and survival. Using data abstracted from the Resource Utilization Among Congestive Heart Failure (REACH) study, a targeted subpopulation of 3471 patients had electrocardiographic, echocardiographic, and clinical data taken from automated sources during the first year of diagnosis. Among the HF population, 1811 (52.2%) had diastolic HF. Prevalence of diastolic HF trended with age, from 46.4% in those less than 45 years to 58.7% in those 85 years or older (p=0.001 for trend). Patients with diastolic HF had a higher mean ejection fraction (55.7% vs. 28.0%), lower left ventricular end-systolic diameter (3.11 vs. 4.74 cm), and lower left atrium: aortic outlet ratio (1.28 vs. 1.38) (p=0.001 for each comparison). Annualized age, sex, and race-adjusted mortality were 11.2% and 13.0% for those with diastolic and systolic HF, respectively (p=0.001). In a large, racially mixed, urban HF population, those with diastolic HF predominate and enjoy better-adjusted survival than counterparts with systolic HF. [ABSTRACT FROM AUTHOR]

Hypothesis/IntroductionThe risks and benefits of angiotensin-converting enzyme (ACE) inhibitors in patients with end-stage renal disease (ESRD) after cardiac events are unknown. We sought to determine the independent effect of ACE inhibitors (ACE-I) on long-term mortality in ESRD patients after cardiac events.Materials and methodsWe analysed a prospective coronary care unit registry and identified 527 ESRD patients, 368 with complete data on medications prescribed, over eight years at a single, tertiary centre.ResultsThe overall mean age was 64.4 13.8 years with 54.9% men, and 59.2% African-American. A total of 143/386 (37.0%) were prescribed ACE-I during the hospital stay for cardiac reasons, including congestive heart failure (CHF) 52.8% and acute coronary syndromes (ACS) 47.2%. There were no significant differences in the rates of hypotension or arrhythmias in those who were treated with ACE-I versus those who were not. Survival analysis over three years, adjusted for known confounders, demonstrated a 37% reduction in all-cause mortality in those who received ACE-I, (p=0.0145).ConclusionsIn the setting of coronary care unit admission for CHF and ACS, ESRD patients selected for ACE-I, did not have increased rates of adverse haemodynamic or arrhythmic complications. The use of ACE-I conferred an independent mortality reduction over long-term follow-up. [ABSTRACT FROM PUBLISHER]

B-type natriuretic peptide (BNP) is a cardiac neurohormone specifically secreted by the cardiac ventricles in response to volume expansion, pressure overload, and resultant increased wall tension. Previous research has shown elevated BNP levels in patients with volume overload caused by end-stage renal disease (ESRD). This pilot study was designed to describe the relative reduction in BNP that occurs as a result of hemodialysis (HD) in relation to baseline left ventricular function. Hemodialysis patients (n = 34) with ESRD were enrolled in a prospective manner. All patients had blinded serum BNP levels measured at the initiation and termination of HD. Levels of BNP were also measured in the dialysate and any residual urine, if available. In addition, monthly urea reduction ratio (URR) and Kt/V were obtained. The most recent measurement of left ventricular ejection fraction (LVEF) by any method was obtained from chart review. The BNP reduction ratio (BNPRR) was calculated by the following expression: pre-BNP-post-BNP/pre-BNP. The mean age was 50.8 years, 50.0% were male, and 55.9% were African American. A mean of 3239.4 mL of fluid was removed during HD. The mean pre-BNP, post-BNP, and change in BNP were 556.3 +/- 451.5 pg/mL, 538.6 +/- 488.3 pg/mL, and -17.6 +/-147.0 pg/mL. Of the 27 patients who had both pre-BNP and post-BNP values in the measurable range (< 1,300 pg/mL), BNP rose in 9 (33.3%) and fell in 18 (66.7%). The BNPRR had the following correlations: volume removed, r = -0.33, P = .07; Kt/V, r = -0.51, P = .01; URR, r = -0.34, P = .09; and change in body weight, r = -0.33, P = .07. The BNPRR was not correlated with time on dialysis or change in blood pressure. A total of 20 patients had LVEF recorded and post-BNP levels in the measurable range. For this group, the BNPRR values stratified by lowest to highest LVEF group were 4.6%, 19.1%, and 21.8%; P = .95 for trend. The BNP values were elevated in ESRD patients and decreased slightly during HD. This change was more pronounced in patients with normal or mildly impaired LVEF. The BNPRR correlated with the volume removed, change in body weight, and Kt/V. Future research with the BNPRR as a potential marker of the adequacy of volume removal in HD is warranted.

The ideal anticoagulant agent would have a fixed oral dose without need for dose adjustment, a wider therapeutic window than that of warfarin, and acceptable bleeding risks without the need for routine coagulation monitoring. Ximelagatran is a new oral agent that, when converted to its active form, melagatran, directly inhibits thrombin, thus blocking its activity and modulating several of its key functions. For the prevention of venous thromboembolism after orthopedic surgery, treatment of venous thromboembolism, and prevention of stroke in patients with atrial fibrillation, clinical trials indicate that ximelagatran meets the criteria for a superior anticoagulant.

Background: Vascular calcification (VC) is a recognized process involved in senescence and atherosclerosis. Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are conditions associated with metabolic disorders related to soft tissue calcification., Methods: We performed a systematic review of the literature confined to patients with CKD or ESRD with clinical observations of VC. Case reports of calciphylaxis were excluded. We identified 30 studies over 20 years: 11 prospective cohort, 7 cross-sectional, 11 case-control, and 1 retrospective cohort; n = 2918 subjects, mean age 51 years, 59% men and 41% women. Imaging methods used included: x-ray 43%, computed tomography 30%, ultrasound 17%, and other methods 10%., Results: The most consistent determinants of VC were older age and dialysis vintage. Eight analyses determined a relationship between VC and measures of calcium-phosphate balance while 20 analyses specifically did not find such a relationship. Three studies suggested the degree of calcium loading, treatment with phosphate binders, or treatment with vitamin D analogues were related to VC. When taken into consideration, the lipid profile (primarily low high-density lipoprotein cholesterol, elevated triglycerides, elevated low-density lipoprotein, and elevated total cholesterol) were predictive factors in four analyses., Conclusions: VC is a common observation in CKD and ESRD and is mainly related to age, length of time on dialysis therapy, and possibly dyslipidemia. The calcium-phosphorus balance and its related treatments are likely not related to this unique form of vascular calcification. Further research into the determinants and potential treatments for vascular calcification is warranted.

The association between chronic kidney disease and cardiovascular death is accounted for, in part, by higher rates of serious arrhythmias. Research shows an independent relationship between worsened renal function and atrial fibrillation, heart block, ventricular tachycardia, ventricular fibrillation, and asystole. These higher rates also associate with underlying structural heart disease including left ventricular hypertrophy, cardiac fibrosis, valvular disease, and left ventricular systolic and diastolic dysfunction. In addition, chronic intermittent ischemia is implicated in the arrhythmias observed during hemodialysis. The superimposed conditions of acidosis and fluxes in both potassium and magnesium also contribute to higher rates of arrhythmias. Baseline estimated glomerular filtration rate is linked to worsened outcomes and increased defibrillation thresholds in patients receiving implantable cardioverter defibrillators. Preventive strategies include meticulous management of electrolytes, baseline treatment for cardiovascular disease, and when indicated, implantable cardioverter defibrillators. Future research into the mechanisms and prevention of sudden cardiac death in patients with chronic kidney disease is warranted., (Copyright 2004 S. Karger AG, Basel)

B-type natriuretic peptide (BNP) is a cardiac neurohormone released as pre-proBNP and then enzymatically cleaved to the N-terminal-proBNP (NT-proBNP) and BNP upon ventricular myocyte stretch. Blood measurements of BNP and NT-proBNP have been used to identify patients with heart failure (HF). Clinical considerations for these tests include their half-lives in plasma, dependence on renal function for clearance, interpretation of their units of measure, and the rapid availability of the test results. The BNP assay is currently used as a diagnostic and prognostic aid in HF and as a prognostic marker in acute coronary syndromes (ACS). In general, a BNP level less than 100 pg/mL excludes acutely decompensated HF. In the absence of renal dysfunction, NT-proBNP has also been shown to be of diagnostic value in HF, related to HF severity, predictive of sudden death, and prognostic for death in ACS. This article will sort out the literature concerning the use of these peptides in a variety of clinical scenarios.

Decreasing levels of renal function act as a major adverse prognostic factor after contrast exposure with or without percutaneous coronary intervention. In chronic kidney disease, the most important risk factor for the development of contrast-induced nephropathy (CIN) is an estimated glomerular filtration rate