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Objective: Leptin is an adipokine with both protective and harmful effects on the cardiovascular (CV) system. Prior studies evaluating the association between leptin and CV outcomes have yielded conflicting results. Thus, we sought to investigate the relationship between leptin and CV events and mortality in patients with chronic stable coronary artery disease (CAD)., Methods: We performed a prospective cohort study of 981 outpatients with stable CAD. Leptin levels were measured in fasting venous samples at baseline. We used proportional hazards models to evaluate the association of baseline leptin with subsequent CV events (myocardial infarction, stroke, transient ischemic attack) and death., Results: During a mean follow-up of 6.2±2.1 years, there were 304 deaths, 112 myocardial infarctions, and 52 strokes/TIAs. In models adjusted for age, sex, and race, low leptin was associated with a 30% increased risk of the combined outcome (HR 1.30, CI 1.05-1.59, p=0.01). After further adjustment for obesity, traditional CV risk factors and biomarkers, low leptin remained associated with a 37% increased risk of events (HR 1.37, CI 1.06-1.76, p=0.02)., Conclusions: Low leptin is associated with increased CV events and mortality in patients with stable coronary artery disease. This association is independent of known factors affecting leptin levels, including gender and obesity., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

Background: We sought to evaluate the association of blood pressure and heart rate response during exercise with myocardial infarction (MI), heart failure, stroke, transient ischemic attack (TIA) and death in ambulatory adults with coronary artery disease., Methods: A study population of 937 patients with stable coronary artery disease underwent treadmill exercise stress testing and was followed for 5 years. Participants were divided into quartiles based on peak SBP change, peak SBP and heart rate. We used multivariable Cox proportional hazards models to evaluate the association of change in SBP and heart rate with subsequent cardiovascular events., Results: The participants with SBP increases in the highest quartile had a decreased rate of hospitalization for heart failure [hazard ratio 0.38, 95% confidence interval (CI), 0.21-0.7; P = 0.002], MI (hazard ratio 0.3, 95% CI 0.15-0.58; P = 0.0004), stroke or TIA (hazard ratio 0.39, 95% CI 0.15-0.98; P = 0.04), and all cause mortality (hazard ratio 0.5, 95% CI 0.33-0.76; P = 0.001). After adjusting for age, history of MI and HTN, use of β blockers, statins and calcium channel blockers, resting heart rate, and SBP, participants with SBP change in the highest quartile remained at lowest risk of MI (hazard ratio 0.31, 95% CI 0.15-0.66, P = 0.002), hospitalization for heart failure (hazard ratio 0.46, 95% CI 0.22-0.97, P = 0.04) and death (hazard ratio 0.52, 95% CI 0.32-0.86, P = 0.01). This association was largely explained by greater exercise capacity in those with the highest SBP change. Change in heart rate had a similar association with cardiovascular events., Conclusion: In ambulatory patients with coronary artery disease, the group with the greatest blood pressure and heart rate increase had the lowest risk of MI, heart failure, stroke or TIA and death. These findings support the notion that a robust blood pressure response predicts favorable outcomes.

Background: Telomere shortening has been proposed as a marker of biological aging. Whether leukocyte telomere length is associated with mortality among patients with stable coronary artery disease (CAD) is unknown., Methods and Results: We measured leukocyte telomere length in 780 patients with stable CAD in a prospective cohort study. Participants were categorized by quartiles of telomere length. Hazard Ratios (HRs) and 95% confidence intervals were calculated for all-cause mortality, heart failure (HF) hospitalization, and cardiovascular (CV) events. After 4.4 years of follow-up there were 166 deaths. Compared with participants in the highest telomere length quartile, those in the lowest quartile were at increased risk of death (age-adjusted HR 1.8; 95% CI 1.2 to 2.9). After multivariate adjustment for clinical (HR 2.1; CI 1.3 to 3.3), inflammatory (HR 2.0; CI 1.2 to 3.2), and echocardiographic (HR 1.9; CI 1.0 to 3.5) risk factors, patients in the lowest quartile of telomere length remained at significantly increased risk of death compared to those in the highest quartile. Patients in the lowest quartile of telomere length were also at significantly increased risk of HF hospitalization (HR 2.6; CI 1.1 to 6.0) but not CV events (HR 1.7; CI 0.9 to 3.5)., Conclusions: Reduced leukocyte telomere length is associated with all-cause mortality in patients with stable CAD. The prognostic value of short telomeres in predicting death is not completely captured by existing clinical, inflammatory, and echocardiographic markers of risk.

The article discusses the long term outcome of bariatric surgery. It reports that sustained weight loss, lower incidences of cardiovascular diseases, diabetes and cancer are some of the benefits from bariatric surgery. The study was conducted in obese controlled Swedish subjects. During a follow up of 20 years following the bariatric procedure, the surgery patients used a 54 mean cumulative hospital days against the 40 days of the control group at a confidence interval (C.I.) of 95 percent. However, the study highlights that the drug costs from the seventh year were lower for patients who underwent the surgery than control patients.

Background: Leukocyte telomere length, an emerging marker of biological age, has been shown to predict cardiovascular morbidity and mortality. However, the natural history of telomere length in patients with coronary artery disease has not been studied. We sought to investigate the longitudinal trajectory of telomere length, and to identify the independent predictors of telomere shortening, in persons with coronary artery disease. Methodology/Principal Findings: In a prospective cohort study of 608 individuals with stable coronary artery disease, we measured leukocyte telomere length at baseline, and again after five years of follow-up. We used multivariable linear and logistic regression models to identify the independent predictors of leukocyte telomere trajectory. Baseline and follow-up telomere lengths were normally distributed. Mean telomere length decreased by 42 base pairs per year (p<0.001). Three distinct telomere trajectories were observed: shortening in 45%, maintenance in 32%, and lengthening in 23% of participants. The most powerful predictor of telomere shortening was baseline telomere length (OR per SD increase = 7.6; 95% CI 5.5, 10.6). Other independent predictors of telomere shortening were age (OR per 10 years = 1.6; 95% CI 1.3, 2.1), male sex (OR = 2.4; 95% CI 1.3, 4.7), and waist-to-hip ratio (OR per 0.1 increase = 1.4; 95% CI 1.0, 2.0). Conclusions/Significance: Leukocyte telomere length may increase as well as decrease in persons with coronary artery disease. Telomere length trajectory is powerfully influenced by baseline telomere length, possibly suggesting negative feedback regulation. Age, male sex, and abdominal obesity independently predict telomere shortening. The mechanisms and reversibility of telomeric aging in cardiovascular disease deserve further study. [ABSTRACT FROM AUTHOR]

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. [Copyright &y& Elsevier]