Background:  Resistin could be the linkage between the adipose tissue and the insulin resistance. In humans, the role of resistin on metabolic and vascular homeostasis is not well defined. The aim of this study was to investigate the possible association between resistin expression and insulin resistance.

BACKGROUND:QT interval prolongation on the surface electrocardiogram (ECG) predicts cardiovascular complications in high-risk subjects, but its prognostic role in uncomplicated hypertension has been understudied. METHODS:For up to 13 years (average, 5.3 years), we followed up 2110 white patients with initially untreated essential hypertension (mean +/- SD age, 49 +/- 12 years; 55% men) without prevalent cardiovascular or renal disease who underwent 12-lead ECG before therapy. We excluded patients with ECG abnormalities including ischemia, necrosis, complete bundle branch block, atrial fibrillation, arrhythmias, and ventricular preexcitation. RESULTS:Heart rate-corrected QT interval (QTc) showed a weak but significant direct association with systolic blood pressure (r = 0.07; P<.001), diastolic blood pressure (r = 0.11; P<.001), and Cornell voltage (r = 0.06; P = .006). During follow-up, 84 patients developed new-onset ischemic heart disease (0.75 event per 100 patient-years). After adjustment (Cox model) for the effects of age, sex, diabetes mellitus, serum cholesterol level, serum creatinine level, smoking, left ventricular hypertrophy, and 24-hour systolic blood pressure, patients with a prolonged QTc (>or=450 milliseconds in women and >or=440 milliseconds in men) had a nearly 2-fold increase in risks of coronary events (hazard ratio, 1.95; 95% confidence interval, 1.12-3.42; P = .02) and cardiovascular death (hazard ratio, 2.05; 95% confidence interval, 1.03-4.37; P = .04). Coronary heart disease risk was independently higher by 33% (95% confidence interval, +7% to +66%; P = .01) for each 32-millisecond increase in QTc. CONCLUSIONS:Prolonged ventricular repolarization is a risk factor for ischemic heart disease and cardiovascular mortality in subjects with uncomplicated hypertension. Its prognostic significance adds to that of several traditional cardiovascular risk factors, including left ventricular hypertrophy.

Adipose tissue secretes bioactive peptides, termed 'adipokines', which act locally and distally through autocrine, paracrine and endocrine effects. In obesity, increased production of most adipokines impacts on multiple functions such as appetite and energy balance, immunity, insulin sensitivity, angiogenesis, blood pressure, lipid metabolism and haemostasis, all of which are linked with cardiovascular disease. Enhanced activity of the tumour necrosis factor and interleukin 6 are involved in the development of obesity-related insulin resistance. Angiotensinogen has been implicated in hypertension and plasminogen activating inhibitor-1 (PAI-1) in impaired fibrinolysis. Other adipokines like adiponectin and leptin, at least in physiological concentrations, are insulin sparing as they stimulate beta oxidation of fatty acids in skeletal muscle. The role of resistin is less understood. It is implicated in insulin resistance in rats, but probably not in humans. Reducing adipose tissue mass, through weight loss in association with exercise, can lower TNF-alpha and IL-6 levels and increase adiponectin concentrations, whereas drugs such as thiazolinediones increase endogenous adiponectin production. In-depth understanding of the pathophysiology and molecular actions of adipokines may, in the coming years, lead to effective therapeutic strategies designed to protect against atherosclerosis in obese patients

Objective Clinicians are often confronted with the incidental finding of isolated minor, non-specific repolarization changes on the electrocardiogram (ECG) in hypertensive patients. The aim of this study was to investigate the prognostic significance of such changes. Design Prospective, observational study. Methods A total of 1970 hypertensive patients without prevalent cardiovascular disease were followed for up to 9.1 years (mean 4.7 years). Patients with ECG abnormalities including ischaemia, previous infarction, bundle branch block, atrial fibrillation and ventricular pre-excitation were excluded. Patients were divided into three groups: normal left ventricular (LV) repolarization (n = 1355); minor repolarization changes (n = 504); and typical LV strain (n = 111). Results During follow-up, 78 patients developed new-onset ischaemic heart disease. The event rates were 0.50, 1.28 and 3.08 per 100 patient-years in the groups with normal repolarization, minor changes, and typical LV strain, respectively (P< 0.001). After adjustment for the effect of age, sex, diabetes, serum cholesterol, smoking, LV hypertrophy and 24-h pulse pressure, the risk for developing coronary events was higher in patients with minor repolarization changes (hazard ratio 2.07, 95% confidence interval 1.23–3.47; P< 0.01) or LV strain (hazard ratio 4.00, 95% confidence interval 2.09–7.65; P< 0.001) than in patients with normal repolarization (reference category). Population-attributable risks were 21 and 14%, respectively. Minor ST-T changes also retained an adverse prognostic value among patients without LV hypertrophy (hazard ratio 1.90, 95% confidence interval 1.08–3.33; P = 0.026). Conclusion We have identified minor, non-specific LV repolarization changes as a novel, independent risk factor for ischaemic heart disease in patients with uncomplicated hypertension.