Visfatin levels are increased in patients with resistant hypertension and are correlated with left ventricular hypertrophy.

OBJECTIVE: The aim of this study was to investigate the possible correlation of serum visfatin levels with resistant hypertension (RHT). PATIENTS AND METHODS: Patients who had undergone ambulatory blood pressure measurements (ABPM) during the outpatient controls were prospectively recruited. Seventy-one patients with RHT and 94 patients with controlled hypertension (CHT) were included in the study. RHT was defined as 'uncontrolled blood pressure (BP) despite using three antihypertensive agents including a diuretic or need of four or more drugs to control BP'. The demographic properties, medications used, and laboratory parameters including visfatin levels were recorded. RESULTS: In the RHT group, left ventricular mass index was significantly higher compared with the CHT group (108.13±26.86 vs. 89.46±24.09 g/m, P<0.01). High-sensitivity C-reactive protein and visfatin levels were significantly higher in the RHT group [4.0 (5.2) vs. 2.3 (3.0) mg/l, P<0.01, and 12.87±4.98 vs. 9.46±4.69 ng/ml, P<0.01, respectively] compared with the CHT group. In the multivariate linear regression model, visfatin level remained as an independent predictor for office systolic BP [B: 2.07, 95% confidence interval (CI): 1.17-2.98, P<0.01]; office diastolic BP (B: 0.71, 95% CI: 0.27-1.16, P<0.01); mean 24-h systolic ABPM (B: 1.46, 95% CI: 0.79-2.13, P<0.01); and mean 24-h diastolic ABPM (B: 0.88, 95% CI: 0.42-1.34, P<0.01) and was also correlated independently with left ventricular mass index (B: 3.13, 95% CI: 2.58-3.99, P<0.01). CONCLUSION: In this cohort of RHT patients diagnosed with ABPM, we have found an independent correlation between higher visfatin levels and the presence of RHT and left ventricular hypertrophy.

Higher copeptin levels are associated with worse outcome in patients with hypertrophic cardiomyopathy.

BACKGROUND: Correlation of increased copeptin levels with various cardiovascular diseases has been described. The clinical use of copeptin levels in patients with hypertrophic cardiomyopathy (HCM) has not been investigated before. HYPOTHESIS: In this study, we aimed to investigate the prognostic value of copeptin levels in patients with hypertrophic cardiomyopathy (HCM). METHODS: HCM was defined as presence of left ventricular wall thickness ≥15 mm in a subject without any concomitant disease that may cause left ventricular hypertrophy. Levels of copeptin and plasma N-terminal probrain natriuretic peptide (NT-proBNP) were evaluated prospectively in 24 obstructive HCM patients, 36 nonobstructive HCM patients, and 36 age- and sex-matched control subjects. Blood samples were collected in the morning between 7 and 9 am after overnight fasting. Patients were followed for 24 months. Hospitalization with diagnosis of heart failure/arrhythmia, implantable cardioverter-defibrillator implantation, and cardiac mortality were accepted as adverse cardiac events. RESULTS: Copeptin and NT-proBNP levels were higher in the HCM group compared with controls (14.1 vs 8.4 pmol/L, P < 0.01; and 383 vs 44 pg/mL, P < 0.01, respectively). Copeptin and NT-proBNP levels were higher in the obstructive HCM subgroup compared with the nonobstructive HCM subgroup (18.3 vs 13.1 pmol/L, P < 0.01; and 717 vs 223 pg/mL, P < 0.01, respectively). In multivariable logistic regression analysis, copeptin and NT-proBNP levels remained as independent predictors of heart failure (P < 0.01 for both) and adverse cardiac events (P < 0.01 for both). CONCLUSIONS: Copeptin and NT-proBNP levels were significantly higher in patients with obstructive HCM, and higher levels were associated with worse outcome.

Contribution of platelets indices in the development of contrast-induced nephropathy.

Contrast-induced nephropathy (CIN) accounts for 10% of hospital-acquired renal failure, causes a prolonged in-hospital stay and represents a powerful predictor of poor clinical outcome. The underlying mechanism of the CIN development remains unclear and seems to be multifactorial. The potential link between platelet indices such as mean platelet volume (MPV) and platelet distribution width (PDW) with CIN is unknown. Herein, we aimed to investigate the correlation between MPV and PDW levels with the development of CIN. The incidence of CIN (20.5%) was prospectively evaluated in 430 patients with diagnosis of acute coronary syndrome. Initial creatinine (1.13 ±â€Š0.25 vs. 1.05 ±â€Š0.27 mg/dl, P = 0.01) and PDW (40.1 ±â€Š20.2 vs. 34.5 ±â€Š19.9%, P = 0.02) levels and the total volume of contrast media used (121 ±â€Š61 vs. 94 ±â€Š42 ml, P = 0.01) were higher in patients who developed CIN. MPV was similar between the two groups (P = 0.80). In a univariate regression analysis, age, increased creatinine, uric acid, phosphate, PDW levels and higher total volume of contrast media used were significantly correlated with CIN incidence. However, in a multivariate analysis, only total volume of CM used [odds ratio (OR) 1.011, 95% confidence interval (CI) 1.006-1.016; P = 0.01], increased age (OR 1.026, 95% CI 1.00-1.052; P = 0.05) and increased PDW levels (OR 1.009, 95% CI 1.00-1.022; P = 0.04) remained as the independent predictors of CIN. Among platelet indices, PDW, but not MPV, was associated with CIN development. The clinical significance of such link remains unclear, but may indicate involvement of platelet activation in CIN pathogenesis.