Background. Prolongation of P‐wave durations and increased P‐wave dispersion are independent predictors of atrial fibrillation (AF). AF is the most common arrhythmia of the general population. Prehypertension, including those with systolic blood pressure ranging from 120–139 mmHg or diastolic blood pressure ranging from 80–89 mmHg was described by JNC7. Prehypertension is the predictor of development of hypertension in the future. Prehypertension is associated with excess cardiovascular morbidity and mortality. In this study, we evaluated relationship between prehypertension and P‐wave dispersion. Methods. Seventy‐eight prehypertensive patients (group 1: mean age 44.6±11.2 years; 45 male) and 78 normotensive patients (group 2: mean age 43.3±7.0 years; 43 male) were enrolled in this study. Standard 12‐lead ECGs were recorded in all patients using a paper speed of 50 mm/s. In all patients, transthoracic echocardiographic examination was performed. Results. Pmax and P‐wave dispersion were significantly higher in group 1 compared with group 2 (103.59±19.8 ms vs 93.59±13.4 ms, p<0.001; 50.51±18.6 ms vs 39.85±10.6 ms, p<0.001, respectively). Conclusion. Pmax and P‐wave dispersion increase in prehypertensive patients compared with normotensive patients. This data might show increased risk of AF in prehypertension.

Aortic valve stenosis is the most common valvular heart disease in the Western world. The most common cause of aortic valve stenosis in adults is calcification of a normal trileaflet or congenital bicuspid valve. Calcific aortic valve stenosis is an active disease process characterized by mechanical stress, endothelial damage, lipid accumulation, inflammation, synthesis of extracellular matrix proteins, and calcification, reminiscent of atherosclerosis in many aspects. Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase which reduces the bioavailability of nitric oxide and begets endothelial dysfunction. The goal of this study was to examine the association between ADMA activity and severity of aortic valve stenosis. One hundred and nine patients were included in this study. Patients were grouped as those with mild aortic stenosis (42 patients, group 1), moderate aortic stenosis (36 patients, group 2), and severe aortic stenosis (31 patients, group 3). ADMA activity was measured by ELISA kit. Mean ADMA activity in group 3 was significantly higher than that in groups 1 and 2 (1.94 ± 0.45 vs. 0.87 ± 0.37 micromol/l, P < 0.001 and 1.94 ± 0.45 vs. 1.34 ± 0.52 micromol/l, P < 0.001, respectively). Serum ADMA activity was positively correlated with mean aortic gradient and maximum aortic gradient and negatively correlated with aortic valve area. Our results showed that serum ADMA activity is higher in patients with severe aortic valve stenosis. ADMA activity is positively correlated with aortic valve stenosis severity. Serum ADMA level may be used as a precious marker to evaluate and follow up the severity of aortic valve stenosis.

Hyperuricemia is associated with poor outcomes in chronic heart failure (HF). We aimed to evaluate whether uric acid (UA) alone or in combination with N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a good predictor of all-cause mortality, HF hospitalization, and the composite endpoint of HF hospitalization or all-cause mortality in chronic HF. UA and NT-proBNP levels were evaluated retrospectively in 861 chronic HF patients with a left ventricular ejection fraction of ≤50%. The patients were compared by dividing them into 4 groups according to the cut-off values of UA and NT-proBNP. Serum UA concentrations were ≥ 7.0 mg/dL in 46.5% of the subjects. With a median follow-up of 30 months, 201 (23.3%) patients died and 308 (35.8%) patients were hospitalized during the study. The all-cause mortality rate was higher in the hyperuricemic group than that of the normouricemic group (p < 0.001). A multivariate Cox regression model revealed that UA and NT-proBNP were independent predictors of all-cause mortality (HR: 1.105, 95% CI: 1.019-1.198, p = 0.016 and HR: 3.743, CI: 2.647-5.292, p < 0.001, respectively). Patients were divided into 4 groups based on UA (≥ 7 and < 7 mg/dL) and NT-proBNP (≥ 2279 and < 2279 ng/L) levels. All-cause mortality, HF hospitalization, and the composite endpoint of HF hospitalization or all-cause mortality rates were higher in the group with high UA and NT-proBNP levels (p < 0.001, p < 0.001, p < 0.001, respectively). Hyperuricemia alone is an independent predictor of all-cause mortality in chronic HF. However, the combination of UA and NT-proBNP appears to be a stronger predictor of poor outcomes.

Background: We aimed to determine whether there is a relationship between the systemic immune-inflammation (SII) index and the recurrence of atrial fibrillation (AF) after successful direct current...