It is classically thought that it is the amount of salt that is critical for driving acute blood pressure responses. However, recent studies suggest that blood pressure responses, at least acutely, may relate to changes in serum osmolality. Here, we test the hypothesis that acute blood pressure responses to salt can be altered by concomitant water loading. Ten healthy patients free of any disease and medication underwent 4 interventions each a week apart in which they took 300 mL of lentil soup with no salt (visit 1), lentil soup with 3 g salt (visit 2), or lentil soup with 3 g salt and 500 mL water (visit 3) or 750 mL water (visit 4). At each visit, hourly blood measurements and blood pressure measurements (baseline, 1st, 2nd, 3rd, and 4th hour) were performed and plasma osmolarity, sodium and copeptin levels were measured. Patients receiving the 3 g salt showed a 6 mOsm/L change in osmolality with a 2.5 mmol/L change in plasma sodium and 10 mm Hg rise in systolic blood pressure at 2 hours. When the same patients drank salty soup with water, the changes in plasma osmolarity, plasma sodium, and blood pressure were prevented. The ability to raise blood pressure acutely with salt appears dependent on changes in plasma osmolality rather than the amount of salt. Our findings suggest that concurrent intake of water must be considered when evaluating the role of salt in blood pressure.

Background Epicardial adipose tissue (EAT) is a cardiometabolic risk factor, and its possible relationship with hypertension has been reported previously. Fragmented QRS (fQRS) detected on electrocardiography (ECG) has been demonstrated to be a marker of myocardial fibrosis. In this study, we aimed to investigate the relationship between the thickness of EAT, and presence of fQRS in hypertensive patients. Methods Consecutive patients who were diagnosed with hypertension were included in the study. ECG and transthoracic echocardiography (TTE) were performed to all patients. fQRS was defined as additional R′ wave or notching/splitting of S wave in two contiguous ECG leads. Thickness of EAT was measured by TTE. Results This study enrolled 69 hypertensive patients with fQRS on ECG and 45 hypertensive patients without fQRS as the control group. Age (P = .869), and gender distribution (P = .751) were similar in both groups. Left atrial diameter (P = .012), interventricular septal thickness (P < .001), posterior wall thickness (P < .001), left ventricular ejection fraction (P = .009), left ventricular mass (P = .006), left ventricular mass ındex (P = .014), left ventricular hypertrophy (P = .003), and EAT thickness (P < .001) were found to be significantly increased in patients with fQRS. In multivariate analysis, among these variables only EAT was observed to be an independent predictor of fQRS (odds ratio:3.306 [95% confidence interval, 0.030‐0.118], P = .001). Conclusion A significant association exists between the presence of fQRS and EAT thickness in hypertensive patients. The presence of fQRS, just as EAT thickness, may be used as a cardiometabolic risk factor in hypertensive patients.

Background: Hyperuricemia may cause acute kidney injury by activating inflammatory, pro-oxidative and vasoconstrictive pathways. In addition, radiocontrast causes an acute uricosuria, potentially leading to crystal formation. We therefore aimed to investigate the effect of urine acidity and urine uric acid level on the development of contrast-induced nephropathy (CIN) in patients undergoing elective coronary angiography. Methods: We enrolled 175 patients who underwent elective coronary angiography. CIN was defined as a >25% increase in the serum creatinine levels relative to basal values 48–72 h after contrast use. Prior to coronary angiography and 48–72 h later, serum uric acid, urea, creatinine, bicarbonate levels, and spot uric acid to creatinine ratio (UACR) were measured. Results: Of the 175 subjects included, 29 (16.6%) developed CIN. Those who developed CIN had a higher prevalence of diabetes, higher UACR (0.60 vs. 0.44, p = 0.014), higher contrast volume, and lower serum sodium level. With univariate analysis of a logistic regression model, the risk of CIN was found to be associated with diabetes (p = 0.0016, OR = 3.8 [95% CI: 1.7–8.7]), urine UACR (p = 0.0027, OR = 9.6 [95% CI: 2.2–42.2]), serum sodium (p = 0.0079, OR = 0.8 [95% CI: 0.77–0.96]), and contrast volume (p = 0.0385, OR = 1.8 [95% CI: 1.03–3.09]). In a multiple logistic regression model with stepwise method of selection, diabetes (p = 0.0120, OR = 3.2 [95% CI: 1.3–8.1]) and UACR (p = 0.0163, OR = 6.9 [95% CI: 1.4–33.4]) were the 2 risk factors finally identified. Conclusions: We have demonstrated that higher urine UACR is associated with the development of CIN in patients undergoing elective coronary angiography.

The findings on TC deciles may be attributed to a comparatively higher death rate in the female (compared with male) bottom decile, reflecting the autoimmune process-induced elevated risk in the lowest decile. Observations on HDLC confirmed presumed pro-inflammatory conversion in levels >50 mg/dL. These results have important clinical implications.

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