Prediction of the left ventricular mass index in hypertensive patients using the product of red cell distribution width and mean corpuscular volume.

The product of red cell distribution width (RDW) and mean corpuscular volume (MCV) has been identified as an indicator of target organ damage in cases of hypertension. However, the role of the RDW-MCV product in assessing carotid alteration, renal damage, and left ventricular hypertrophy in patients with hypertension has not been elucidated. In this cross-sectional study, a total of 1115 participants with hypertension were included. The RDW and MCV at admission were measured using an automated hematology analyzer. Organ damage was determined by the left ventricular mass index (LVMI), carotid intima-media thickness, and estimated glomerular filtration rate. The prevalence rates of carotid alteration and left ventricular hypertrophy were 57.0% and 18.0%, respectively. A higher RDW-MCV product and RDW were observed in hypertensive patients who developed carotid alteration. After adjusting for potential confounding factors, the correlations of the RDW-MCV product (P = .285) and RDW (P = .346) with carotid alteration were not significant. Moreover, the analysis of variance showed no significant correlation between RDW and LVMI (P = .186). However, the RDW-MCV product was higher in individuals with a high LVMI compared to those with a normal LVMI. Multivariable linear regression analysis revealed that the RDW-MCV product was independently associated with the LVMI (ß = 2.519, 95% CI: 0.921-4.116; P = .002), but not the estimated glomerular filtration rate (ß = -0.260, 95% CI: -2.031-1.511; P = .773). An elevated RDW-MCV product may be a predictor for left ventricular hypertrophy in patients with hypertension.

Circ_0006251 mediates the proliferation and apoptosis of vascular smooth muscle cells in CAD via enhancing TET3 and PPM1B expression.

Coronary artery disease (CAD) is a serious global problem that has been considered to be a major cause of death. Circular RNAs (circRNAs) as a key player in the regulation of cardiac progression and disease. Nevertheless, most circRNAs are poorly understood. In our research, we discussed the circ_TET3 (circ_0006251) function in the development of CAD. Firstly, circ_0006251 expression was measured through RT-qPCR analysis. Functional results prove the clear functionality of circ_0006251 for CAD. In addition, mechanism experiments including RIP, RNA pull-down and luciferase reporter results were applied to delve into the mechanisms of regulation of circ_0006251 in CAD. Results showed that Circ_0006251 expression was notably increased in PDGF-BB-induced VSMCs cells. Moreover, circ_0006251 interference mitigated the VSMCs cells proliferation and stimulated apoptosis after being treated with PDGF-BB. Furthermore, circ_0006251 targeted TET3 and PPM1B via sponging miR-361-3p, thereby contributing to CAD occurrence. In conclusion, Circ_0006251 could be identified as a biomarker for CAD which might shed light on the diagnosis and therapy of CAD.

Multiplicative interaction between mean corpuscular volume and red cell distribution width with target organ damage in hypertensive patients.

BACKGROUND: Accumulating evidence suggests that increased red cell distribution width (RDW) and mean corpuscular volume (MCV) were both poor prognostic factors for patients with cardiovascular diseases. Recently, the multiplicative interaction between RDW and MCV has been observed for predicting mortality in elderly patients without anemia; however, the relationship between the product of RDW-MCV and hypertension-induced target organ damage (TOD) has not been evaluated. METHODS: We performed a cross-sectional study in 1115 hypertensive patients. RDW and MCV were determined using automated hematology analyzers. Prevalence of TOD was evaluated by estimated glomerular filtration rate, carotid intima-media thickness, and left ventricular mass index. RESULTS: The prevalence of TOD was observed to be increased with the RDW or product of RDW-MCV quartiles. Moreover, RDW, MCV and product of RDW-MCV were significantly higher in patients with TOD compared to those without TOD. According to two logistic regression models, the associations of RDW and MCV with TOD were lost after adjustment for other factors. However, product of RDW-MCV remains an independent predictor of TOD, with per 0.4 fL increase in the product of RDW-MCV associated with a 16% increased risk of TOD (P=.012). CONCLUSIONS: The inclusion of MCV by calculating the product of RDW-MCV appears to enhance the association of RDW with TOD.