Left ventricular diastolic dysfunction (LVDD) is common in hypertension and is a predictor of increased cardiovascular risk, however the effect of LVDD, detected by new guideline, on major adverse cardiac events (MACE) is unknown in hypertensive patients without known cardiovascular disease. The present study aims to evaluate LVDD in a community hypertension cohort study and assess the effect of LVDD on MACE. we studied 283 asymptomatic nonischemic patients with hypertension who had baseline echocardiogram between 2012 and 2014. Patients were followed for MACE (myocardial infarction, coronary revascularization procedures, heart failure, stroke, all-cause mortality) with mean follow-up of 5.4 years. A Cox proportional hazards model was used to assess the association of LVDD with MACE. At baseline, 35 of the 283 hypertensions were diagnosed with LVDD (12.3%) and 25 patients were women (15.5%). Women had higher frequency of LVDD than men (8%). During follow-up, there were 26.6% patients occurring MACE in the LVDD group at baseline, 9.9% patients occurring MACE in the group with normal diastolic function. In multivariable Cox regression analyses, LVDD was a stronger predictor of MACE (HR: 2.5; 95% CI: 1.20 to 5.25; c- statistics 0.805) than E/e′ ratio (HR: 1.13; 95% CI: 1.04 to 1.22). LVDD was strongly associated with MACE in hypertension patients.

Background: Atherosclerosis is the most common cause of cardiovascular disease, accompanied by high mortality and poor prognosis. Low-density lipoprotein (LDL) and its oxidized form oxidized low-density lipoprotein (oxLDL) play an important role in atherosclerosis. This article will explore the role of the lncRNA COLCA1 (colorectal cancer associated 1)/hsa-miR-371a-5p/SPP1 (secreted phosphoprotein 1) pathway in oxLDL in causing human coronary artery endothelial cells (HCAECs) inflammation and related biological function changes.Methods: OxLDL was used to stimulate HCAECs. The inflammatory response and biological function changes of HCAECs were analyzed, total RNA-seq was performed on HCAECs before and after stimulation, and RT-Qpcr (real-time quantitative PCR) was used to verify the differential genes. Interference of the expression of COLCA1 in HCAECs was performed by siRNA interference technology to verify the role of COLCA1 in the biological function changes of HCAECs after oxLDL stimulation, and further prove that COLCA1 affects SPP1 through hsa-miR-371a-5p.Results: OxLDL can affect the oxidative stress response of HCAECs, which in turn affects the apoptosis and wound healing ability of HCAECs. COLCA1 and SPP1 were highly expressed after oxLDL stimulation, while hsa-miR-371a-5p was the opposite. After COLCA1 interference, the oxidative stress level of HCAECs stimulated by oxLDL decreased, the apoptosis level also significantly decreased, and the wound healing ability was enhanced. After simultaneous COLCA1 interference and recovery of the expression of hsa-miR-371a-5p, these improved functions disappeared. The dual-luciferase assay confirmed that hsa-miR-371a-5p and COLCA1, hsa-miR-371a-5p and SPP1 has binding targets.Conclusions: OxLDL can up-regulate the expression of COLCA1 in HCAECs, which in turn affects the intracellular COLCA1/hsa-miR-371a-5p/SPP1 pathway to regulate the level of oxidative stress in cells. This in turn affects the level of apoptosis and wound healing ability, which causes cells to produce a continuous inflammatory response.

To compare the predictive value of mortality between left ventricular hypertrophy (LVH) defined by Chinese thresholds and defined by international guidelines in hypertension individuals and investigate better indexation methods for LVH in Chinese population. We included 2454 community hypertensive patients with Left ventricular mass (LVM) and relative wall thickness. LVM was indexed to body surface area (BSA), height2 7 and height 1 7. The outcomes were all‐cause and cardiovascular mortality. Cox proportional hazards models were used to explore the association between LVH and the outcomes. C‐statistics and time‐dependent receiver operating characteristic curve (ROC) was used to evaluate the value of those indicators. During a median follow‐up of 49 months (interquartile range 2–54 months), 174 participants (7.1%) died from any cause (n = 174), with 71 died of cardiovascular disease. LVM/BSA defined by the Chinese thresholds was significantly associated with cardiovascular mortality (HR: 1.63; 95%CI: 1.00‐2.64). LVM/BSA was significantly associated with all‐cause mortality using Chinese thresholds (HR: 1.56; 95%CI: 1.14‐2.14) and using Guideline thresholds (HR: 1.52; 95%CI: 1.08‐2.15). LVM/Height1.7 was significantly associated with all‐cause mortality using Chinese thresholds (HR: 1.60; 95%CI: 1.17‐2.20) and using Guideline thresholds (HR: 1.54; 95%CI: 1.04‐2.27). LVM/Height2.7 was not significantly associated with all‐cause mortality. C‐statistics indicated that LVM/BSA and LVM/Height1.7 by Chinese thresholds had better predictive ability for mortality. Time‐ROC indicated that only LVM/Height1.7 defined by Chinese threshold had incremental value for predicting mortality. We found that in community hypertensive populations, race‐specific thresholds should be used to classify LV hypertrophy related to mortality risk stratification. LVM/BSA and LVM/Height1.7 are acceptable normalization method in Chinese hypertension.