Clinical value of long non-coding RNA KCNQ1OT1 in estimating the stenosis, lipid level, inflammation status, and prognostication in coronary heart disease patients.

Abstract

Long non-coding RNA KQT-like subfamily, member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) could regulate lipid metabolism, vascular smooth muscle cell function, inflammation, and atherosclerosis. This study aimed to evaluate whether lncRNA KCNQ1OT1 could serve as a biomarker for reflecting coronary heart disease (CHD) patients' disease situation and prognosis. LncRNA KCNQ1OT1 expression was determined in peripheral blood mononuclear cells from 267 CHD patients, 50 disease controls (DCs) (unexplained chest pain), and 50 healthy controls (HCs) by the RT-qPCR method. TNF-α, IL-17A, VCAM-1, and ICAM-1 were determined by the ELISA procedure in serum from CHD patients only. The mean (95% confidential interval) follow-up duration was 16.0 (15.3-16.8) months. LncRNA KCNQ1OT1 was highest in CHD patients, followed by DCs, and lowest in HCs (p < 0.001). LncRNA KCNQ1OT1 could distinguish the CHD patients from DCs (area under the curve [AUC]: 0.757) and from the HCs (AUC: 0.880). LncRNA KCNQ1OT1 was positively associated with triglyceride (p=0.026), low-density lipoprotein cholesterol (p=0.023), cardiac troponin I (p=0.023), and C-reactive protein (p=0.001). Besides, lncRNA KCNQ1OT1 was also positively linked with the Gensini score (p=0.008). Furthermore, lncRNA KCNQ1OT1 was positively related to the TNF-α (p < 0.001), IL-17A (p=0.008), and VCAM-1 (p=0.003). LncRNA KCNQ1OT1 was elevated in CHD patients with MACE compared to those without MACE (p=0.006); moreover, lncRNA KCNQ1OT1 high was associated with shorter MACE-free survival (p=0.018). Circulating lncRNA KCNQ1OT1 expression not only reflects the stenosis degree, blood lipid level, and inflammation status but also predicts the MACE risk, while a large-scale study is needed for verification.