Prevalence of Coronary Artery Disease in Patients Undergoing Valvular Heart Surgery.

BACKGROUND: The risk of coronary artery disease (CAD) in different valve dysfunction has been unclear. METHODS: We reviewed patients, who underwent valve heart surgery and coronary angiography from 2008 to 2021, at our center. RESULTS: A total of 7,932 patients were included in the present study, and 1,332 (16.8%) had CAD. The mean age of the study cohort was 60.5±7.9 years, and 4,206 (53.0%) were male. CAD was 21.4% in aortic disease, 16.2% in mitral valve disease, 11.8% in isolated tricuspid valve disease, and 13.0% in combined aortic and mitral valve disease. Patients with aortic stenosis were older than those with regurgitation (63.6±7.4 years vs. 59.5±8.2 years, P < 0.001), and the CAD risks also were higher (28.0% vs. 19.2%, P < 0.001). The age difference was minimal (60.6±8.2 years vs. 59.5±6.7 years, P = 0.002) between patients with mitral valve regurgitation and stenosis, but the risks of CAD were twice high in regurgitation (20.2% vs. 10.5%, P < 0.001). When the type of valve impairment was not considered, non-rheumatic etiology, advanced age, male sex, hypertension, and diabetes were independent predictors of CAD. CONCLUSION: In patients undergoing valve surgery, the prevalence of CAD was influenced by conventional risk factors. Importantly, CAD also was associated with the type and etiology of valve diseases.

Alteration in microRNA-25 expression regulate cardiac function via renin secretion.

Heart failure arises from diverse cardiovascular diseases, including hypertension, ischemic disease and atherosclerosis, valvular insufficiency, myocarditis, and contractile protein mutations. MicroRNAs are dysregulated in heart failure, but identification of the specific microRNAs involved remains incomplete. Here, we evaluate miR-25 expression in the peripheral blood from healthy, dilated cardiomyopathy (DCM), remote infarct (OMI), hypertensive heart disease (HHD), and HHD resulting in heart failure (HHDF) using q-PCR. Interestingly, we discovered miR-25 expression in humans is initially decreased at the onset of heart failure but is later increased in end-stage heart failure. We also show that overexpression of miR-25 in normal mice causes cardiomyocyte fibrosis and apoptosis. However, inhibition of miR-25 in normal mice led to activate renin-angiotensin system (RAS) and high blood pressure, mild heart dilation. Notably, the miR-25 cluster knock-out mice was also characterized high blood pressure and no obvious cardiac function alteration. RNA sequencing showed the alteration of miR-25 target genes in angomir-treated mice, including the renin secretion signal related gene. In vitro, cotransfection with the miR-25 antagomir repressed luciferase activity from a reporter construct containing the Pde3a and Cacnalc untranslated region. In summary, miR-25 expression during different stages of heart disease, offers a new perspective for the role of miR-25 function in heart failure.