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Abstract Background: It has been shown that seropositive patients with rheumatoid arthritis are susceptible to cardiovascular disease. Methods In this cross-sectional research, we evaluated patients with RA who were referred to our clinic from October 2017 to August 2018. All patients underwent transthoracic echocardiography and determination of plasma autoantibodies after being refused admission of concomitant CVD. Result We investigated 135 patients with RA. In addition, the plasma measurements of anti-citrullinated protein and anti-modified citrullinated vimentin antibodies were negatively correlated with left ventricular ejection fractions. The receiver operating characteristic curve revealed that anti-MCV antibody titer u2265547. 5 indicates reduced LVEF with a sensitivity of 85 percent and specificity of 93%. Conclusions The results revealed a strong inverse correlation between anti-MCV antibody titer and LVEF, according to the authors. These findings show that anti-MCV's use is promising for cardiac screening and early detection of cardiac systolic dysfunction.
Source link: https://doi.org/10.1186/s12872-020-01676-x
Quercetin's cardiovascular disease models and attributed to senolysis have mainly been investigated. We hypothesized that Q could mitigate murine cardiac arrest resulting from HFD by reestablishing the myocardial microcirculation. For six months, C57BL/6J mice were fed standard chow or HFD for six months and then treated with Q or vehicle 5-day biweekly for ten weeks. In HFD vs. control mice, the ejection fraction was lower in HFD vs. control mice, but it was much higher in HFD+Q mice. Cardiomyocyte hypertrophy, antioxidant overload, and vascular rarefaction were all reduced by cardiac fat accumulation and reduced HFD-induced cardiac fibrosis, cardiovascular fat accumulation, oxidative stress, and vascular rarefaction. Cardiac senescence was not present in any group. In vitro, ox-LDL reduced HUVEC tube formation rate, which Q effectively improved. Quercetin can specifically induce angiogenesis and decrease myocardial oxidative stress in the murine HFD-fed murine heart independently of senolytic activity.
Source link: https://doi.org/10.1155/2021/8875729
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