A new infectious outbreak sustained by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is now spreading all around the world. The aim of this study was to evaluate the prognostic value of left ventricular global longitudinal strain (LV-GLS) and right ventricular longitudinal strain (RV-LS) in patients with coronavirus disease 2019 (COVID-19). In this prospective, single-center study, data were gathered from patients treated for COVID-19 between April 15 and April 30, 2020. Two-dimensional echocardiography (2-DE) and speckle tracking echocardiography (STE) images were obtained for all patients. Patients were divided into three groups: those with severe COVID-19 infection, those with non-severe COVID-19 infection, and those without COVID-19 infection (the control group). Data regarding clinical characteristics and laboratory findings were obtained from electronic medical records. The primary endpoint was in-hospital mortality. A total of 100 patients hospitalized for COVID-19 were included in this study. The mean age of the severe group (n = 44) was 59.1 ± 12.9, 40% of whom were male. The mean age of the non-severe group (n = 56) was 53.7 ± 15.1, 58% of whom were male. Of these patients, 22 died in the hospital. In patients in the severe group, LV-GLS and RV-LS were decreased compared to patients in the non-severe and control groups (LV-GLS:

CFR is impaired in subjects with prehypertension, but this impairment is not as severe as that in hypertension.

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Although uric acid (UA) is considered as an antioxidant, the relationship between serum UA levels and cardiovascular diseases is not clear yet. Higher brachial artery resting diameter (BD), impaired brachial artery flow-mediated dilatation (FMD), increased carotid intima-media thickness (IMT), decreased aortic distensibility (AoD), and increased aortic stiffness index (AoSI) and elastic modulus (AoEM) are predictors for development and/or progression of atherosclerosis. In this study, BD, FMD, carotid IMT, AoD, AoSI and AoEM were studied in healthy subjects with UA concentrations in physiological range. One hundred 24 healthy volunteers between 26 and 55 years of age were included in this study. Each subject had a serum UA levels in normal range. Carotid IMT, BD and brachial FMD were measured by means of high-resolution vascular ultrasound. AoD, AoSI, AoEM were examined by transthoracic echocardiography. Endothelium-dependent dilatation (EDD) was assessed by establishing reactive hyperemia and endothelium-independent dilatation (EID) was determined by using sublingual isosorbide dinitrate. Although carotid IMT and EDD were significantly correlated with UA concentrations (r = 0.346, p < 0.0001; r = -0.255, p < 0.05, respectively), EID measurements were not significantly correlated with serum UA concentrations (r = - 0.105, p > 0.05). In addition, AoSI and AoEM were significantly correlated with serum UA levels (r = 0.368, p < 0.0001; r = -0.366, p < 0.0001, respectively), and there was a significant inverse correlation between AoD and serum UA concentrations (r = -0.366, p < 0.0001). Furthermore, in multivariate analysis, we found that serum UA concentrations were correlated with increased carotid IMT, reduced FMD and increased aortic stiffness independent of other cardiovascular risk factor (beta = 256, p = 0.002; beta = -193, p = 0.03; beta = 0.295, p < 0.0001, respectively). In healthy subjects, increased serum UA concentrations, even in physiological range, are a risk factor for increased carotid IMT, reduced FMD and increased aortic stiffness independent of other cardiovascular risk factor, and other factors related to the metabolic syndrome.

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