Galectin-3 as a Novel Biomarker for Predicting Clinical Outcomes in Hospitalized COVID-19 Patients.

BACKGROUND: Galectin-3 has been shown to play a key pathophysiological role in pulmonary associated inflammatory response and lung fibrosis in COVID-19 and is a mediator for viral adhesion. However, there is limited data about its potential role in severity and prognosis of COVID-19. This study aimed to investigate the predictive role of serum galectin-3 concentrations in the severe clinical outcomes of hospitalized COVID-19 patients: the severity of pneumonia, in-hospital mortality, and the need for intensive care unit (ICU) admission. METHODS: This single-center study included 68 patients with laboratory- and radiologically-confirmed COVID-19 admitted to our emergency department. The study population was divided into patients with primary clinical out-comes (n = 32) and those without (n = 36). The need for ICU admission and/or in-hospital mortality were the primary clinical endpoints. The study group was also classified based on pneumonia severity: severe or mild/moderate. Blood samples were collected within 48 hours of admission to estimate serum galectin-3 concentrations. RESULTS: Multivariate regression analysis showed that lower concentrations of galectin-3 and arterial oxygen saturation (SpO2) were independently associated with the primary clinical outcomes (OR = 0.951, p = 0.035; OR = 0.862, p = 0.017, respectively); increased concentrations of galectin-3 were an independent predictor of severe pneumonia (OR = 1.087, p = 0.016). In the receiver operating characteristics curve analysis, serum galectin-3 concentrations at hospital admission predicted pneumonia severity with 52.1% sensitivity and 90% specificity with a cutoff of 38.76 ng/mL. CONCLUSIONS: Circulating galectin-3 at hospital admission could be a useful biomarker for identifying COVID-19 patients at high risk for severe pneumonia.

Doppler-derived strain imaging detects left ventricular systolic dysfunction in children with Turner syndrome.

OBJECTIVES: Children with Turner syndrome (TS) are at increased risk of cardiovascular disease (CVD), but associations with subclinical CVD are not well-characterized. The purpose of this study was to assess myocardial function using strain imaging (SI) by echocardiography in children with TS and without known CVD. METHODS: The study included 48 children with TS aged 4-16 years and 20 healthy control children. Children with TS were excluded if they had a cardiac malformation, a decreased left ventricular (LV) systolic function, or any chronic disease. Each child had an echocardiographic examination with conventional echocardiography and one-dimensional longitudinal strain (1DST) echocardiography. RESULTS: Septal and lateral systolic strain (S) and strain rate (SR) values, which are indicative of longitudinal myocardial function, were significantly decreased in TS patients. However, LV ejection fraction (LVEF) and LV fractional shortening (LVFS) was not significantly different between groups. LV mass index (LVMi), interventricular septum (IVS) thickness, LV posterior wall (LVPW) thickness, and left atrial (LA) diameter index were significantly higher in TS children compared to controls. Peak transmitral flow velocity in late diastole (peak A) was significantly higher, whereas peak transmitral flow velocity in early diastole (peak E), deceleration time (DT), and the ratio of early to late diastolic filling were significantly lower, in TS patients. CONCLUSION: Reduced LV systolic S and SR in children with TS may indicate early myocardial dysfunction before any detectable change in LVEF.

Impact of vitamin D insufficiency on the epicardial coronary flow velocity and endothelial function.

OBJECTIVE: Increasing evidence suggests a relationship between vitamin D (VD) insufficiency and cardiovascular disease. The present study evaluated the effect of VD insufficiency on epicardial coronary flow rate, subclinical atherosclerosis, and endothelial function. METHODS: The present study was cross-sectional and observational. We enrolled 222 consecutive patients who had undergone coronary angiography for suspected ischemic heart disease and were found to have normal or near-normal coronary arteries. Thereafter, 25(OH)D3 levels were measured and the coronary flow rate was assessed using the thrombolysis in myocardial infarction frame count. Slow coronary flow (SCF) was defined as a thrombolysis in myocardial infarction frame count greater than 27/frame. Endothelial function was assessed by brachial artery flow-mediated dilatation. Carotid intima-media thickness, an indicator of subclinical atherosclerosis, was measured using B-mode ultrasonography. RESULTS: The mean level of 25(OH)D3 was 31.8 ng/ml, and 47% (n=106) of the patients had insufficient 25(OH)D levels (<30 ng/ml). Baseline characteristics were similar between VD-insufficient and VD-sufficient groups. The incidence of SCF was significantly higher in the VD-insufficient group than in patients with sufficient VD (relative risk=3.5, 95% confidence interval=1.1-10.5, P=0.01). After adjusting for cardiovascular disease risk factors, VD insufficiency was independently associated with SCF. The linear regression analysis showed that VD insufficiency was correlated independently with % flow-mediated dilatation (ß=0.424, P<0.001) and carotid intima-media thickness (ß=0.43, P<0.001). CONCLUSION: A strong association was found between VD insufficiency and the SCF phenomenon. In addition, VD insufficiency was associated with endothelial dysfunction and subclinical atherosclerosis. We believe that further studies are required to clarify the role of VD in patients with SCF.