[Hypoxia and inflammation are risk factors for acute myocardial injury in patients with coronavirus disease 2019].

OBJECTIVE: To investigate the risk factors for acute myocardial injury in coronavirus disease 2019 (COVID-19) patients. METHODS: This is a retrospective analysis of a COVID-19 cohort, in which 149 confirmed COVID-19 patients enrolled were divided into the group of myocardial injury (19 cases) and the group of non-myocardial injury (130 cases). Myocardial injury was defined according to Fourth universal definition of myocardial infarction released by European Society of Cardiology (ESC) in 2018, that cardiac troponin (cTn) was above 99th percentile of the reference level. Clinical information and results of laboratory tests of the eligible patients were collected. Factors associated with myocardial injury in COVID-19 patients were evaluated. RESULTS: Compared with the group of non-injury, the patients in the group of injury were older and had a larger proportion of severe or critical cases (P < 0.05), higher respiratory rate and lower percutaneous oxygen saturation (SpO2) without oxygen therapy on admission (P < 0.05). All inflammatory indexes except for tumor necrosis factor α (TNF-α) showed significant elevation in the patients of the group of injury (P < 0.05). Analyzed by Spearman correlation test, we showed that the levels of circulatory cTnI were in positive correlation with the levels of high-sensitivity C-reactive protein (hs-CRP), ferritin, receptor of interleukin-2 (IL-2R), interleukin-6 (IL-6) and interleukin-8 (IL-8) (ρ > 0, P < 0.05). Lower SpO2 without oxygen therapy on admission (OR: 0.860, 95%CI: 0.779-0.949, P=0.003) and higher plasma IL-6 levels (OR: 1.068, 95%CI: 1.019-1.120, P=0.006) were independent risk factors for acute myocardial injury in the patients with COVID-19 by multivariate Logistic regression analyses. CONCLUSION: Hypoxic state and inflammation may play a key role in the pathogenesis of acute myocardial injury in COVID-19 patients.

[Relationship between angiopoietin-2 and vascular endothelial factor and vasodilation function in hypertensive patients].

Objective: To analyze the relationship between angiopoietin 2 (Ang2) and vascular endothelial factor and vasodilation function in hypertensive patients. Methods: Patients with new onset grade 1~2 hypertension (n=40) and healthy control group (n=25) wereenrolledprospectively. Serum Ang2 and nitric oxide (NO), nitric oxide synthase (eNOS), endothelin-1 (ET-1) were measured in both groups. Flow-mediated vasodilation (FMD) were measured in hypertensive patients. The above indicators were reviewed in hypertensive patients after antihypertensive treatment until blood pressure<140/90 mmHg. Results: Compared with the control group, serum Ang2 (P=0.049) and ET-1 (P<0.001) were significantly higher. Serum NO (P<0.001) and eNOS (P<0.001) was significantly lower in the hypertensive group. Compared with baseline, serum Ang2 (P=0.049) and ET-1 (P<0.001) were decreased significantly, meanwhile serum NO (P<0.001) and eNOS (P<0.001) were significantly increased. Serum Ang2 after antihypertensive treatment was not significantly different from that of the control group, but no statistical difference was observed in FMD after antihypertensive therapy. Correlation analysis found that serum Ang2 was positively correlated with mean arterial pressure (R=0.432, P<0.001), and negative correlated with serum NO(R=-0.374, P=0.001) and FMD (R=-0.368 0, P=0.002). Multiple linear regression found that serum Ang2 was independently associated with body mass index, mean arterial pressure, and serum NO. Conclusion: Serum Ang 2 can reflect the degree of endothelial and vasodilation impairment in hypertensive patients. Antihypertensive therapy can improve endothelial function, but whether it can restore damaged vasodilation function needs further verification.