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Objective No data are available to develop uniform recommendations for reperfusion therapies in ST-segment elevation myocardial infarction (STEMI) during the coronavirus disease 2019 (COVID-19) pandemic. We aimed to fill the evidence gap regarding STEMI reperfusion strategy during the COVID-19 era. Methods Clinical characteristics and outcomes for 17 patients with STEMI who received fibrinolysis during the COVID-19 pandemic were compared with 20 patients who received primary percutaneous coronary intervention (PPCI), and were further compared with another 41 patients who received PPCI in the pre-COVID-19 period. Results In patients with STEMI, fibrinolysis achieved a comparable in-hospital and 30-day primary composite end point, as compared with those who received PPCI during the COVID-19 pandemic. No major bleeding was detected in either group. Compared patients with STEMI who received PPCI in the pre-COVID-19 period, we found a remarkable extension of chest pain onset-to-first medical contact (FMC) and FMC-to-wire crossing times, significantly increased number and length of stents, and much worse thrombolysis in myocardial infarction flow in patients with STEMI who received PPCI during the COVID-19 pandemic. Conclusion Owing to its considerable efficacy and safety and advantages in conserving medical resources, we recommend fibrinolysis as a reasonable alternative for STEMI care during the COVID-19 pandemic.

ObjectivesThe higher than expected PFO rate in CS patients has raised concerns that paradoxical embolism maybe the pathophysiologic mechanism for strokes. However, only a small proportion of pathogenic PFOs cause CS. Therefore, accurate recognition of patients with pathogenic PFOs among all CS patients could guide clinical decision making in selecting the most appropriate treatment. The aim of this study was to devise a new algorithm to stratify cryptogenic stroke (CS) patients into pathogenic patent foramen ovale (p‐PFO)‐ and non‐p‐PFO‐related patients.MethodsA total of 1201 patients with acute ischemic stroke were recruited from two different medical centers, and 253 CS patients were identified. Of the 253 patients, 111 were diagnosed with PFO using contrast transcranial Doppler. Data on medical histories, neuroimaging and laboratory tests were compared in CS patients with or without PFO.ResultsCompared with PFO‐negative CS patients, PFO‐positive CS patients showed younger onset age, lower incidence of hypertension and dyslipidemia, characteristic infarction pattern in magnetic resonance imaging and specifically altered platelet activity and coagulation function. Based on the above information, we constructed a PFO judgment formula (Hr‐PFOJ) by means of feature weight estimation and predictive performance evaluation to predict pathogenic PFO in CS patients with a sensitivity of 76.3% and a specificity of 66.5%.InterpretationsHr‐PFOJ judgment formula is a useful screening tool for identification of patients with pathogenic PFO who may benefit from PFO‐related treatment.

KeywordsCoronary artery disease · MicroRNA-136-3p · Cardiac microvascular endothelial cells · EIF5A2 · Rho A/ROCK signaling pathway Abstract Objective: Coronary artery disease (CAD) is a cardiovascular disease that poses a fatal threat to human health, and the identification of potential biomarkers may help to delineate its pathophysiological mechanisms. Accumulating evidence has implicated microRNAs (miRNAs) in the pathogenesis and development of cardiovascular diseases. The present study aims to identify the expression of miRNA-136-3p (miR-136-3p) in CAD and further investigate its functional relevance in myocardial injury both in vitro and in vivo. Methods: Initially, CAD models were induced in rats by high-fat diet and intraperitoneal injection of pituitrin. Next, the effect of overexpressed miR-136-3p on cardiac function and pathological damage in myocardial tissue, cardiomyocyte apoptosis, oxidative stress and inflammatory response were assessed in CAD rats. Rat cardiac microvascular endothelial cells (CMECs) were isolated and cultured by the tissue explant method, and the CMEC injury model was induced by homocysteine (HCY). The function of miR-136-3p in vitro was further evaluated. Results: miR-136-3p was poorly expressed in the myocardial tissue of CAD rats and CMEC injury models. In vivo assays indicated that overexpressed miR-136-3p could improve cardiac function and alleviate pathological damage in myocardial tissue, accompanied by reduced oxidative stress and inflammatory response. Moreover, in vitro assays suggested that overexpression of miR-136-3p enhanced proliferation and migration while inhibiting apoptosis of HCY-stressed CMECs. Notably, we revealed that EIF5A2 was a target gene of miR-136-3p, and miR-136-3p inhibited EIF5A2 expression and activation of the Rho A/ROCK signaling pathway. Conclusion: In conclusion, the overexpression of miR-136-3p could potentially impede myocardial injury in vitro and in vivo in CAD through the blockade of the Rho A/ROCK signaling pathway, highlighting a potential miR-136-3p functional relevance in the treatment of CAD.

Objective: This study was designed to investigate the effects of leukocyte Rho kinase activity and serum Cystatin C (Cys C) on cardiovascular events in patients with acute coronary syndrome (ACS). Methods: A total of 48 patients with ST-segment elevation myocardial infarction (STEMI), 23 patients with non-ST-segment elevation myocardial infarction (NSTEMI), 25 patients with unstable angina (UA) and 20 patients with no-acute coronary syndrome as control from January 2017 to June 2018 in Tianyou Hospital affiliated to Wuhan University of Science and Technology were selected in this study. Western blot was used to detect the leukocyte Rho kinase activity and Elisa kit was used to measure serum Cys C. Univariate and multivariate analysis were used to analyze the influencing factors of cardiovascular events in ACS patients. Results: The activity of leukocyte Rho kinase and serum Cys C were gradually reduced in the STEMI, NSTEMI and UA patients, but all significantly higher than that in No-ASC patients, and there was a positive correlation between leukocyte Rho kinase activity and serum Cys C in ACS patients (r = 0.516, P < .001). The activity of leukocyte Rho kinase was positively correlated with the levels of serum TNF-α (r = 0.634, P < .001), IL-6 (r = 0.578, P < .001), IL-8 (r = 0.582, P < .001) in ACS patients, and the level of Cys C was positively correlated with the levels of serum TNF-α (r = 0.634, P < .001), IL-6 (r = 0.578, P < .001), IL-8 (r = 0.582, P < .001) in ACS patients. Univariate and multivariate analysis showed that the leukocyte Rho kinase activity (HR = 2.994, 95%CI = 1.328–6.054, P < .0001) and the levels of serum Cys C (HR = 1.692, 95%CI = 1.028–2.124, P < .0001) were independent influencing factors of cardiovascular events in ACS patients. Conclusion: The leukocyte Rho kinase activity and serum Cystatin C are high in acute coronary syndrome patients, and are the independent influencing factors of cardiovascular events in ACS patients.