2021年 · 第01卷第01期

The coexistence of coronary artery disease (CAD) and atrial fibrillation (AF) is common in clinical practice. Patients with CAD require antiplatelet therapy to reduce the occurrence of myocardial ischemic events. However, patients with AF at high risk of thromboembolism require oral anticoagulants to reduce the occurrence of thromboembolic events such as stroke. In cases where CAD coexists with AF, the combined use of antiplatelet and anticoagulation therapy can effectively reduce the risk of ischemic and thromboembolic events but increase the risk of bleeding at the same time. The optimal antithrombotic regimen in patients with both CAD and AF has been controversial in clinical practice. In recent years, the expert consensuses on antithrombotic therapy in patients with AF presenting with acute coronary syndrome and/or undergoing percutaneous coronary intervention have been successively released in Europe and North America, and have been updated in a timely manner. In contrast, the guidelines on antithrombotic therapies in China are lacking. Based on published clinical evidence, this consensus incorporated relevant international and Chinese guidelines, consensuses, and expert recommendations, and addressed the issues encountered in the clinical practice of antithrombotic therapy in patients with AF and different types of CAD. The current guideline is of great significance to guide treatment in patients with both CAD and AF in China.

Objective: Previous studies indicated that patients with atrial fibrillation (AF) and moderate-to-severe chronic kidney disease (CKD) are at a higher risk of thromboembolism and bleeding during anticoagulation. Whether mild CKD is associated with an increased risk of thromboembolism and bleeding in AF patients remains unknown. This study aimed to evaluate the impact of mild CKD on thromboembolism and major bleeding among patients with AF. Methods: Baseline serum creatinine was available in 17,559 of 25,512 patients enrolled in the China-AF study between August 2011 and December 2018. After excluding those who underwent AF ablation or with moderate-to-severe CKD, 7191 non-valvular AF patients (2059 with mild CKD and 5132 with normal renal function) with regular follow-up for at least 6 months were included. Primary outcomes were the time to the first occurrence of thromboembolic and major bleeding events. Results: Over a mean follow-up of (44.4 ± 23.4) months, 639 thromboembolism and 231 major bleeding events occurred. The crude incidence rates of thromboembolism were higher in the mild CKD group than that of the normal renal function group (3.0/100 person-years vs. 2.2/100 person-years, P < 0.0001), while the crude incidence rates of major bleeding were comparable between the two groups (1.0/100 person-years vs. 0.8/100 person-years, P= 0.076). After multivariate analyses, mild CKD was not associated with an increased risk of thromboembolism (HR = 1.05, 95% CI: 0.89-1.25, P= 0.547) or major bleeding (HR = 1.11, 95% CI: 0.84-1.47, P= 0.476). Conclusions: Mild CKD was not an independent risk factor of thromboembolism or major bleeding in patients with AF.

Objective: Coronavirus disease 2019 (COVID-19) is a global public health crisis. There are no specific antiviral agents for the treatment of SARS-CoV-2. Information regarding the effect of Abidol on in-hospital mortality is scarce. The present study aimed to evaluate the treatment effect of Abidol for patients with COVID-19 before and after propensity score matching (PSM). Methods: This retrospective cohort study analyzed 1019 patients with confirmed COVID-19 in China from December 22, 2019 to March 13, 2020. Patients were divided to Abidol (200 mg, tid, 5-7 days, n = 788, 77.3%) and No-Abidol (n = 231, 22.7%) groups. The primary outcome was the mortality during hospitalization. Results: Among 1019 COVID-19 patients, the age was (60.4 ± 14.5) years. Abidol-treated patients, compared with No-Abidol-treated patients, had a shorter duration from onset of symptoms to admission, less frequent renal dysfunction, lower white blood cell counts (lymphocytes <0.8) and erythrocyte sending rate, lower interleukin-6, higher platelet counts and plasma IgG and oxygen saturation, and less frequent myocardial injury. The mortality during hospitalization before PSM was 17.9% in Abidol group and 34.6% in No-Abidol (hazard ratio (HR) = 2.610, 95% confident interval (CI): 1.980-3.440), all seen in severe and critical patients. After PSM, the in-hospital death was 13.6% in Abidol and 28.6% in No-Abidol group (HR= 2.728, 95% CI: 1.598-4.659). Conclusions: Abidol-treatment results in less in-hospital death for severe and critical patients with COVID-19. Further randomized study is warranted to confirm the findings from this study.

Endothelial dysfunction characterized by impaired endothelium-dependent vaso-relaxation is one of the earliest detectable pathological events in smoking, diabetes, and many cardiovascular diseases including hypertension, atherosclerosis. Overwhelming data from human and animals demonstrate that the endothelial dysfunction associated with diabetes is due to the local formation of oxidants and free radicals. However, the mechanisms by which diabetes instigates oxidative stress, and those by which oxidative stress perpetuates endothelial dysfunction are the subjects of intensive research in the last 3 decades. The studies from us and others have demonstrated that adenosine monophosphate-activated protein kinase (AMPK), a well-characterized energy sensor and modulator, serves as a highly efficient sensor as AMPK can be activated by very low levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) generated by physiological, pharmacological, and pathologic stimuli (redox sensor). Interestingly, oxidants-activated AMPK feedback lowers the levels of ROS by either suppressing ROS/RNS from reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and mitochondria or by increasing the levels of antioxidant enzymes (redox modulator). Further, our studies demonstrate that AMPK’s functions as a redox sensor and modulator are vital to maintain endothelial cell function under physiological conditions. Finally, we discover that under chronic oxidative stress or large influx of ROS, AMPK is particularly susceptible to inhibition by ROS. We conclude that oxidative inactivation of AMPK in diabetes perpetuates oxidative stress and accelerates atherosclerosis in diabetes.