Volume 01 · Issue 01 · 2021

中华心脏病学会会长

约瑟夫·A·希尔

菲利普创造

瓦伦丁·福斯特

简·弗里德曼

王继光

安宰俊久

马长生

心血管疾病（CVDs）已被公认为全球死亡的主要原因。据估计，2017年心血管疾病导致全球1780万人死亡，比2007年增加了21.1%。^[1]中国是心血管疾病负担最高的国家之一，中风和缺血性心脏病是中国死亡的前两大原因。^[2]庞大的CVDs人群、高死亡率和高致残率以及对社会和经济的巨大负担极大地促进了全球对CVDs研究的投资，使其成为医学领域发展最快的学科。基于近期全球范围内CVDs防治的重大进展，随着新冠肺炎疫情带来的变化，本文就与CVDs相关的几个关键课题的现状和前景提出了一些设想。

自1847年德国著名病理学家沃格尔首次观察到动脉斑块中存在胆固醇以来，^[1]动脉粥样硬化(AS)被认为是一种胆固醇贮积疾病，其特征在于胆固醇在动脉壁中的被动沉积。十年后，Virchow，^[2]一位著名的病理学家指出，AS并不是真正的“脂肪过程的结果，而是炎症的直接产物”。不幸的是，这些早期观察并没有引起心血管界的太多关注。直到19世纪末，病理学家才开始认识到AS是一种炎症性疾病，^[3]经过许多小组，特别是Libby在血管生物学的新领域多年的研究。^[4,5,6]从这一刻起，对于在该领域工作的许多医生和科学家来说，发现一种安全有效的AS抗炎疗法一直是一个圣杯，但实际上是一场艰苦的战斗。

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.

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.

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).

Mild CKD was not an independent risk factor of thromboembolism or major bleeding in patients with AF.

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).

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.

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).

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.