2021年 · 第01卷第01期

President of Chinese Society of Cardiology

Joseph A. Hill

Filippo Crea

Valentin Fuster

Jane Freedman

Ji-Guang Wang

Toshihisa Anzai

Changsheng Ma

Cardiovascular diseases (CVDs) have been recognized as the leading cause of death worldwide. It is estimated that CVDs led to 17.8 million deaths worldwide in 2017, increased by 21.1% from 2007.^[1]China is one of the countries that have the highest burden of CVDs with stroke and ischemic heart disease being the top two overall causes of deaths in China.^[2]The massive population with CVDs, the high mortality rate and disability rate, and the great burden to the society and the economy have significantly promoted investments in CVDs research globally, making it the fastest growing discipline in the medical field. Based on the recent major progress in CVDs prevention and treatment worldwide, with the changes brought by the COVID-19 pandemic, this article puts forward some ideas on the present situation and prospect of several key topics related to CVDs.

Since 1847 when Vogel, an eminent German pathologist, first observed that cholesterol was present in arterial plaques,^[1]atherosclerosis (AS) has been regarded as a cholesterol storage disease characterized by a passive deposition of cholesterol in the artery wall. One decade later, Virchow,^[2]a renowned pathologist, stated that AS is not really "a consequence of a fatty process but a direct product of inflammation" . Unfortunately, these early observations did not attract much attention from the cardiovascular community. It was not until the end of 19 century that pathologists began to recognize AS as an inflammatory disease,^[3]after many years of research in the new field of vascular biology by a number of groups, notably the one by Libby.^[4,5,6]From this moment, the discovery of a safe and effective anti-inflammatory therapy for AS has been a Holy Grail, but in reality a tough battle, for many physicians and scientists working in this field.

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.