Dear Editor,

We read with great interest the article entitled “Hydroxychloroquine and Cardiovascular Events in Patients with Rheumatoid Arthritis” [1] previously published in the journal Cardiovascular Drugs and Therapy. We searched for and read some previous studies on the relationship between hydroxychloroquine (HCQ) and cardiovascular disease (CVD). We would like to discuss some points about the effect of HCQ on CVD in patients with rheumatoid arthritis (RA).

In this article, the authors [1] found that HCQ was associated with lower rates of major adverse cardiac events (MACE) (HR: 0.827, 95% CI: 0.8,0.86) in patients with RA [1]. This study indicated that HCQ plays a protective role in CVD in patients with RA. Some previous studies also supported this view. Shapiro et al. revealed that the use of HCQ is independently associated with decreased risk for cardiovascular morbidity among patients with RA [2]. Similarly, a systematic review and meta-analysis suggested that HCQ was associated with a reduced risk of CVD in patients with rheumatic diseases [3]. All the above studies indicated that HCQ is beneficial to the cardiovascular system.

The cardiotoxicity of HCQ became an increased concern with its use in COVID-19 patients. A retrospective, observational study found that HCQ could increase the risk of QT interval prolongation and torsades de pointes tachycardia, especially when used with azithromycin [4]. A review of the toxicity of HCQ indicated that HCQ is a generally well-tolerated medication. Short-term (days to weeks) toxicity includes gastrointestinal effects and rarely glucose abnormalities, dermatologic reactions, and neuropsychiatric events. Long-term (years) toxicities include retinopathy, neuromyotoxicity, and cardiotoxicity including conduction abnormalities and cardiomyopathy. Deaths from overdoses of HCQ most often result from cardiovascular collapse [5].

In conclusion, patients with RA can obtain heart benefits from HCQ. We think this may be due to the stronger anti-inflammatory effect of HCQ than its cardiotoxicity in patients with RA. However, the specific mechanism involved in reducing MACE occurrence is unclear. More basic and clinical research is required to further clarify the effect of HCQ on CVD in patients with RA. More importantly, we hope that the toxicity of HCQ to the heart can be further studied in other diseases, not only in rheumatic diseases.