Chronic exposure to mercury increases arrhythmia and mortality post-acute myocardial infarction in rats

Front Physiol. 2023 Oct 19:14:1260509. doi: 10.3389/fphys.2023.1260509. eCollection 2023.

Abstract

Introduction: Mercury (Hg) is a heavy metal that causes a variety of toxic effects in eukaryotic cells. Previous studies have reported detrimental effects of mercury toxicity in the cardiovascular system. Given the importance of understanding the relationship between Hg and cardiovascular disease, we sought to investigate if the Hg could worsen the myocardial repercussions following ischemic injury. We demonstrated that once mercury toxicity is established, it can influence the outcome of myocardial infarction (MI). Methods: Male Wistar rats received intramuscular injections of either saline (NaCl 0.9%) or mercuric chloride (HgCl2, first dose of 4.6 μg/kg, and subsequent doses of 0.07 μg/kg/day) for 4 weeks. Three weeks post-exposure, we induced transmural infarction in the left ventricle free wall through coronary artery occlusion surgery. Results: ECG recordings obtained from MI groups demonstrated alterations in the rhythm of the heartbeat/heart electrical activity, as expected, including ventricular extrasystoles and ventricular tachycardia. However, the MI group exposed to Hg (MI-Hg) exhibited augmented ventricular extrasystoles and ventricular tachycardia compared to the MI group. Also, Basckó coefficient revealed that the arrhythmic events-after MI-were aggravated by Hg exposure. Discussion: Our results indicate that the significantly increased mortality in MI-Hg groups when compared to MI (21%, MI vs 32%, MI-Hg) is correlated with greater occurrence of arrhythmias. In conclusion, this study further supports the idea that exposure to mercury (Hg) should be recognized as a significant risk factor that exacerbates the impact of cardiac ischemic injury, potentially leading to an increased mortality rate among patients experiencing acute MI.

Keywords: arrhythmias; eletrocardiogram; mercury; mortality; myocardial infarction.

Grants and funding

The authors declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants from No. 48511935/2009 PRONEX—FAPES/CNPq (Fundação de Amparo à Pesquisa do Espírito Santo/Conselho Nacional de Desenvolvimento Cientifico e Tecnológico), No. 44181/2014-9 Edital Universal/CNPq, No. 84324600/2018 Edital FAPES/CNPq 24/2018, and FAPES CAPEX 019/2022-20226C3F7. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.