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Bisphenol A (BPA) exposure perturbs cardiac electrical conduction in excised rat hearts
Author(s) -
Posnack Nikki Gillum,
Jaimes Rafael,
Asfour Huda,
Swift Luther M,
Wengrowski Anastasia M,
Sarvazyan Narine,
Kay Matthew W
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.706.7
Subject(s) - bisphenol a , electrical conduction system of the heart , qrs complex , cardiology , medicine , pr interval , in vivo , qt interval , population , electrophysiology , acute exposure , heart rate , endocrinology , electrocardiography , chemistry , biology , blood pressure , epoxy , microbiology and biotechnology , organic chemistry , environmental health
Bisphenol A (BPA) is used to produce polycarbonate plastics and epoxy resins that are used in everyday products. Biomonitoring studies indicate that >;90% of the population is routinely exposed to BPA. Recent studies reported alarming correlations between increased BPA urinary concentrations and cardiovascular disease; yet the direct effects of BPA on the heart are unknown. Our goal was to measure BPA's effect on cardiac impulse propagation ex vivo , using excised rat hearts. BPA exposure (1–100 μM) resulted in delayed atrioventricular conduction, prolonged PR segment, lengthened QRS interval and alteration of QRS morphology, decreased epicardial conduction velocity and prolonged action potential duration. These effects were observed after acute exposure (<15min), underscoring the potential detrimental effects in humans with continuous exposure. Higher BPA exposure (100 μM) also resulted in dropped ventricular beats and eventually led to complete heart block. Our results show that acute BPA exposure is cardiotoxic and perturbs electrical conduction in excised rat hearts. These findings emphasize the importance of examining BPA's effect on heart electrophysiology and determining whether chronic in vivo exposure can exacerbate conduction abnormalities in patients with pre‐existing heart conditions and other high‐risk populations. Supported by the NIH (F32 ES019057).