摘要：Background: Epidemiological evidence suggests that a majority of deaths attributed to secondhand smoke (SHS) exposure are cardiovascular related. However, to our knowledge, the impact of SHS on cardiac electrophysiology, Ca 2 + handling, and arrhythmia risk has not been studied. Objectives: The purpose of this study was to investigate the impact of an environmentally relevant concentration of SHS on cardiac electrophysiology and indicators of arrhythmia. Methods: Male C57BL/6 mice were exposed to SHS [total suspended particles (THS): 3.0 ± 0.1 mg / m 3 , nicotine: 0.4 ± 0.2 mg / m 3 , carbon monoxide: 12.4 ± 1.6 ppm , or filtered air (FA) for 4, 8, or 12 wk ( n = 4 – 5 / group ]. Hearts were excised and Langendorff perfused for dual optical mapping with voltage- and Ca 2 + -sensitive dyes. Results: At slow pacing rates, SHS exposure did not alter baseline electrophysiological parameters. With increasing pacing frequency, action potential duration (APD), and intracellular Ca 2 + alternans magnitude progressively increased in all groups. At 4 and 8 wk, there were no statistical differences in APD or Ca 2 + alternans magnitude between SHS and FA groups. At 12 wk, both APD and Ca 2 + alternans magnitude were significantly increased in the SHS compared to FA group ( p < 0.05 ). SHS exposure did not impact the time constant of Ca 2 + transient decay ( τ ) at any exposure time point. At 12 wk exposure, the recovery of Ca 2 + transient amplitude with premature stimuli was slightly (but nonsignificantly) delayed in SHS compared to FA hearts, suggesting that Ca 2 + release via ryanodine receptors may be impaired. Conclusions: In male mice, chronic exposure to SHS at levels relevant to social situations in humans increased their susceptibility to cardiac alternans, a known precursor to ventricular arrhythmia. https://doi.org/10.1289/EHP3664
