Division of Cardiology, University of California, San Francisco, San Francisco, California.
Division of Cardiology, University of California, San Francisco, San Francisco, California; Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California.
Heart Rhythm. 2023 Jan;20(1):76-86. doi: 10.1016/j.hrthm.2022.09.021. Epub 2022 Nov 15.
The emergence of a plethora of new tobacco products marketed as being less harmful than smoking, such as electronic cigarettes and heated tobacco products, and the increased popularity of recreational marijuana have raised concerns about the potential cardiovascular risk associated with their use.
The purpose of this study was to investigate whether the use of novel tobacco products or marijuana can cause the development of proarrhythmic substrate and eventually lead to arrhythmias.
Rats were exposed to smoke from tobacco, marijuana, or cannabinoid-depleted marijuana, to aerosol from electronic cigarettes or heated tobacco products, or to clean air once per day for 8 weeks, following by assays for blood pressure, cardiac function, ex vivo electrophysiology, and histochemistry.
The rats exposed to tobacco or marijuana products exhibited progressively increased systolic blood pressure, decreased cardiac systolic function with chamber dilation, and reduced overall heart rate variability, relative to the clean air negative control group. Atrial fibrillation and ventricular tachycardia testing by ex vivo optical mapping revealed a significantly higher susceptibility to each, with a shortened effective refractory period and prolonged calcium transient duration. Histological analysis indicated that in all exposure conditions except for air, exposure to smoke or aerosol from tobacco or marijuana products caused severe fibrosis with decreased microvessel density and higher level of sympathetic nerve innervation.
These pathophysiological results indicate that tobacco and marijuana products can induce arrhythmogenic substrates involved in cardiac electrical, structural, and neural remodeling, facilitating the development of arrhythmias.
大量新型烟草产品的出现,如电子烟和加热烟草产品,被宣传为比吸烟危害更小,以及娱乐用大麻的普及,引发了人们对其使用相关潜在心血管风险的担忧。
本研究旨在探究新型烟草产品或大麻的使用是否会导致致心律失常基质的形成,并最终导致心律失常。
大鼠每天暴露于烟草、大麻或大麻素耗尽的大麻烟雾、电子烟或加热烟草产品的气溶胶或清洁空气中一次,持续 8 周,然后进行血压、心功能、离体电生理学和组织化学检测。
与清洁空气阴性对照组相比,暴露于烟草或大麻产品的大鼠表现出逐渐升高的收缩压、心室扩张导致的心收缩功能降低以及整体心率变异性降低。通过离体光学映射进行的心房颤动和室性心动过速检测显示,每种情况的易感性显著增加,有效不应期缩短,钙瞬变持续时间延长。组织学分析表明,除空气暴露外,所有暴露条件下,暴露于烟草或大麻产品的烟雾或气溶胶都会导致严重的纤维化,微血管密度降低,交感神经支配水平升高。
这些病理生理学结果表明,烟草和大麻产品可诱发涉及心脏电、结构和神经重构的致心律失常基质,促进心律失常的发生。