Marijuana and electronic cigarettes increase the risk of arrhythmias

In a recent study published in Heartbeat The journal, researchers at the University of California, San Francisco, evaluated the association between different types of marijuana inhalation or use of tobacco products with ventricular and atrial arrhythmias.

The effect of traditional tobacco smoking on coronary artery disease is well understood. However, the effects of smoking on the mechanisms of arrhythmia and arrhythmia need further research. Modern tobacco products such as electronic cigarettes (e-cigs) and hot tobacco products (HTPs) and the increasing popularity of legalized marijuana have complicated the situation. These products are generally considered safer than tobacco cigarettes. However, although non-traditional tobacco products and marijuana may pose a new threat to the cardiovascular system, there is little understanding of the effect of smoking or vaping on arrhythmias.

Study: Increased susceptibility to atrial and ventricular arrhythmias caused by various types of inhaled tobacco or marijuana products.  Image credit: Hazem Kamal/Shutterstock

Stady: Increased susceptibility to atrial and ventricular arrhythmias caused by various types of inhaled tobacco or marijuana products. Image credit: Hazem Kamal/Shutterstock

about studying

In this study, researchers determined whether the use of new types of tobacco or marijuana can lead to an arrhythmia substrate, which ultimately leads to arrhythmias.

In this study, male and female Sprague-Dawley rats aged eight to 10 weeks were used and were divided into groups of five to 16. In order to simulate the active smoking or vaping observed in humans, conscious rats were exposed to an aerosol or pulsed smoke. Each rat underwent exposure five days a week for two months with one session per day. Each of these sessions consisted of 10 cycles conducted over five minutes to estimate the consumption of a single vaping session or cigarette. Two of the 18 animals in the tobacco cigarette group died at the start of the study on day 1 and day 14. They were replaced, and no other animals died. Mice were exposed to either e-cigarettes (JUUL), HTPs (IQOS), Marlboro Red cigarettes (CIG), marijuana (MJ), or placebo (pb-MJ).

The team measured an arrhythmia stimulation test, telemetry, echocardiography, systolic blood pressure (SBP), and visual mapping during or after exposure. To incrementally determine chronic effects, a tail cuff was used to measure conscious SBP on the first day of exposure and at the end of the second, fourth, sixth and eighth weeks. On each day of measurement, SBP was estimated twice, once each before and after that day’s single exposure, to estimate the acute effect for that day.

The team also performed optical mapping of the heart ex vivo eight weeks after exposure to measure the heart’s sensitivity to arrhythmias from the right and left ventricles and atria and to determine their electrophysiological properties. The length of the action potential at 80% repolarization (APD).80) and calcium transients at 80% depolarization (CATD80) were measured.


The results of the study showed that all non-weather conditions significantly altered SBP. Cigarette smoke, IQOS aerosol, and Juul aerosol had the same effect on SBP: they all significantly increased SBP on the first day of exposure, with moderate improvements in the following days. However, unlike tobacco products, each acute exposure to marijuana lowers SBP. On the other hand, pb-MJ did not reduce SBP but increased it in a manner similar to tobacco products.

Pre-exposure values ​​showed that chronic exposure to the products assessed gradually raised baseline SBP from 0.130 mmHg after two weeks of exposure to 0.140 mmHg after four weeks and 0.150 mmHg after eight weeks of exposure. Norepinephrine concentrations in serum samples were significantly different in mice exposed to marijuana or tobacco products compared to air after eight weeks of exposure. At the same time, angiotensin levels showed no difference.

After eight weeks of exposure, the differences in partial area and ejection fraction in all non-aerobic cohorts were lower than at baseline. In the non-aerobic groups, the left ventricular (LV) end-systolic and left ventricular (LV) end-diastolic volumes gradually increased. By eight weeks after exposure, end-diastolic and low-pressure end-diastolic volumes had increased significantly compared to baseline in all non-aerobic groups. In addition, the LV block also increased compared to the pneumatic and baseline cohorts. Also, exposure to all conditions except air resulted in left atrial diameter enlargement by the fourth week of exposure, with enlargement continuing until the eighth week. These results indicate that tobacco and marijuana use caused LV dysfunction with enlargement of the heart chambers. This indicates that smoking and vaping are associated with impaired LV and remodeling function.

When compared with air, all tobacco products facilitated the induction of atrial fibrillation overall. Overall, 37.5% of mice exposed to MJ and 50% of mice exposed to Pb-MJ developed AF. However, the mice exposed to air did not develop atrial fibrillation. The rate of VT-inducible due to air exposure was 0%, CIG was 62.5%, Joule 71.43%, IQOS was 37.5%, MJ 75%, Pb-MJ was 37.5%. AF rates were significant only for CIG, JUUL, and MJ. More than half of the cases of tachycardia were caused by excessive speed. The LA, LV, and right atrium (RA) effective refractory periods were shorter in the non-aerobic groups. Furthermore, the non-aired cohorts had a shorter APD80 with a longer CATD80 compared to the airless control groups with different speed cycle lengths.

Overall, the results of the study showed that marijuana and tobacco can cause changes in the structural, electrical, and neurological remodeling of the heart, which facilitate the occurrence of arrhythmias.

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