In a recent study published in the journal Heart Rhythm, researchers from the University of California, San Francisco, evaluated the relationship between different types of inhaled marijuana or the use of tobacco products with ventricular and atrial arrhythmias.
The impact of conventional smoking on coronary artery disease is well understood. However, the effects of smoking on proarrhythmic mechanisms and cardiac arrhythmia need further research. Modern tobacco products such as electronic cigarettes (e-cigs) and heated tobacco products (HTP) and the increasing popularity of legalized marijuana have complicated the situation. These products are popularly considered safer than tobacco cigarettes. However, although non-traditional tobacco products and marijuana may be a new threat to the cardiovascular system, there is little understanding of the impact of smoking or vaping on cardiac arrhythmias.
Study: Increased vulnerability to atrial and ventricular arrhythmias caused by different types of inhaled tobacco or marijuana products. Image credit: Hazem.m.kamal / Shutterstock
About the study
In the present study, the researchers determined whether the use of new types of tobacco or marijuana can lead to a proarrhythmic substrate, which ultimately results in arrhythmias.
For this study, eight- to 10-week-old male and female Sprague-Dawley rats were used and divided into groups of five to 16. To mimic active smoking or vaping seen in humans, the conscious rats were exposed to an aerosol or pulsating smoke. Each rat was exposed five days a week for two months with one session per day. Each of these sessions consisted of 10 cycles performed for five minutes to estimate the consumption of a vaping session or a cigarette. Two of the 18 animals in the tobacco cigarette group at the start of the study died on days 1 and 14. They were replaced and no other animals died. Rats were exposed to electronic cigarettes (JUUL), HTP (IQOS), Marlboro Red cigarettes (CIG), marijuana (MJ), or marijuana placebo (pb-MJ).
The team measured arrhythmia inducibility tests, electrocardiographic telemetry, echocardiography, systolic blood pressure (SBP), and optical mapping during or after exposure. To identify chronic effects over time, 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 measurement day, SBP was estimated twice, once before and after that day’s single exposure, to estimate that day’s acute effect.
The team also performed ex vivo optical mapping of the heart eight weeks after exposure to measure the heart’s susceptibility to arrhythmias in the right and left ventricles and atria and determine their electrophysiological characteristics. The duration of an action potential at 80% repolarization (APD80) and of a calcium transient at 80% repolarization (CATD80) were measured.
results
The findings of the study showed that all non-aerial conditions dramatically changed SBP. Cigarette smoke, IQOS aerosol, and JUUL aerosol had the same effect on SBP: all significantly increased SBP on the first day of exposure, with modest improvements on subsequent days. However, unlike tobacco products, each acute exposure to marijuana reduced 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 evaluated products gradually increased baseline SBP from 0.130 mm Hg after two weeks of exposure to 0.140 mm Hg after four weeks and 0.150 mm Hg after eight weeks of exposure Norepinephrine concentrations in serum samples were significantly different in rats exposed to marijuana or tobacco products compared to air eight weeks after exposure. At the same time, angiotensin levels showed no variation.
After eight weeks of exposure, the changes in fractional area and ejection fraction in all non-aerial cohorts were lower than they were at baseline. In the no-air groups, left ventricular (LV) end-diastolic and left ventricular end-systolic volumes increased gradually. Eight weeks after exposure, LV end-diastolic and LV end-systolic volumes had increased significantly compared with baseline in all nonair groups. In addition, LV mass was also increased compared to the air and baseline cohorts. Furthermore, exposure to all conditions except air caused left atrial (LA) diameter to expand at the fourth week of exposure, and the expansion continued until the eighth week. These results suggested that tobacco and marijuana use caused LV dysfunction with enlargement of the heart chambers. This indicated that smoking and vaping are related to LV dysfunction and remodeling.
Compared with air, all tobacco products facilitated the overall induction of AF. Overall, 37.5% of rats exposed to MJ and 50% of rats exposed to pb-MJ developed AF. However, air-exposed rats did not develop AF. VT induction rate due to air exposure was 0%, CIG 62.5%, JUUL 71.43%, IQOS 37.5%, MJ 75% and bp -MJ of 37.5%. AF rates were significant only for CIG, JUUL, and MJ. More than half of all cases of tachycardia were caused by excessive pacing. The effective refractory periods (ERPs) of the LA, LV, and right atrium (RA) were shorter in the nonaerial groups. In addition, the non-air cohorts had a shorter APD80 with a longer CATD80 compared to the air control groups with different rhythm cycle lengths.
Overall, the results of the study showed that marijuana and tobacco could cause changes in the structural, electrical and neuronal remodeling of the heart, facilitating the occurrence of arrhythmias.
Journal reference:
- Huiliang Qiu, Hao Zhang, Daniel D. Han, Ronak Derakhshandeh, Xiaoyin Wang, Natasha Goyal, Mina Navabzadeh, Poonam Rao, Emily E. Wilson, Leila Mohammadi, Jeffrey E. Olgin, Matthew L. Springer, Increased vulnerability to ‘atrial and ventricular arrhythmias caused by different types of inhaled tobacco or marijuana products, heart rhythm, 2022, ISSN 1547-5271, DOI: https://doi.org/10.1016/j.hrthm.2022.09.021, https://www.sciencedirect.com/science/article/pii/S1547527122024869