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Both marijuana and e-cigarettes increase the risk of heart arrhythmias
In a recent study published in the Heart Rhythm journal, researchers at the University of California, San Francisco examined the relationship between different types of inhaled marijuana or tobacco product use with ventricular and atrial arrhythmias. The effects of conventional tobacco smoking on coronary artery disease are well understood. However, the effects of smoking on proarrhythmic mechanisms and cardiac arrhythmias require further research. Modern tobacco products such as electronic cigarettes (e-cigs) and heated tobacco products (HTPs) and the increasing popularity of legalized marijuana have complicated the situation. These products are generally considered safer than tobacco cigarettes. Although non-traditional tobacco products and marijuana pose a novel threat to the cardiovascular system...
Both marijuana and e-cigarettes increase the risk of heart arrhythmias
In a recently published study in the heart rhythm Journal, researchers at the University of California, San Francisco, examined the relationship between different types of inhaled marijuana or tobacco product use with ventricular and atrial arrhythmias.
The effects of conventional tobacco smoking on coronary artery disease are well understood. However, the effects of smoking on proarrhythmic mechanisms and cardiac arrhythmias require further research. Modern tobacco products such as electronic cigarettes (e-cigs) and heated tobacco products (HTPs) and the increasing popularity of legalized marijuana have complicated the situation. These products are generally considered safer than tobacco cigarettes. Although non-traditional tobacco products and marijuana may pose a novel threat to the cardiovascular system, there is little understanding of the effects of smoking or vaping on cardiac arrhythmias.
About studying
In the present study, researchers determined whether the use of new varieties of tobacco or marijuana can result in a proarrhythmic substrate that ultimately leads to arrhythmias.
For this study, male and female Sprague-Dawley rats between eight and ten weeks of age were used and divided into groups of five to 16. To mimic the active smoking or vaping observed in humans, conscious rats were exposed to pulsating aerosol or smoke. Each rat was exposed five days per week with one session per day for two months. Each of these sessions consisted of 10 cycles performed over 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 either electronic cigarettes (JUUL), HTPs (IQOS), Marlboro Red cigarettes (CIG), marijuana (MJ), or placebo marijuana (pb-MJ).
The team measured arrhythmia inducibility testing, electrocardiographic telemetry, echocardiography, systolic blood pressure (SBP), and optical mapping during or after exposure. To identify progressively 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 measurement day, SBP was estimated twice, once before and after each exposure on that day, to estimate the acute effect of that day.
The team also performed ex vivo optical cardiac mapping eight weeks after exposure to measure the heart's susceptibility to arrhythmias from the right and left ventricles and atria and to determine their electrophysiological properties. The length of an action potential at 80% repolarization (APD80) and a calcium transient at 80% repolarization (CATD80) were measured.
Results
The study results showed that all non-air conditions drastically changed SBP. Cigarette smoke, IQOS aerosol, and JUUL aerosol all had the same effect on systolic blood pressure: they all significantly increased systolic blood pressure on the first day of exposure, with moderate improvements in subsequent days. However, unlike tobacco products, any acute exposure to marijuana decreased SBP. On the other hand, pb-MJ did not decrease SBP but increased it in a manner similar to tobacco products.
Pre-exposure values showed that chronic exposure to the products evaluated gradually increased 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 eight weeks after exposure in rats exposed to marijuana or tobacco products compared to air. At the same time, the angiotensin levels showed no fluctuations.
After eight weeks of exposure, area fraction variations and ejection fraction were lower in all non-air cohorts than at baseline. In non-air groups, left ventricular (LV) end-diastolic and LV end-systolic volumes gradually increased. Eight weeks after exposure, end-diastolic and LV end-systolic volumes were significantly increased compared to baseline in all non-air groups. Furthermore, LV mass also increased compared to air cohorts and baseline. Additionally, exposure to all conditions except air caused the left atrium (LA) diameter to increase until the fourth week of exposure, with the enlargement lasting until the eighth week. These results suggested that tobacco and marijuana use caused LV dysfunction with enlargement of the heart chambers. This suggested that smoking and vaping are associated with LV dysfunction and remodeling.
Compared to air, all tobacco products facilitated overall AF induction. Overall, 37.5% of MJ-exposed rats and 50% of pb-MJ-exposed rats developed atrial fibrillation. However, rats exposed to air did not develop AF. The VT-inducible rate by air exposure was 0%, CIG 62.5%, JUUL 71.43%, IQOS 37.5%, MJ 75%, and pb-MJ 37.5%. AF rates were significant only for CIG, JUUL, and MJ. More than half of all cases of tachycardia were caused by overdrive pacing. Effective refractory periods (ERPs) for LA, LV, and right atrium (RA) were shorter in the non-air groups. Furthermore, non-air cohorts had a shorter APD80 with a longer CATD80 compared to air control groups at different stimulation cycle lengths.
Overall, the study results showed that marijuana and tobacco can cause changes in the structural, electrical and neural remodeling of the heart, facilitating the occurrence of arrhythmias.
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, Erhöhte Anfälligkeit für atriale und ventrikuläre Arrhythmien, die durch verschiedene Arten von inhalierten Tabak- oder Marihuanaprodukten verursacht werden, 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
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