Quitting smoking may significantly lower risk of atrial fibrillation, unravels research
Quitting cigarettes can significantly lower a person's risk of atrial fibrillation (AFib) compared to those who continue to smoke, according to a study published today in JACC: Clinical Electrophysiology. The findings show that the benefits of quitting start right away, suggesting that it is possible to reverse the risk of negative health outcomes.
“The findings provide a compelling new reason to show current smokers that it’s not too late to quit and that having smoked in the past doesn’t mean you’re ‘destined’ to develop AFib,” said senior author Gregory Marcus, MD, MAS, a cardiologist at the University of California, San Francisco. “Even for the current and longtime smoker, AFib can still be avoided.”
Smoking is greatly associated with an increased risk of AFib, an irregular and often rapid heart rhythm. It has potentially serious health consequences and is linked with a significant risk of stroke, heart failure and overall mortality. Rates of AFib are rising, creating a need to identify lifestyle changes that can reduce risk.
“There’s strong evidence that smoking increases the risk of AFib, but the benefits of quitting smoking have been less certain,” Marcus said. “We wanted to determine whether quitting smoking could lower a person’s risk of developing AFib or if the risk would stay the same.”
The team analyzed UK Biobank data on more than 146,700 current and former smokers. Participants’ smoking habits and health outcomes were tracked for around 12 years.
They found that former smokers had around 13% lower risk of AFib than people who were still smoking. Surprisingly, researchers also found that those who quit smoking during the study had an 18% lower risk of AFib than people who smoke, showing a significantly lower risk than former smokers.
“This is likely a testament to the potency of reducing atrial fibrillation risk pretty shortly after quitting,” Marcus said.
Previous research that looked at the connection between smoking and AFib was observational, making it difficult to prove a causal relationship.
“While the current study is also observational, our findings lend credence to the idea that smoking may truly cause AFib,” Marcus said.
Future research could focus on explaining the mechanisms underlying the relationship between smoking and AFib, potentially identifying new therapeutic targets to prevent and treat it.
Study limitations include the possibility of recall bias in self-reported smoking status, the variability of the number of completed serial lifestyle questionnaires, and unmeasured confounding that may have contributed to the results, such as participant lifestyle or access to support in preventative health.
Reference:
Justin T. Teraoka, Janet J. Tang, Francesca N. Delling, Eric Vittinghoff, and Gregory M. Marcus, Smoking Cessation and Incident Atrial Fibrillation in a Longitudinal Cohort, JACC Clinical Electrophysiology, DOI: 10.1016/j.jacep.2024.06.019.
