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Smoking is known to promote negative cardiovascular outcomes, but what is the relative effect of smoking on different manifestations of cardiovascular disease? Banks and colleagues addressed this question using a large database of adults without a prior history of cardiovascular disease. Their research was published in the July 3, 2019, issue of BMC Medicine.[1]
The risk for heart failure in general was raised with current smoking in this study, but the effect of former smoking and cumulative lifetime dose of cigarettes on the risk for heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF) are not well understood. The current study addresses these issues.
A study that used observational data from the Atherosclerosis Risk in Communities (ARIC) shows a significant association between cigarette smoking and increased risk for HFpEF and HFrEF.
Researchers found that the risk for HFpEF and HFrEF increased in conjunction with pack-years, duration, and intensity of smoking, indicating that longer, more intense exposure results in elevated risk.
"There was a dose-response relationship between smoking and heart failure overall, as well as [HFpEF] and [HFrEF]," said Kunihiro Matsushito, MD, PhD, from John Hopkins Bloomberg School for Public Health and John Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Baltimore, Maryland.
Smoking cessation significantly reduced the incidence of HF, but an elevated risk associated with previous smoking still existed decades later.
The results of this study "demonstrate that the excess risk created by smoking may last up to 30 years, and I think that clearly tells the importance of preventing smoking in the first place, but also encouraging current smokers to quit as soon as possible because the excess risk may last long," added Dr Matsushito.
The article was published in the June 14 issue of the Journal of the American College of Cardiology.[2]
A Modifiable Risk FactorPrevention is "crucial" for HF, and specifically HFpEF, they note. "Since there are not many treatment options for that condition, it's critical that we try to prevent the occurrence of heart failure with preserved ejection fraction," said Dr Matsushita.
Using data from the ARIC study, the authors looked at outcomes in 9345 participants to determine whether there is an association between cigarette smoking and smoking cessation with incident acute decompensated HF overall, HFrEF, or HFpEF.
Baseline was January 1, 2005; adjudication for potential HF cases started at the beginning of 2005. Data from clinic exams and annual/semiannual phone interviews were used. Patients with previous HF or those with missing variables of interest were excluded from the study.
Mean age of the study cohort was 70.4±5.7 years, 57.3% of participants were women, and 20.8% were Black. Of the 9345 participants, 823 (8.8%) were current smokers, 4547 (48.7%) were former smokers, and 3975 (42.5%) were never smokers.
Pack-years of smoking showed an association with HF after adjustment for potential confounders. Participants with less than 10 pack-years of smoking did "not necessarily" have an increased risk for overall HF, they note. Participants with 10 to 25 pack-years had a borderline increased risk for overall HF (hazard ratio [HR], 1.19; 95% CI, 0.99-1.44), and those with 25 or more pack-years had an approximately 2-fold increased risk for overall HF.
Results for HFpEF and HFrEF were similar with continuous smoking. The HR per increment of 10 pack-years was 1.16 (95% CI, 1.12-1.20) for HFpEF and 1.09 (95% CI, 1.05-1.13) for HFrEF.
Smoking intensity and duration showed graded associations with overall HF, HFpEF, and HFrEF, the authors note.
Longer duration of smoking cessation was associated with less risk for HF, but compared with never smokers, there was still a significant elevated risk for HF from 20 to 30 years after cessation (HR, 1.34; 95% CI, 1.07-1.67).
However, participants with smoking cessation of more than 30 years had a risk for HF, HFpEF, and HFrEF similar to that of never smokers. There was a 50% lower risk for both types of HF among participants who remained abstinent for 30 years compared with current smokers.
Cigarette smoking is associated with increased risk for HFrEF because cigarette smoking is a significant risk factor for coronary heart disease, a major cause of HFrEF, the authors note. "However, the etiological link between cigarette smoking and the development of HFpEF remains unclear," they write.
The authors reported some limitations to their findings. First, using self-reported smoking status could result in measurement error. Second, baseline data were not available precisely at the beginning of 2005; however, the authors found consistent results using visit 1 as a baseline. Third, 15% of HF events could not be categorized into HF subtypes because of missing information. Fourth, there could have been residual confounding, as with any observational study.
Last, the data used in this study were for cigarette smoking only, so it is "unknown" whether the results would apply to cigars, pipes, secondhand smoke, or e-cigarettes.
Smoking Cessation an Important ToolIn an accompanying editorial, the authors acknowledge that despite the advances in treatment for HF, prevention remains at the forefront.[3]
"Smoking is a major cause of all types of heart failure, with detrimental effects that may persist several years after cessation. The focus on both heart failure with systolic dysfunction and heart failure without systolic dysfunction is particularly timely and confirms the multidimensional detrimental effects of smoking on cardiac pathophysiology," Dr Biondi-Zoccai,from Sapienza University of Rome, told theheart.org | Medscape Cardiology.
The editorial also notes that although the study did not examine exposure to other substances, such as cannabis, cigars, pipes, heat-not-burn devices, vaping, and smokeless tobacco, it reinforces the efforts to minimize those exposures.
Dr Biondi-Zoccai added that decreasing exposure to such things as passive smoking and household or environmental pollution would also be beneficial.
The ARIC study is funded by federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services. The authors have disclosed no relevant financial relationships. Dr Biondi-Zoccai has consulted for Cardionovum, Crannmedical, Innovheart, Meditrial, Opsens Medical, Replycare, and Terumo. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
J Am Coll Cardiol. 2022;79:2298-2305, 2306.2309.