A study that used observational data from the Atherosclerosis Risk in Communities (ARIC) study shows a significant association between cigarette smoking and increased risk for heart failure (HF) both with preserved (HFpEF) and reduced ejection fraction (HFrEF).
Researchers found 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 heart failure with reduced ejection fraction and heart failure with preserved ejection fraction,” said Kunihiro Matsushito, MD, PhD, John Hopkins Bloomberg School for Public Health and John Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Baltimore.
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 Matsushito.
The article was published in the June 14 issue of the Journal of the American College of Cardiology.
A Modifiable Risk Factor
Improvements have been made over the past few decades, but the prognosis of HF is “still devastating,” with a 1-year mortality of about 30% after diagnosis, the authors write.
Prevention 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 Matsushita.
Using data from the ARIC study, the authors looked at outcomes in 9345 participants to determine if there is an association between cigarette smoking and smoking cessation with incident acute decompensated HF overall, and HFrEF, and HFpEF.
Baseline was January 1, 2005; adjudication for potential HF cases started at the beginning of 2005. Data from clinic exams and annual/semi-annual phone interviews were used. Patients with previous HF or those with missing variables of interest were excluded from the study.
To determine smoking duration, the authors used cumulative years of smoking before visit 1 for each participant, as well as the years during follow-up. Smoking intensity was assessed at visits 1 to 4. The authors then calculated pack-years of smoking as the average number of cigarettes per day divided by 20, multiplied by the duration of smoking in years.
The authors assessed years since smoking cessation by calculating baseline age minus the recalled age of cessation plus cumulative years of cessation during follow-up.
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.
Over a median follow-up of 13 years, there were 1215 cases of incident acute decompensated HF: 555 of HFpEF, 492 of HFrEF, and 168 of HF with unknown LVEF.
The adjusted incidence rate per 1000 person-years for HF was 9.7 (95% CI, 8.7 – 10.6) for never smokers, 13.5 (95% CI, 12.5 – 14.6) for former smokers, and 20.1 (95% CI, 16.7 – 23.5) for current smokers. Similar results were seen for the incidence of HFpEF and HFrEF.
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], 11.19; 95% CI, 0.99 – 1.44), and those with 25 or more pack-years had an approximately twofold 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).
A similar pattern was seen when they analyzed the HF subtypes separately, but the HR for HFrEF in smoking cessation from 20 to 30 years was not statistically significant.
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, second-hand smoke, or e-cigarettes. “Given the increased prevalence of e-cigarette use, future studies are warranted to explore this topic,” they conclude.
Smoking Cessation an Important Tool
In an accompanying editorial, Giuseppe Biondi-Zoccai, MD, MSTAT, Sapienza University of Rome, Latina, Italy, and Mediterranea Cardiocentro, Napoli, Italy; Mariangela Peruzzi, MD, PhD, Mediterranea Cardiocentro, Sapienza University of Rome; and Giacomo Frati, MD, Sapienza University of Rome, Latina, and IRCCS NEUROMED, Pozzilli, Italy, acknowledge that despite the advances in treatment for HF, prevention remains at the forefront.
“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,” Biondi-Zoccai told theheart.org | Medscape Cardiology.
The editorial highlights the importance of motivating current smokers to stop, and emphasizes the importance of continuing abstinence for those who have quit.
“By highlighting the important causal role of smoking on heart failure, we may inform people at large, not only patients, that if they wish to avoid developing heart failure, they must avoid smoking or discontinue smoking if they are currently doing it,” added Biondi-Zoccai.
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.
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 Institutes, National Institute of Health, and the Department of Health and Human Services. The authors have no conflict of interest to disclose. 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. Abstract, Editorial
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