Smoking ‘important’ modifiable risk factor for HF
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Current smoking was associated with elevated risk for HF in a dose-response manner, according to a new analysis of the ARIC cohort.
“Our results strengthened the evidence that smoking is an important modifiable risk factor for HF and highlighted the importance of smoking prevention and cessation for the prevention of HF, including HF [with preserved ejection fraction],” Ning Ding, MD, ScM, data analyst at the Johns Hopkins Bloomberg School of Public Health, and colleagues wrote in the Journal of the American College of Cardiology.
Ding and colleagues analyzed 9,345 participants from the ARIC cohort (mean age, 70 years; age range, 61 to 81 years; 57% women; 21% Black) who were free from HF at baseline in 2005 to quantify the association between cigarette smoking and smoking cessation and development of HFpEF or HF with reduced ejection fraction.
In a median follow-up of 13 years, 1,215 patients developed HF. Compared with never smokers, current smokers were more likely to have a HF event (adjusted HR = 2.36; 95% CI, 1.92-2.9), a HFpEF event (aHR = 2.28; 95% CI, 1.67-3.1) or a HFrEF event (aHR = 2.16; 95% CI, 1.55-3), according to the researchers.
Former smokers were also more likely than never smokers to develop HF, but not to the same extent as current smokers (aHR for HF = 1.36; 95% CI, 1.19-1.55; aHR for HFpEF = 1.31; 95% CI, 1.08-1.59; aHR for HFrEF = 1.36; 95% CI, 1.1-1.68), Ding and colleagues wrote.
The results varied by pack-years of smoking, as participants who smoked for longer had greater risk for HF compared with those who smoked for a shorter duration (aHR per 10 pack-years = 1.14; 95% CI, 1.11-1.16), the researchers wrote.
Elevated risk for HF persisted for 20 to 30 years after smoking cessation, but “there was an approximately 50% lower risk for both phenotypes of HF among those who remained abstinent for over 30 years compared with current smokers,” Ding and colleagues wrote.
“Smoking should indeed be leveraged into detailed risk prediction, possibly within dedicated frameworks that can include epigenetics and machine learning algorithms,” Giuseppe Biondi-Zoccai, MD, MStat, from the department of medical-surgical sciences and biotechnologies, Sapienza University of Rome, Latina, Italy, and colleagues wrote in a related editorial.
“The fight against smoking in all of its forms should continue, while proactively promoting smoking cessation and offering effective smoking cessation interventions to all individuals, especially those at heightened risk of heart failure,” Biondi-Zoccai and colleagues wrote.
Reference:
Perspective
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Even though HFpEF and HFrEF are recognized as separate pathophysiologic entities, hospitalization and death rates are equally high in both diseases. Cigarette smoking independently increases the risk for developing either phenotype, and this risk remains present even after adjusting for the strongest traditional risk factors (ie, hypertension, CHD).
The prevalence of the HFpEF phenotype is rising, treatment options for it remain very limited once the syndrome develops, and morbidity and mortality from HFpEF is devastating. The direct association between cigarette smoking and HF, coupled with the overall poor prognosis that persists even with implementation of all the currently available therapies, should be incorporated in our efforts to counsel patients on cigarette smoking.
Education regarding the risks of developing congestive HF in addition to other major health risks caused by cigarette smoking (ie, CAD, cancer) should be included in community-based smoking cessation initiatives.
Mechanistic studies trying to identify the true pathways by which cigarette smoking increases incident HF risk, especially as it relates to coronary microvascular function, are needed.
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