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Active smoking is associated with increased left ventricular (LV) mass and decreased diastolic function, according to a study published in Circulation: Cardiovascular Imaging.
Smokers without overt coronary artery disease have higher rates of heart failure compared with nonsmokers in epidemiological studies. But data on the link between smoking and LV mass have been inconsistent. Smoking may also have an effect on risk factors for cardiovascular remodeling, such as blood pressure and arterial stiffness, that could account for changes in cardiac structure and function.
Researchers led by Scott D. Solomon, MD, of Brigham and Women’s Hospital, used data from the Atherosclerosis Risk in Communities (ARIC) study to clarify the relationship between smoking status and LV structure and function.
Transthoracic echocardiography was performed on 4580 participants without overt heart failure, coronary artery disease, or valvular disease. Study participants were grouped into categories of never, former, and current smokers.
Current smokers, compared with never smokers, had significantly greater LV mass index (80.4 vs 76.7 g/m2; P <.001) and LV mass/volume ratio (1.93 vs 1.83 g/mL; P <.001). Participants who actively smoked also had more LV hypertrophy (15% vs 9% of nonsmokers; P =.008) and worse diastolic dysfunction (E/E’ ratio 11.7 vs 10.9 in nonsmokers; P <.001).
Among current smokers, cumulative cigarette exposure, as measured by estimated pack-years and years of smoking, correlated with increased measures of LV mass and worse diastolic function (P <.01 for all comparisons).
No significant differences in echocardiographic parameters were found between former smokers and never smokers.
“The main finding of our study is that smoking may increase the risk for heart failure by causing the heart to hypertrophy, or become thicker, which worsens myocardial pump function,” Dr Solomon told Cardiology Advisor.
“The good news is that these effects seem to be somewhat reversible with smoking cessation. But we don’t know how fast these changes occur and how fast they reverse with smoking cessation,” he added.
The correlation between smoking and heart structure and function could not be accounted for by smoking-induced changes in blood pressure or arterial stiffness, as measured by carotid-femoral pulse wave velocity, which were similar in all smoking groups.
“We don’t know the exact mechanisms by which smoking contributes to alterations in cardiac structure and function,” Dr Solomon concluded. “This is certainly an area that requires for further research.”
