Key result
Smoking was associated with higher pericardial adipose tissue volume compared to non-smoking (231 vs. 201 mL, p=0.03) and an increased odds of elevated PAT (OR 2.92; 95% CI 2.31-3.61; p<0.001).
Why the study?
Pericardial adipose tissue is associated with atherosclerotic and inflammatory processes and related to coronary heart disease prevalence, but the effect of smoking on its extent required determination.
Does smoking increase pericardial adipose tissue volume in asymptomatic patients?
Observational (n=1,217)
Does smoking increase pericardial adipose tissue volume in asymptomatic patients?
Smoking is independently associated with increased pericardial adipose tissue volume, highlighting a potential mechanism for increased inflammatory and atherosclerotic risk in smokers.
Smoking was associated with higher pericardial adipose tissue volume; leaves open its incremental value for risk prediction or targeted interventions.
Background: Pericardial adipose tissue (PAT), a visceral fat depot directly located to the heart, is associated with atherosclerotic and inflammatory processes. The extent of PAT is related to the prevalence of coronary heart disease and might be used for cardiovascular risk prediction. This study aimed to determine the effect of smoking on the extent of PAT. Methods: We retrospectively examined 1217 asymptomatic patients (490 females, age 58.3 ± 8.3 years, smoker n = 573, non-smoker n = 644) with a multislice CT scanner and determined the PAT volume. Coronary risk factors were determined at inclusion, and a multivariate analysis was performed to evaluate the influence of smoking on PAT independent from accompanying risk factors. Results: The mean PAT volume was 215 ± 107 mL in all patients. The PAT volume in smokers was significantly higher compared to PAT volume in non-smokers (231 ± 104 mL vs. 201 ± 99 mL, p = 0.03). Patients without cardiovascular risk factors showed a significantly lower PAT volume (153 ± 155 mL, p < 0.05) compared to patients with more than 1 risk factor. Odds ratio was 2.92 [2.31, 3.61; p < 0.001] for elevated PAT in smokers. Conclusion: PAT as an individual marker of atherosclerotic activity and inflammatory burden was elevated in smokers. The finding was independent from metabolic risk factors and might therefore illustrate the increased inflammatory activity in smokers in comparison to non-smokers.
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Zimmermann et al. (2021) conducted an observational in Asymptomatic patients (n=1,217). Smoking vs. Non-smokers was evaluated on Pericardial adipose tissue (PAT) volume and elevated PAT (OR 2.92, 95% CI 2.31-3.61, p=<0.001). Smoking was associated with higher pericardial adipose tissue volume compared to non-smoking (231 vs. 201 mL, p=0.03) and an increased odds of elevated PAT (OR 2.92; 95% CI 2.31-3.61; p<0.001).
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