Modified effect of active or passive smoking on the association between age and abdominal aortic calcification: a nationally representative cross-sectional study

Abstract

ObjectiveThe deleterious effects of smoking on atherosclerosis were well known; however, the interaction among ageing, smoking and atherosclerosis remains unclear. This study tested the hypothesis that the association between age and vascular calcification, a critical mark of atherosclerosis, was modified by smoking.DesignCross-sectional study.SettingA nationally representative sample, the National Health and Nutrition Examination Surveys 2013–2014.ParticipantsThis study included 3140 adults aged 40–80 years with eligible data for abdominal aortic calcification (AAC). Active and passive smoking exposure was identified through self-reports and tobacco metabolites (serum cotinine and urinary 4-methylnitrosamino-3-pyridyl-1-butanol).Primary outcome measuresAAC score was determined using dual-energy X-ray absorptiometry (DXA) scans. OR was estimated using the logistic regression method to assess the association between age and the presence of severe or subclinical AAC stratified by smoking exposure. The survey-weighted Wald test was used to evaluate potential interactions.ResultsAAC was positively associated with age in the general population. After adjustment for age, sex, race/ethnicity and other cardiovascular risk factors, age was significantly associated with the odds of severe AAC (OR for each 5-year increase in age: 1.66, 95% CI 1.48 to 1.87, p<0.001). As expected, the association between age and vascular calcification was especially stronger in smokers than in never smokers (p value for interaction ≤0.014). According to spline fitting, the progression of vascular calcification was significantly increased after 45 years in smokers compared with that after 60 years in never smokers. Quitting smoking may compromise the deleteriousness of the vascellum especially in younger adults. However, the difference in age-related calcification among never smokers with or without secondhand smoke exposure was minor, regardless of the definition by self-report, serum cotinine, or urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol.ConclusionsSmoking significantly accelerated the progression of age-related subclinical atherosclerosis. Early smoking cessation should be encouraged among young smokers. The effect of passive smoking exposure on arteriosclerosis should be assessed further.

Analysis of the Risk Factors for Free Flap Necrosis in Soft Tissue Reconstruction of the Lower Limbs

“…After smoking, hypoxia and hypercapnia cause a rapid increase in erythrocyte volume, and a large number of aggregated platelets increase blood viscosity and affect blood circulation. Increased smoking can increase the risk of vascular embolism and vascular crisis in the free flap 25 . Simultaneously, smoking can increase nitric oxide (NO) in the blood, and NO can competitively bind to hemoglobin, decreasing blood oxygen 26 .…”

“…Increased smoking can increase the risk of vascular embolism and vascular crisis in the free flap. 25 Simultaneously, smoking can increase nitric oxide (NO) in the blood, and NO can competitively bind to hemoglobin, decreasing blood oxygen. 26 Mlodinow 7 found that a long smoking history significantly increases the risk of flap necrosis after mastectomy.…”

Vascular Calcification Heterogeneity from Bench to Bedside: Implications for Manifestations, Pathogenesis, and Treatment Considerations

“…A systematic review summarized that biological sex has important effects on the risk of VC [31], and Wu et al speculated that biological sex-related differences in VC probability could result from differential expression or levels of vitamin D, anti-calcific molecules (matrix Gla protein), soluble klotho, and other hormones (parathyroid hormone, fibroblast growth factor-23, and sclerostin). Noxious environmental stimuli, such as active and passive smoking [32], cadmium exposure [33], and air pollution [34] have also been suggested as modifiers of the probability of VC worsening. Dietary fiber content has also been found to modulate the risk of VC development and worsening among those with CKD [35].…”

Imaging Early Life Cardiovascular Phenotype

“…Moreover, smoking cessation has been shown to reduce the deleterious effects of smoking on abdominal aortic atherosclerosis. [111][112][113] In the CARDIA study, The AAC score was an early indicator of atherosclerosis as it reflects atherosclerotic CVD when CAC is zero. 114 The prevalence of AAC was 53% among young adults, 114 and AAC scores were generally found to be higher than CAC scores.…”