Association between alpha1-antitrypsin (α1-AT) levels, lipid profile and ventilatory pulmonary function in predicting the cardiovascular risk in simptomatic smokers

Background: Cigarette smoke oxidants can cause oxidative inactivation of methionine residues of α1-AT, leading to lipid binding, with dyslipidemia, inflammation and endothelial dysfunction, the early stage of atherosclerosis. The aim of the study was to assess the relationship between serum α1-AT levels, pulmonary function and lipids in predicting the risk of cardiovascular disease among symptomatic smokers adult subjects in an Out-patient Pulmonology Health Unit. Methods: 100 respiratory symptomatic adults mean aged 53.34±9.69 year-old, were grouped in smokers (current and former heavy smokers) (n=64) and nonsmokers (n=36). Demographic, anthropometric, pack-years smoking, serum α1-AT, plasma lipid profile {(total cholesterol-TC, low density lipoprotein cholesterol-LDLc, high density lipoprotein cholesterol-HDLc, triglycerides-TG, nonhigh density lipoprotein cholesterol-nonHDLc, very low density lipoprotein cholesterol-VLDL), by which were calculated lipid indices}, were performed. All subjects underwent spirometry according to the international recommendations. Lung function was expressed as forced vital capacity (FVC% predicted), forced expiratory volume in one second (FEV1% predicted), Forced Expiratory volume in 1 second/Forced Vital Capacity ratio (FEV1/FVC% predicted). Cardiovascular disease risk was evaluated through Framingham Risk Score (FRS). Statistical analysis included Spearman correlations tests and one-way ANOVA test. Results: α1-AT (p=0.008), FEV1 (p=0.008), FVC (p=0.03) was significantly lower, while LDLc/HDLc ratio (p=0.01), Atherogenic Index of Plasma (AIP) (p=0.04), FRS (p=0.003) increased in smokers versus nonsmokers. In smokers, statistically significant correlations were found between α1-AT and FVC (r=-0.26;p=0.03); FEV1/FVC ratio (r=0.30;p=0.01); TC (r=0.35;p=0.003); LDLc (r=0.27; p=0.02); nonHDLc (r=0.26;p=0.03). Conclusions: α1-AT interacts with lipid oxidation pathways, decreasing in smokers. A better understanding of the relationships between smoking, oxidative modifications of α1-AT, lung function and, lipid profile can better predict the risk of heart disease. Smoking is a modifiable health risk factor and tobacco cessation may prevent the occurence of cardiovascular diseases.