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(Stroke. 2004;35:438.)
© 2004 American Heart Association, Inc.

Original Contributions

Synergistic Effect of Apolipoprotein E Polymorphisms and Cigarette Smoking on Risk of Ischemic Stroke in Young Adults

Alessandro Pezzini, MD; Mario Grassi, PhD; Elisabetta Del Zotto, MD; Elena Bazzoli, MD; Silvana Archetti, PhD; Deodato Assanelli, MD; Nabil Maalikjy Akkawi, MD; Alberto Albertini, MD Alessandro Padovani, MD, PhD

From Clinica Neurologica (A.P., E. Del Z., E.B., N.M.A., A.P.), Clinica Cardiologica (D.A.), and III Laboratorio di Analisi, Biotecnologie (S.A., A.A.), Università degli Studi di Brescia, Brescia, and Istituto di Statistica Medica e Biometrie, Università degli Studi di Pavia, Pavia (M.G.), Italia.

Correspondence to Alessandro Pezzini, Clinica Neurologica, Università degli Studi di Brescia, P. le Spedali Civili, 1, 25100 Brescia, Italia. E-mail ale_pezzini{at}hotmail.com

Background and Purpose— The effect of apolipoprotein E (APOE) polymorphisms on stroke risk may be influenced by the coexistence of modifiable predisposing conditions. We explored the interactions of APOE genotypes and conventional risk factors in a case-control study of young adults with cerebral infarct.

Methods— We analyzed 124 consecutive patients (age, 34.7±7.3 years) and 147 age- and sex-matched controls. APOE genotypes were determined by restriction fragment-length polymorphism analysis.

Results— The prevalence of the 4 allele and 34 genotype was slightly higher in cases than in controls (0.125 versus 0.071 and 0.242 versus 0.136, respectively). Carriers of the 34 genotype and 4 allele were associated with an increased risk of stroke on multivariate analysis compared with the 33 genotype and non-4 carriers, respectively (odds ratio [OR], 2.29; 95% confidence interval [CI], 1.10 to 4.76; and OR, 2.27; 95% CI, 1.13 to 4.56). ORs for stroke were 2.99 (95% CI, 1.64 to 5.45), 2.69 (95% CI, 1.25 to 5.77), and 5.39 (95% CI, 1.59 to 18.30) for smokers with the 33 genotype, nonsmokers with the 34 genotype, and smokers with the 34 genotype, respectively, compared with nonsmokers with the 33 genotype. Similar results were obtained when 4 carriers and non-4 carriers were compared in the same interaction model. No significant interaction between APOE and hypertension was found.

Conclusions— In young adults, the APOE 4 allele and cigarette smoking act synergistically, increasing an individual’s propensity to have a cerebral ischemic event. This finding may help in determining an individual’s predisposition to stroke and more targeted preventive interventions.

Key Words: apolipoproteins • cigarette smoking • polymorphism • risk factors

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