Smoking and a complement gene polymorphism interact in promoting cardiovascular disease morbidity and mortality

G. J. Arason, J. Krámer, B. Blaskó, R. Kolka, P. Thorbjornsdottir, K. Einarsdóttir, A. Sigfúsdóttir, S. T. Siguroarson, G. Sigurosson, Z. Rónai, Z. Prohászka, M. Sasvári, S. Böovarsson, G. Thorgeirsson, G. Füst

Research output: Article

19 Citations (Scopus)

Abstract

We have demonstrated previously that carriers of a genotype called C4B*Q0 (silent allele of the C4B gene) have a substantially increased risk to suffer from myocardial infarction or stroke, and are selected out from the healthy elderly population. Because smoking carries a major risk for cardiovascular disease (CVD), it seemed worthwhile to study if these two factors interact. Study 1 involved 74 patients with angina pectoris (AP), 85 patients with recent acute myocardial infarction (AMI) and 112 survivors of a previous AMI and 382 controls from Iceland. Study 2 involved 233 patients with severe CVD and 274 controls from Hungary. Smoking habits were registered for each subject. The number of C4A and C4B genes was determined by phenotyping or genotyping. Compared to controls, C4B*Q0 carrier frequency was significantly higher at diagnosis in Icelandic smokers with AP (P = 0.005) and AMI (P = 0.0003) and Hungarian smokers with severe coronary artery disease (P = 0.023), while no such difference was observed in non-smoking subjects. Age-associated decrease in C4B*Q0 observed previously in two remote Caucasian populations was found, in the present study, to be associated strongly with smoking, and to already occur in smokers after age 50 years both in Iceland and Hungary. Our findings indicate that the C4B*Q0 genotype can be considered as a major covariate of smoking in precipitating the risk for AMI and associated deaths.

Original languageEnglish
Pages (from-to)132-138
Number of pages7
JournalClinical and Experimental Immunology
Volume149
Issue number1
DOIs
Publication statusPublished - júl. 2007

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Cardiovascular Diseases
Smoking
Myocardial Infarction
Morbidity
Mortality
Iceland
Hungary
Genes
Angina Pectoris
Genotype
Population
Habits
Survivors
Coronary Artery Disease
Stroke
Alleles

ASJC Scopus subject areas

  • Immunology

Cite this

Smoking and a complement gene polymorphism interact in promoting cardiovascular disease morbidity and mortality. / Arason, G. J.; Krámer, J.; Blaskó, B.; Kolka, R.; Thorbjornsdottir, P.; Einarsdóttir, K.; Sigfúsdóttir, A.; Siguroarson, S. T.; Sigurosson, G.; Rónai, Z.; Prohászka, Z.; Sasvári, M.; Böovarsson, S.; Thorgeirsson, G.; Füst, G.

In: Clinical and Experimental Immunology, Vol. 149, No. 1, 07.2007, p. 132-138.

Research output: Article

Arason, GJ, Krámer, J, Blaskó, B, Kolka, R, Thorbjornsdottir, P, Einarsdóttir, K, Sigfúsdóttir, A, Siguroarson, ST, Sigurosson, G, Rónai, Z, Prohászka, Z, Sasvári, M, Böovarsson, S, Thorgeirsson, G & Füst, G 2007, 'Smoking and a complement gene polymorphism interact in promoting cardiovascular disease morbidity and mortality', Clinical and Experimental Immunology, vol. 149, no. 1, pp. 132-138. https://doi.org/10.1111/j.1365-2249.2007.03391.x
Arason, G. J. ; Krámer, J. ; Blaskó, B. ; Kolka, R. ; Thorbjornsdottir, P. ; Einarsdóttir, K. ; Sigfúsdóttir, A. ; Siguroarson, S. T. ; Sigurosson, G. ; Rónai, Z. ; Prohászka, Z. ; Sasvári, M. ; Böovarsson, S. ; Thorgeirsson, G. ; Füst, G. / Smoking and a complement gene polymorphism interact in promoting cardiovascular disease morbidity and mortality. In: Clinical and Experimental Immunology. 2007 ; Vol. 149, No. 1. pp. 132-138.
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abstract = "We have demonstrated previously that carriers of a genotype called C4B*Q0 (silent allele of the C4B gene) have a substantially increased risk to suffer from myocardial infarction or stroke, and are selected out from the healthy elderly population. Because smoking carries a major risk for cardiovascular disease (CVD), it seemed worthwhile to study if these two factors interact. Study 1 involved 74 patients with angina pectoris (AP), 85 patients with recent acute myocardial infarction (AMI) and 112 survivors of a previous AMI and 382 controls from Iceland. Study 2 involved 233 patients with severe CVD and 274 controls from Hungary. Smoking habits were registered for each subject. The number of C4A and C4B genes was determined by phenotyping or genotyping. Compared to controls, C4B*Q0 carrier frequency was significantly higher at diagnosis in Icelandic smokers with AP (P = 0.005) and AMI (P = 0.0003) and Hungarian smokers with severe coronary artery disease (P = 0.023), while no such difference was observed in non-smoking subjects. Age-associated decrease in C4B*Q0 observed previously in two remote Caucasian populations was found, in the present study, to be associated strongly with smoking, and to already occur in smokers after age 50 years both in Iceland and Hungary. Our findings indicate that the C4B*Q0 genotype can be considered as a major covariate of smoking in precipitating the risk for AMI and associated deaths.",
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AU - Thorbjornsdottir, P.

AU - Einarsdóttir, K.

AU - Sigfúsdóttir, A.

AU - Siguroarson, S. T.

AU - Sigurosson, G.

AU - Rónai, Z.

AU - Prohászka, Z.

AU - Sasvári, M.

AU - Böovarsson, S.

AU - Thorgeirsson, G.

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