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

G J Arason1, J Kramer, B Blaskó

  • 1Department of Immunology, Institute for Medical Laboratory Sciences, Landspítali University Hospital, Reykjavík, Iceland. garason@lsh.is

Clinical and Experimental Immunology
|April 12, 2007
PubMed

Insights

The C4B*Q0 genotype significantly increases cardiovascular disease risk, especially when combined with smoking. This interaction accelerates the age-related decline of C4B*Q0 carriers, particularly after age 50.

Area of Science:

  • Genetics
  • Cardiovascular Disease Research
  • Epidemiology

Background:

  • The C4B*Q0 genotype is linked to increased risk of myocardial infarction and stroke.
  • Smoking is a major risk factor for cardiovascular disease (CVD).
  • The interaction between C4B*Q0 genotype and smoking requires investigation.

Purpose of the Study:

  • To investigate the interaction between the C4B*Q0 genotype and smoking in relation to cardiovascular disease risk.
  • To determine if smoking modifies the association between C4B*Q0 and CVD outcomes.

Main Methods:

  • Two studies were conducted with participants from Iceland and Hungary.
  • Smoking habits, C4A and C4B gene counts were assessed.
  • C4B*Q0 carrier frequency was compared between cases and controls, stratified by smoking status.

Main Results:

  • C4B*Q0 carrier frequency was significantly higher in smokers with angina pectoris, acute myocardial infarction (AMI), and severe coronary artery disease compared to controls.
  • No significant difference in C4B*Q0 frequency was observed in non-smoking subjects.
  • The age-associated decrease in C4B*Q0 was strongly associated with smoking, occurring after age 50 in smokers.

Conclusions:

  • The C4B*Q0 genotype acts as a significant covariate with smoking in precipitating the risk for AMI and associated deaths.
  • Smoking exacerbates the risk associated with the C4B*Q0 genotype.
  • These findings highlight the critical interplay between genetic predisposition and environmental factors in CVD development.

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