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Effects of total pathogen burden on coronary artery disease risk and C-reactive protein levels
J Zhu1, A A Quyyumi, J E Norman
1Cardiovascular Research Institute, Washington Hospital Center, DC 20010, USA.
Insights
Infections contribute to coronary artery disease (CAD) risk. Higher pathogen burden, indicated by antibodies to multiple infectious agents, correlates with increased CAD risk and elevated C-reactive protein (CRP) inflammation markers.
Area of Science:
- Infectious disease epidemiology
- Cardiovascular medicine
- Immunology
Background:
- Infection and inflammation are implicated in the development of coronary artery disease (CAD).
- The relationship between cumulative pathogen exposure and CAD risk requires further investigation.
- C-reactive protein (CRP) serves as a key biomarker for systemic inflammation.
Purpose of the Study:
- To investigate the association between pathogen burden and CAD risk.
- To determine if increased pathogen burden correlates with elevated CRP levels.
- To explore the role of infectious agents in the pathogenesis of atherosclerosis.
Main Methods:
- Evaluated 233 patients for CAD using coronary angiography.
- Assessed immunoglobulin-G (IgG) antibody seropositivity for cytomegalovirus (CMV), Chlamydia pneumoniae, hepatitis A virus (HAV), herpes simplex virus type 1 (HSV-1), and HSV type 2.
- Measured C-reactive protein (CRP) levels in blood samples.
Main Results:
- 68% of patients had evidence of CAD.
- Increasing pathogen burden was significantly associated with increased CAD risk, even after adjusting for traditional risk factors.
- Pathogen burden was also significantly associated with elevated CRP levels, suggesting an inflammatory link.
Conclusions:
- Cumulative exposure to pathogens (pathogen burden) is a significant risk factor for CAD.
- Infectious agents may contribute to atherosclerosis development through inflammatory pathways.
- Pathogen burden is a relevant predictor of systemic inflammation as indicated by CRP levels.
Abstract:
Infection and inflammation have been suggested to play roles in coronary artery disease (CAD). We hypothesized that: (1) CAD risk is associated with the aggregate number of pathogens (pathogen burden), and (2) increased pathogen burden is associated with elevated levels of C-reactive protein (CRP), a marker of inflammation. We evaluated 233 patients for CAD. Blood samples from each patient were tested for immunoglobulin-G (IgG) antibodies to cytomegalovirus (CMV), Chlamydia pneumoniae, hepatitis A virus (HAV), herpes simplex virus type 1 (HSV-1) and HSV type 2 (HSV-2), and for the CRP levels. Of the 233 study subjects, 68% had evidence of CAD by coronary angiography. Although the prevalence of seropositivity for each pathogen tended to be higher in the patients with CAD than those without, only the association between CAD and seropositivity to HAV was significant in multivariate analysis. Over 75% of study subjects had been exposed to > or =3 of the 5 pathogens tested, and analysis determined that increasing pathogen burden was significantly associated with increasing CAD risk, even after adjustment for traditional CAD risk factors. The prevalence of CAD was 48%, 69%, and 85% in individuals with antibodies to < or =2 pathogens, to 3 or 4 pathogens, and to 5 pathogens, respectively. A similar association between increasing pathogen burden and CRP levels was also found. The pathogen burden remained a significant predictor of CRP levels after multivariate analysis. Our data suggest that infection does play a role in the genesis of atherosclerosis. However, the risk posed by infection is related to the pathogen burden that may contribute to CAD through inflammatory responses.