Evaluation of C-reactive protein, an inflammatory marker, and infectious serology as risk factors for coronary artery disease and myocardial infarction.
OBJECTIVE
We sought to test whether C-reactive protein (CRP) and seropositivity to any of three infectious agents are associated with angiographic coronary artery disease (CAD) and clinical myocardial infarction (MI).


BACKGROUND
CRP, an inflammatory marker, is reported to predict risk of MI. The stimulus for CRP is unknown but might include infection. Chlamydia pneumoniae, cytomegalovirus and Helicobacter pylori have been linked to risk of MI or CAD.


METHODS
Blood samples were collected from 363 patients undergoing coronary arteriography and tested for CRP and IgG titers to the infectious agents.


RESULTS
CRP was higher in patients with CAD (1.32 mg/dl [SE 0.22, n = 80] vs. 0.58 mg/dl [SE 0.11 mg/dl, n = 109], p = 0.004) and in those with MI (2.05 mg/dl [SE 0.36, n = 47] vs. 0.54 mg/dl [SE 0.08, n = 133], p = 0.0002) than in respective control subjects. Seropositivity for each agent was present in a high proportion of patients with CAD (58% to 77%) or MI (54% to 75%) as well as in control subjects (no CAD: 46% to 74%; no MI: 50% to 77%). However, subjects seropositive to both C. pneumoniae and H. pylori had an increased prevalence of CAD (odds ratio [OR] 2.6, p = 0.02) and MI (OR 2.0, p = 0.15) and tended to have higher CRP levels (1.07 mg/dl [SE 0.16]) than those seronegative to both infectious agents (0.53 mg/dl [SE 0.10], p = 0.06).


CONCLUSIONS
CRP is elevated in patients with CAD (more than twofold) and in those with MI (fourfold). Infectious serology is highly prevalent in both patients and control subjects. Seropositivity to both C. pneumoniae and H. pylori (but not one agent alone) may predict increased risk and may be associated with higher CRP levels. Infectious serology may be less predictive than previously suggested, but the cause of inflammation in CAD and MI deserves further study.
Anderson
J L
JL
University of Utah School of Medicine, Department of Internal Medicine, LDS Hospital, Salt Lake City, USA. jeffrey_anderson@merck.com
Carlquist
J F
JF
Muhlestein
J B
JB
Horne
B D
BD
Elmer
S P
SP
D000328:Adult; D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism*; D016993:Chlamydophila pneumoniae / Q000276:immunology; D017023:Coronary Angiography; D003327:Coronary Disease / Q000175:diagnosis* / Q000276:immunology; D003587:Cytomegalovirus / Q000276:immunology; D005260:Female; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000276:immunology; D012307:Risk Factors; D012680:Sensitivity and Specificity; D018746:Systemic Inflammatory Response Syndrome / Q000175:diagnosis* / Q000276:immunology
D007074:Immunoglobulin G; D018836:Inflammation Mediators; D002097:C-Reactive Protein