Does chronic Chlamydia pneumoniae infection increase the risk of myocardial injury? Insights from patients with non-ST-elevation acute coronary syndromes.
BACKGROUND
Cumulative evidence suggests a positive association between Chlamydia pneumoniae (Cpn) infection and risk of future coronary events among patients with stable coronary artery disease. However, its prognostic role in unstable coronary syndromes is less well defined. Because Cpn immunoglobulin A (IgA) may be a more reliable indicator of chronic infection than immunoglobulin G (IgG), we speculated that in patients with non-ST-elevation acute coronary syndromes (ACS), this marker might serve as a more useful prognostic tool. Accordingly, we evaluated plasma samples acquired at presentation in 178 patients with ACS for a possible association between Cpn IgA titer and biochemical evidence of myocardial injury.


METHODS
Cpn IgG (positive if > or =1:32), and IgA titers (positive if > or =1:16) were measured by use of the microimmunofluorescence technique in 70 patients with ACS in whom myocardial injury developed associated with their presenting events (elevated CK-MB and/or troponin I); and in 108 patients with ACS without such injury. The odds ratios (ORs) for myocardial injury associated with consecutive antibody titers were determined for each of Cpn IgG and IgA. Multiple logistic regression was applied to adjust for key baseline characteristics.


RESULTS
Median age of subjects was 64 years; 63% were male and 33% were smokers. The median antibody titers among those with and without myocardial injury respectively were as follows: IgG (1:128 vs 1:128), IgA (1:32 vs <1:16, P =.2). The adjusted ORs for myocardial injury associated with consecutive IgA titers were as follows: IgA > or =1:16, adjusted OR 1.49 (P =.22); > or =1:32, OR 1.95 (P =.04); > or =1:64, OR 1.37 (P =.38); > or =1:128, OR 0.77 (P =.55). No significant trend was found for any IgG titer.


CONCLUSIONS
Among patients with non-ST-elevation ACS, a Cpn IgA > or =1:32 at presentation was associated with a significantly higher risk of myocardial injury complicating the presenting event.
Wong
Brian Y L
BY
University of Alberta, Edmonton, Alberta, Canada.
Gnarpe
Judy
J
Teo
Koon K
KK
Ohman
E Magnus
EM
Prosser
Connie
C
Gibler
W Brian
WB
Langer
Anatoly
A
Chang
Wei-Ching
WC
Armstrong
Paul W
PW
D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D000907:Antibodies, Bacterial / Q000097:blood*; D002690:Chlamydia Infections / Q000453:epidemiology / Q000276:immunology* / Q000503:physiopathology; D016993:Chlamydophila pneumoniae / Q000276:immunology*; D002908:Chronic Disease; D003327:Coronary Disease / Q000097:blood / Q000276:immunology* / Q000382:microbiology* / Q000503:physiopathology; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood*; D007074:Immunoglobulin G / Q000097:blood; D007527:Isoenzymes / Q000097:blood; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011446:Prospective Studies; D016036:Seroepidemiologic Studies; D014336:Troponin / Q000097:blood
D000907:Antibodies, Bacterial; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007527:Isoenzymes; D014336:Troponin; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form