Serologic markers of persistent chlamydia pneumonia infection and long-term prognosis after successful coronary stenting - 28/08/11
, Olga A Papadaki, MD a, Paraskevi K Psarogianni, MD a, Maria A Thoma, MD a, George K Andrikopoulos, MD a, Pelagia C Batika, RN a, Christina G Poulopoulou, MD a, Kyriaki G Trifinopoulou, MD a, Christopher D Olympios, MD a, Stefanos G Foussas, MD, FESC, FACC aAbstract |
Background |
Previous studies have shown an incremental role of inflammation in late prognosis following coronary stenting (CS). In particular, high preprocedural levels of plasma C-reactive protein (CRP) have been related to increased hazard of late ischemic complications. Persistent Chlamydia pneumoniae (Cp) infection, detected by positive IgA anti-Cp titers, may be associated with this inflammatory process and portend a high risk of late adverse prognosis after CS.
Methods |
A total of 483 consecutive patients with either stable or unstable coronary syndromes were followed-up for 1 year after successful CS. The composite of cardiac death, myocardial infarction, rehospitalization for rest-unstable angina, and exertional angina, whichever occurred first, was the clinical end point. Additionally, the rate of in-stent restenosis and progression of coronary artery disease during this period were evaluated. Anti-Cp titers and plasma CRP levels were measured before the procedure.
Results |
Positive immunoglobulin A (IgA), but not positive immunoglobulin G (IgG), titers were significantly associated with high plasma CRP levels in patients with unstable coronary syndromes (P = .005), but not in those with stable angina (P = .7). Moreover, positive IgA titers were significantly related to increased risk of both the composite clinical end point (P = .04) and progression of coronary artery disease (P < .001) in patients with unstable coronary syndromes but not in those with stable angina. Neither positive IgA nor positive IgG titers were associated with the rate of in-stent restenosis.
Conclusions |
Persistent Cp infection may drive an inflammatory response in the coronary vasculature and portends an adverse late outcome after CS in patients with unstable coronary syndromes.
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Vol 146 - N° 6
P. 1082-1089 - décembre 2003 Retour au numéro
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