Serologic Markers of Persistent Chlamydia Pneumonia Infection
Serologic Markers of Persistent Chlamydia Pneumonia Infection
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.
Although coronary stenting (CS) is a well-established therapy in patients with coronary artery disease, a significant proportion of successfully treated patients experience late nonfatal or fatal ischemic events. The pathophysiologic mechanisms for these late events include in-stent restenosis (ISR) or progression of coronary artery disease (PRCAD) in untreated native vessels. Moreover, several studies have recently suggested the incremental role of inflammation in long-term prognosis after either simple angioplasty or CS, and high preprocedural levels of plasma C-reactive protein (CRP) have been shown to portend an increased risk of late ischemic complications. However, despite the mounting evidence, the signals that initiate or maintain this inflammatory process are unknown. It has been hypothesized that viral or bacterial infectious agents may participate in this process and Chlamydia pneumoniae (Cp) is one of the most likely candidates.
Since the first report by Saikku et al of positive immunoglobulin A (IgA) or immunoglobulin G (IgG) anti-Cp titers in patients with acute myocardial infarction or chronic coronary artery disease, a resurgence of interest has been focused on the possible pathophysiologic link between Cp infection and either the manifestations of coronary atherosclerosis or adverse long-term outcomes after coronary angioplasty with or without stent implantation. Thus many prospective studies have been subsequently conducted in different population groups, but the derived results were inconsistent.
However, the presence of Cp has been demonstrated by experimental methods in atherosclerotic coronary plaques but not in nonatherosclerotic coronary lesions or normal arteries. Moreover, Cp is an obligatory intracellular bacterium that has the tendency to cause persistent infection, usually reflected by positive IgA anti-Cp titers (positive IgG anti-Cp titers alone do not distinguish past bacterial exposure from persistent infection), and may drive a chronic inflammatory reaction in coronary vasculature or other tissues. In particular, cytokines produced by Cp-infected macrophages, located in coronary atherosclerotic plaques, may trigger an ongoing inflammatory response (detected by elevated plasma CRP levels), and thus an increased prothrombotic state and smooth muscle cell proliferation, all of which favor atherothrombotic complications and restenosis after CS. It is therefore possible that preprocedural IgA anti-Cp titers may be indicative of an increased underlying cardiovascular inflammatory response, which could be associated with an increased risk of late adverse prognosis after successful CS. The purpose of this study was to evaluate this hypothesis.
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.
Although coronary stenting (CS) is a well-established therapy in patients with coronary artery disease, a significant proportion of successfully treated patients experience late nonfatal or fatal ischemic events. The pathophysiologic mechanisms for these late events include in-stent restenosis (ISR) or progression of coronary artery disease (PRCAD) in untreated native vessels. Moreover, several studies have recently suggested the incremental role of inflammation in long-term prognosis after either simple angioplasty or CS, and high preprocedural levels of plasma C-reactive protein (CRP) have been shown to portend an increased risk of late ischemic complications. However, despite the mounting evidence, the signals that initiate or maintain this inflammatory process are unknown. It has been hypothesized that viral or bacterial infectious agents may participate in this process and Chlamydia pneumoniae (Cp) is one of the most likely candidates.
Since the first report by Saikku et al of positive immunoglobulin A (IgA) or immunoglobulin G (IgG) anti-Cp titers in patients with acute myocardial infarction or chronic coronary artery disease, a resurgence of interest has been focused on the possible pathophysiologic link between Cp infection and either the manifestations of coronary atherosclerosis or adverse long-term outcomes after coronary angioplasty with or without stent implantation. Thus many prospective studies have been subsequently conducted in different population groups, but the derived results were inconsistent.
However, the presence of Cp has been demonstrated by experimental methods in atherosclerotic coronary plaques but not in nonatherosclerotic coronary lesions or normal arteries. Moreover, Cp is an obligatory intracellular bacterium that has the tendency to cause persistent infection, usually reflected by positive IgA anti-Cp titers (positive IgG anti-Cp titers alone do not distinguish past bacterial exposure from persistent infection), and may drive a chronic inflammatory reaction in coronary vasculature or other tissues. In particular, cytokines produced by Cp-infected macrophages, located in coronary atherosclerotic plaques, may trigger an ongoing inflammatory response (detected by elevated plasma CRP levels), and thus an increased prothrombotic state and smooth muscle cell proliferation, all of which favor atherothrombotic complications and restenosis after CS. It is therefore possible that preprocedural IgA anti-Cp titers may be indicative of an increased underlying cardiovascular inflammatory response, which could be associated with an increased risk of late adverse prognosis after successful CS. The purpose of this study was to evaluate this hypothesis.