C-Reactive Protein and Increased Risk of Clinical Restenosis
C-Reactive Protein and Increased Risk of Clinical Restenosis
Background: Restenosis after percutaneous coronary intervention (PCI) constitutes a serious complication in the treatment of cardiovascular disease, but known risk factors do not fully account for the observed restenosis risk. Preliminary studies of infection or inflammation in restenosis report varied results. We tested whether C-reactive protein (CRP) or pathogen burden (seropositivity to 0, 1, 2, or 3 pathogens, of Chlamydia pneumoniae [Cpn], cytomegalovirus [CMV], or Helicobacter pylori [Hpy]) predict clinical restenosis after percutaneous coronary intervention (PCI).
Methods: Blood samples were collected from 415 patients undergoing PCI, and levels of plasma CRP and antibodies to Cpn, CMV, and Hpy were measured. The patient's medical history, demographics, and procedural data were recorded. Patient end points were determined for as long as 6 months as a means of evaluating the incidence of clinical restenosis and major adverse cardiac events.
Results: The average patient age was 62 years, and 80% of patients were male. Fifty-eight patients (14%) experienced clinical restenosis, whereas 17 patients (4%) died or had an acute myocardial infarction. After adjusting for 19 possible predictors, we found the pathogen burden (P-trend = .04, adjusted odds ratio [OR] 1.5 per number of pathogens) and minimum luminal diameter (P = .003, OR 1.8 per mm decrease) to be significant predictors of clinical restenosis. Male sex was a nonsignificant predictor of restenosis (P = .06, OR 2.2), but CRP was not significant after adjustment (P-trend = .10, OR 0.73 per tertile).
Conclusion: Pathogen burden was associated with clinical coronary restenosis, an association that deserves further exploration and evaluation. CRP, a marker of inflammation, was not associated with an increased risk of restenosis.
Percutaneous coronary intervention (PCI), including balloon angioplasty, intracoronary stent deployment, and a variety of atherectomy procedures, has become an accepted approach to coronary revascularization, with procedural success rates often reaching higher than 95%. Despite excellent procedural results, and even with the aggressive use of coronary stents, PCI remains plagued by the troublesome complication of late restenosis. The pathophysiologic characteristics of restenosis remain relatively poorly understood, but appear to differ fundamentally from those of primary atherosclerosis in that intimal hyperplasia tends to play a more important role than lipid accumulation. Currently known clinical and angiographic predictors of restenosis include such characteristics as patient sex, diabetes mellitus, lesion length, postprocedural minimum luminal diameter (MLD), and whether coronary stents were used. However, these factors account for only a small proportion of the total incidence of restenosis, and so the search for others continues.
Recently, a large body of information has been published about a potential role of inflammation in the pathogenesis of atherosclerosis. It appears to occur directly via the action of inflammatory cells within the atherosclerotic plaque and indirectly through systemic inflammatory mediators such as C-reactive protein (CRP). Mounting evidence also indicates that various forms of chronic infection may contribute to the pathogenesis of atherosclerosis. Epidemiologic associations between cardiovascular events and an exposure history (seropositivity) to infectious agents are reported for several suspect organisms, including Chlamydia pneumoniae (Cpn), cytomegalovirus (CMV), and Helicobacter pylori (Hpy), although reported results have not always been consistent. Additionally, significant associations between the number of various infectious agents to which a patient is exposed, or the "pathogen burden," and the development or progression of atherosclerosis have been reported.
Although restenosis may have different mechanisms than coronary artery disease (CAD) development, the connection between restenosis and some traditional cardiovascular risk factors (eg, diabetes mellitus) suggests that some factors can influence both processes. Inflammation and infection, although not necessarily associated with one another, individually merit evaluation for association to restenosis because of the potential for CAD-related factors to also influence restenosis. The objective of this study was to determine whether the pathogen burden (seropositivity to 0, 1, 2, or 3 pathogens, including CMV, Hpy, or Cpn) or baseline CRP level is associated with clinical restenosis in a population undergoing PCI at a single care center.
Background: Restenosis after percutaneous coronary intervention (PCI) constitutes a serious complication in the treatment of cardiovascular disease, but known risk factors do not fully account for the observed restenosis risk. Preliminary studies of infection or inflammation in restenosis report varied results. We tested whether C-reactive protein (CRP) or pathogen burden (seropositivity to 0, 1, 2, or 3 pathogens, of Chlamydia pneumoniae [Cpn], cytomegalovirus [CMV], or Helicobacter pylori [Hpy]) predict clinical restenosis after percutaneous coronary intervention (PCI).
Methods: Blood samples were collected from 415 patients undergoing PCI, and levels of plasma CRP and antibodies to Cpn, CMV, and Hpy were measured. The patient's medical history, demographics, and procedural data were recorded. Patient end points were determined for as long as 6 months as a means of evaluating the incidence of clinical restenosis and major adverse cardiac events.
Results: The average patient age was 62 years, and 80% of patients were male. Fifty-eight patients (14%) experienced clinical restenosis, whereas 17 patients (4%) died or had an acute myocardial infarction. After adjusting for 19 possible predictors, we found the pathogen burden (P-trend = .04, adjusted odds ratio [OR] 1.5 per number of pathogens) and minimum luminal diameter (P = .003, OR 1.8 per mm decrease) to be significant predictors of clinical restenosis. Male sex was a nonsignificant predictor of restenosis (P = .06, OR 2.2), but CRP was not significant after adjustment (P-trend = .10, OR 0.73 per tertile).
Conclusion: Pathogen burden was associated with clinical coronary restenosis, an association that deserves further exploration and evaluation. CRP, a marker of inflammation, was not associated with an increased risk of restenosis.
Percutaneous coronary intervention (PCI), including balloon angioplasty, intracoronary stent deployment, and a variety of atherectomy procedures, has become an accepted approach to coronary revascularization, with procedural success rates often reaching higher than 95%. Despite excellent procedural results, and even with the aggressive use of coronary stents, PCI remains plagued by the troublesome complication of late restenosis. The pathophysiologic characteristics of restenosis remain relatively poorly understood, but appear to differ fundamentally from those of primary atherosclerosis in that intimal hyperplasia tends to play a more important role than lipid accumulation. Currently known clinical and angiographic predictors of restenosis include such characteristics as patient sex, diabetes mellitus, lesion length, postprocedural minimum luminal diameter (MLD), and whether coronary stents were used. However, these factors account for only a small proportion of the total incidence of restenosis, and so the search for others continues.
Recently, a large body of information has been published about a potential role of inflammation in the pathogenesis of atherosclerosis. It appears to occur directly via the action of inflammatory cells within the atherosclerotic plaque and indirectly through systemic inflammatory mediators such as C-reactive protein (CRP). Mounting evidence also indicates that various forms of chronic infection may contribute to the pathogenesis of atherosclerosis. Epidemiologic associations between cardiovascular events and an exposure history (seropositivity) to infectious agents are reported for several suspect organisms, including Chlamydia pneumoniae (Cpn), cytomegalovirus (CMV), and Helicobacter pylori (Hpy), although reported results have not always been consistent. Additionally, significant associations between the number of various infectious agents to which a patient is exposed, or the "pathogen burden," and the development or progression of atherosclerosis have been reported.
Although restenosis may have different mechanisms than coronary artery disease (CAD) development, the connection between restenosis and some traditional cardiovascular risk factors (eg, diabetes mellitus) suggests that some factors can influence both processes. Inflammation and infection, although not necessarily associated with one another, individually merit evaluation for association to restenosis because of the potential for CAD-related factors to also influence restenosis. The objective of this study was to determine whether the pathogen burden (seropositivity to 0, 1, 2, or 3 pathogens, including CMV, Hpy, or Cpn) or baseline CRP level is associated with clinical restenosis in a population undergoing PCI at a single care center.
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