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Percutaneous coronary intervention (PCI), which includes percutaneous transluminal coronary angioplasty (PTCA) and coronary stenting, has continued expanding its role in the management of coronary atherosclerosis. Major advances in the technical aspects of PCI (especially coronary stents) have had a favorable impact on both early and long-term outcomes(1). Although bare-metal stents have dramatically reduced the incidence of angiographic (>50% stenosis at site of previous PCI) and clinical restenosis (repeat coronary intervention prompted by evidence of recurrent ischemia) compared with balloon angioplasty, restenosis within the stent occurs in 15–30% of cases and has remained a limitation to the long-term success of PCI. The pathogenesis of restenosis is multifactorial and includes smooth muscle cell proliferation and migration, extracellular matrix production, organization of thrombus, elastic recoil, and negative remodeling. Stent implantation, in particular, precipitates arterial intimal cellular proliferation and extracellular matrix synthesis mediated largely by inflammatory processes(2). Because of these considerable contributions of inflammation, preprocedural measurement of the inflammatory marker C-reactive protein (CRP) has been proposed as a method to identify patients at higher risk of restenosis. The report from Rittersma et al.(3) in this issue, however, adds to the aggregate base of evidence that should shift the clinician’s focus from recurrence at a focal site of recent intervention to prevention of events related to vulnerable atheroma elsewhere in the coronary bed.Data regarding the relationship between …

Preprocedural C-Reactive Protein for Risk Prediction Before Percutaneous Coronary Intervention (PCI): A US Perspective