The implications of renal impairment among patients undergoing percutaneous coronary intervention.
The clinical implications of even mild impairment of renal function in percutaneous coronary interventions (PCI) have, to date, been poorly appreciated. The progressive loss of renal function is marked by the onset of a thrombo-inflammatory state not unlike what occurs in progressive coronary artery disease (CAD). In the presence of renal insufficiency, procedural success is reduced, peri-procedural myocardial infarction (MI) is more frequent and increased late mortality, myocardial ischemia and target vessel revascularization are more common. Vessel stenting reduces the rate of target vessel revascularization in renal failure patients, but fails to impact the frequency of peri-procedural ischemic events. Consequently, a rational, evidence-based approach to adjunctive anticoagulation in renal failure patients undergoing PCI is warranted if per-procedural ischemic events are to be better managed. Unfortunately, current recommendations are hampered by a paucity of clinical trial evidence specifically examining the efficacy of available therapies. In an attempt to go beyond this lack of clinical evidence, some therapeutic insight may be drawn from the known hemostatic derangements associated with renal impairment. These changes include a well-described decreased in platelet aggregatory activity and an increase in thrombin generation. While more definitive clinical trial evidence of adjunctive anticoagulation efficacy among patients with renal impairment is in process, this article will briefly review the pathophysiological changes associated with renal impairment, as well as the evidence supporting each of the current therapeutic options available to the interventional cardiologist.
Sica
Domenic
D
Section of Clinical Pharmacology and Hypertension, Division of Nephrology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA.
D015906:Angioplasty, Balloon, Coronary; D001777:Blood Coagulation / Q000502:physiology; D001792:Blood Platelets / Q000473:pathology; D003324:Coronary Artery Disease / Q000150:complications / Q000188:drug therapy / Q000628:therapy; D018450:Disease Progression; D019317:Evidence-Based Medicine; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D051437:Renal Insufficiency / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D016896:Treatment Outcome
D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors