Use of statins prior to percutaneous coronary intervention reduces myonecrosis and improves clinical outcome.
Primary and secondary prevention with statins reduce major cardiac events in patients with coronary artery disease. The impact of pretreatment with statins prior to percutaneous coronary intervention (PCI) is not well established. The objective of this study was to determine if pretreatment with statins prior to PCI reduce myonecrosis and improve clinical outcome. One hundred nineteen consecutive patients with acute coronary syndrome who underwent PCI were identified. We compared the incidence of myonecrosis defined as peak elevation of CK-MB or CK three time above upper limit of normal within 24 hr and the 6-month cardiovascular event rate (death, nonfatal myocardial infarction unrelated to PCI, target vessels revascularization, and unstable angina requiring hospitalization) among patients who received statins prior to PCI (n = 63) to those who did not (n = 56). Pretreated patients were more likely to have history of myocardial infarction or revascularization (63% vs. 43%; P = 0.015), hyperlipidemia (80% vs. 48%; P = 0.001), hypertension (83% vs. 49%; P = 0.02), and use of angiotensin-converting enzyme inhibitor (62% vs. 38%; P = 0.008). The rest of baseline characteristics were similar between the two groups, including use of glycoprotein IIb/IIIa inhibitors, number of diseased vessels, and type of lesions. Patients pretreated with statins had a significantly lower incidence of myonecrosis (2% vs. 10%; P = 0.04) at 24 hr and a significantly lower clinical event (CE) rate at 6 months (17% vs. 21%; P = 0.015). Of patients not pretreated with statins, 72% were taking statins at 6 months as compared to 98% of pretreated patients. After adjusting for all baseline characteristics, use of statins prior to PCI was associated with a marked decrease in risk of all CEs (OR = 0.2; CI = 0.06-0.63; P = 0.006). Statin therapy prior to PCI may reduces peri-PCI myonecrosis and late cardiac events. These results need to be confirmed in large prospective randomized trials.
Chang
Su Min
SM
Section of Cardiology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Yazbek
Naji
N
Lakkis
Nasser M
NM
D015906:Angioplasty, Balloon, Coronary; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000453:epidemiology / Q000628:therapy; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D015994:Incidence; D007527:Isoenzymes / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000628:therapy; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009336:Necrosis; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000627:therapeutic use; D011237:Predictive Value of Tests; D011446:Prospective Studies; D040242:Risk Reduction Behavior; D013577:Syndrome; D016896:Treatment Outcome
D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007527:Isoenzymes; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form