Effects of receipt of chronic statin therapy before the onset of acute myocardial infarction: a retrospective study in patients undergoing primary percutaneous coronary intervention

Clin Ther. 2006 Nov;28(11):1812-9. doi: 10.1016/j.clinthera.2006.11.003.

Abstract

Background: Studies have reported an association between receipt of statin therapy and a reduction in complications after elective percutaneous coronary intervention (PCI). However, there are limited data on the effects of chronic statin therapy before the occurrence of an acute myocardial infarction (AMI).

Objective: This study investigated whether administration of chronic statin therapy before AMI was associated with a reduction in reperfusion injury in AMI patients undergoing PCI.

Methods: This was a retrospective study of consecutive patients with a first AMI who underwent successful reperfusion therapy with PCI within 24 hours after the onset of AMI between April 1998 and October 2003. Patients were stratified according to whether they had or had not been receiving chronic statin therapy for > or = 1 month before the onset of AMI. The following end points were compared after PCI: electrocardiographic resolution of ST segment elevation, defined as a reduction of > or = 50% from the initial value; achievement of Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow; corrected TIMI frame count (cTFC); maximum serum creatine kinase (CK) level; and the type and frequency of ventricular arrhythmias.

Results: The study enrolled 386 patients, 40 of whom had been receiving statin therapy before the onset of AMI. The clinical characteristics of the 2 groups were similar at baseline, with the exceptions of a significantly higher rate of hyperlipidemia in the statin group compared with the nonstatin group (P < 0.001), significantly greater chronic use of aspirin therapy (P < 0.001), and significantly greater chronic use of antihypertensive medications (beta-blockers: P = 0.004; angiotensin-converting enzyme inhibitors/angiotensin II-receptor blockers: P = 0.007; calcium channel blockers: P = 0.006). Electrocardiographic ST segment resolution after PCI was observed in 87.5% and 69.9% of the statin and nonstatin groups, respectively (hazard ratio [HR]: 3.01; 95% CI, 1.15-7.90; P = 0.025). Achievement of TIMI grade 3 flow after PCI was seen in 95.0% of the statin group and 83.5% of the nonstatin group (HR: 3.75; 95% CI, 0.88-16.0; P = NS). Patients treated with a statin had a significantly lower mean (SD) maximum CK level compared with the nonstatin group (2300 [1449] vs 3538 [3170] IU/mL, respectively; P = 0.015) and a lower cTFC after PCI (18.8 [4.0] vs 24.2 [14.2]; P = 0.017). The difference in reperfusion arrhythmias between groups was not statistically significant. After adjustment for baseline covariates, pretreatment with a statin was found to be an independent predictor of ST segment resolution after PCI (HR: 2.95; 95% CI, 1.08-8.09; P = 0.035) and prevention of impaired coronary flow (HR: 3.00; 95% CI, 1.63-5.55; P < 0.001).

Conclusion: In this study, receipt of chronic statin therapy before the onset of AMI was associated with improvement in epicardial perfusion and a reduction in myocardial necrosis after PCI.

Publication types

  • Clinical Trial
  • Comparative Study

MeSH terms

  • Adrenergic beta-Antagonists / administration & dosage
  • Adrenergic beta-Antagonists / adverse effects
  • Aged
  • Angioplasty, Balloon, Coronary* / adverse effects
  • Calcium Channel Blockers / administration & dosage
  • Calcium Channel Blockers / adverse effects
  • Female
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / administration & dosage*
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / adverse effects
  • Male
  • Middle Aged
  • Myocardial Infarction / complications
  • Myocardial Infarction / physiopathology
  • Myocardial Infarction / therapy*
  • Myocardial Reperfusion Injury / etiology
  • Myocardial Reperfusion Injury / physiopathology
  • Myocardial Reperfusion Injury / prevention & control*
  • Retrospective Studies

Substances

  • Adrenergic beta-Antagonists
  • Calcium Channel Blockers
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors