Withdrawal of statins increases event rates in patients with acute coronary syndromes.
BACKGROUND
HMG-CoA Reductase Inhibitors (statins) reduce cardiac event rates in patients with stable coronary heart disease. Withdrawal of chronic statin treatment during acute coronary syndromes may impair vascular function independent of lipid-lowering effects and thus increase cardiac event rate.


RESULTS
We investigated the effects of statins on the cardiac event rate in 1616 patients of the Platelet Receptor Inhibition in Ischemic Syndrome Management (PRISM) study who had coronary artery disease and chest pain in the previous 24 hours. We recorded death and nonfatal myocardial infarction during the 30-day follow-up. Baseline clinical characteristics did not differ among 1249 patients without statin therapy, 379 patients with continued statin therapy, and 86 patients with discontinued statin therapy after hospitalization. Statin therapy was associated with a reduced event rate at 30-day follow-up compared with patients without statins (adjusted hazard ratio, 0.49 [95% CI, 0.21 to 0.86]; P=0.004). If the statin therapy was withdrawn after admission, cardiac risk increased compared with patients who continued to receive statins (2.93 [95% CI, 1.64 to 6.27]; P=0.005) and tended to be higher compared with patients who never received statins (1.69 [95% CI, 0.92 to 3.56]; P=0.15). This was related to an increased event rate during the first week after onset of symptoms and was independent of cholesterol levels. In a multivariate model, troponin T elevation (P=0.005), ST changes (P=0.02), and continuation of statin therapy (P=0.008) were the only independent predictors of patient outcome.


CONCLUSIONS
Statin pretreatment in patients with acute coronary syndromes is associated with improved clinical outcome. However, discontinuation of statins after onset of symptoms completely abrogates this beneficial effect.
Heeschen
Christopher
C
University Hospital Frankfurt, Germany.
Hamm
Christian W
CW
Laufs
Ulrich
U
Snapinn
Steven
S
Böhm
Michael
M
White
Harvey D
HD
D000208:Acute Disease; D002784:Cholesterol / Q000097:blood; D002986:Clinical Trials as Topic; D015897:Comorbidity; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000401:mortality*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005500:Follow-Up Studies; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects* / Q000627:therapeutic use; D015994:Incidence; D008148:Lovastatin / Q000009:adverse effects / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000139:chemically induced* / Q000453:epidemiology; D016017:Odds Ratio; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D017035:Pravastatin / Q000009:adverse effects / Q000627:therapeutic use; D016016:Proportional Hazards Models; D012307:Risk Factors; D019821:Simvastatin / Q000009:adverse effects / Q000627:therapeutic use; D013375:Substance Withdrawal Syndrome; D015996:Survival Rate; D016896:Treatment Outcome; D014336:Troponin / Q000097:blood; D014481:United States / Q000453:epidemiology
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010975:Platelet Aggregation Inhibitors; D014336:Troponin; D006493:Heparin; D002784:Cholesterol; D008148:Lovastatin; D019821:Simvastatin; D017035:Pravastatin