Statin Administration Before Percutaneous Coronary Intervention - Statin Administration Before PCI

Jan 31, 2005
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Date Published:
01/01/2004
Date Updated:
01/31/2005
Original Posted Date:
01/31/2005
References

Description:

The goal of the trial was to evaluate the effect of administration of statin therapy prior to percutaneous coronary intervention (PCI) on the development of periprocedural non-Q-wave myocardial infarction (MI).

Hypothesis:

Treatment with statin therapy for at least three days prior to PCI would be associated with a reduction in periprocedural MI in patients undergoing elective PCI.

Study Design

Study Design:

Patients Enrolled: 451
Mean Follow Up: Hospital discharge
Mean Patient Age: Mean age 63 years
Female: 13

Patient Populations:

Not taking statins and scheduled for elective PCI in de novo lesions in native coronary arteries

Exclusions:

Abnormal baseline CK-MB and/or cardiac troponin I levels

Primary Endpoints:

Large non-Q-wave MI, defined as CK-MB >5 times ULN

Drug/Procedures Used:

Patients not on statin therapy who were scheduled for elective PCI were randomized to either statin therapy (n=226) or no treatment (n=225). Statin therapy was started at least three days prior to PCI. Type and dose of statin was at the discretion of the physician. All patients were given a prescription for a statin after the procedure. Blood samples were drawn prior to PCI and at 6 and 12 hours after PCI to assess creatinine kinase myocardial isoenzyme (CK-MB) and troponin I.

Concomitant Medications:

Aspirin (325 mg) and ticlopidine (250 mg bid) or clopidogrel (75 mg daily); unfractionated heparin (70 IU/kg intravenous bolus plus additional boluses to maintain activated clotting time >300 seconds) during the procedure

Principal Findings:

Statin treatment was started an average of 17 days prior to PCI in the treatment group, with 84% of patients on statin therapy for ≥2 weeks. Simvastatin was the most frequently used statin (39%), followed by atorvastatin and pravastatin (29% each) and fluvastatin (3%). At the time of the procedure, low-density lipoprotein was lower in the statin group (93 mg/dl vs. 121 mg/dl, p<0.001), as was total cholesterol (168 mg/dl vs. 193 mg/dl, p<0.001).

Elevated C-reactive protein occurred less often in the statin group (13.8% vs. 27%, p=0.007). Angiographic characteristics were similar, including diameter stenosis (79% each pre-PCI and 4% each post-PCI), TIMI flow grade 2/3 (16% each pre-PCI and 84% each post-PCI), and lesion length (15 mm each).

Peak CK-MB post-PCI was lower in the statin group than the control group (median 1.70 vs. 2.20 ng/ml, p=0.015), as was peak troponin I (median 0.13 vs. 0.21 ng/ml, p=0.033). Large non-Q-wave MI, defined as CK-MB >5 times the upper limit of normal (ULN) occurred less frequently in the statin group (8.0% vs. 15.6%, odds ratio [OR] 0.47, p=0.012). Troponin I elevation >5 times the ULN also occurred less frequently in the statin group (23.5% vs. 32%, OR 0.65, p=0.043). In a multivariate model, statin therapy remained associated with a lower rate of CK-MB >5 times ULN post-PCI (OR 0.33, p=0.023), as did angiographic procedural complications (OR 9.36, p<0.001) and age >65 years (OR 2.58, p=0.031).

Interpretation:

Among patients undergoing elective PCI, treatment with at least three days of statin therapy prior to PCI was associated with a reduction in large non-Q-wave MI compared with no statin therapy. These findings were similar to that of the randomized, double-blind ARMYDA trial, which showed a reduction in periprocedural MI associated with atorvastatin therapy prior to PCI. The authors of the present study hypothesized that the benefit associated with statin therapy may be due to an increase in plaque stability, attributable to lower LDL or less inflammation.

One limitation of the present trial was the open-label manner of the control group. Additionally, the study did not prespecify the duration of therapy prior to PCI or the statin or dose.

References:

Briguoria C, Colombo A, Airoldi F, et al. Statin administration before percutaneous coronary intervention: impact on periprocedural myocardial infarction. Eur Heart J 2004;25:1822-8.

Keywords: Odds Ratio, Inflammation, Myocardial Infarction, Isoenzymes, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Fatty Acids, Monounsaturated, Creatinine, Heptanoic Acids, Constriction, Pathologic, Simvastatin, Percutaneous Coronary Intervention, Lipoproteins, LDL, Pyrroles, Cholesterol, C-Reactive Protein, Troponin I, Indoles, Pravastatin, Coronary Vessels


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