Use of Rosuvastatin Prior to Angioplasty Does Not Influence Troponin I Release Following Angioplasty


November 9, 2012

November 9, 2012 — A study found that the use of rosuvastatin prior to angioplasty did not influence the levels of troponin I, a sensitive indicator of muscle damage. Results were presented at the 24th annual Transcatheter Cardiovascular Therapeutics (TCT) scientific symposium, sponsored by the Cardiovascular Research Foundation (CRF).

Previous randomized studies have suggested that pretreatment with statins may reduce a periprocedural myocardial infarction (PMI) in patients with stable and/or unstable angina during an angioplasty or percutaneous coronary intervention (PCI). The purpose of this international, multicenter, randomized study was to investigate the effect of a one-day rosuvastatin loading therapy on troponin I (TnI) release in patients with stable or unstable angina undergoing PCI. Troponin is a protein that is released when the heart muscle has been damaged (for example, during a heart attack). The more damage there is to the heart, the greater the amount of troponin levels there will be in the blood.

Researchers assessed more than 1,700 patients for eligibility in the trial. Four hundred and seventy-eight patients with stable or unstable (troponin-negative) angina pectoris were enrolled and randomized in a 1:1 ratio. Patients in the experimental group were given 20 mg of rosuvastatin 12 hours prior to coronary angiography and 20 mg immediately prior to PCI (220 analyzable patients). Those in the control group underwent PCI without loading statin therapy (225 analyzable patients). In patients taking statins, rosuvastatin was added to their established statin therapy.

The serum concentration of troponin was measured at baseline, 6 to 12 hours after PCI, and 16 to 24 hours after PCI. The primary endpoint was the incidence of troponin l (Tnl) microleak defined as TnI elevation >1.5x upper limit of normal (ULN), and the secondary endpoint was the incidence of PMI defined as TnI elevation >3x ULN. The incidence of primary and secondary endpoint in the rosuvastatin vs. control group was 13.6% vs. 12.0% (p=0.61) and 8.2% vs. 7.1% (p=0.67), respectively.

While the incidence of the primary endpoint did not differ by inflammatory status as measured by c-reactive protein (CRP), in a secondary and exploratory analysis, patients with a c-reactive protein level ≥2.0 mg/l had a decreased release of post-PCI TnI in the rosuvastatin group (0.032 μg/l vs. 0.056 μg/l; p = 0.045).

“One-day, high-dose rosuvastatin loading therapy did not reduce the occurrence of troponin microleak after angioplasty or periprocedural heart attack. However, these results suggest that, in patients with an advanced inflammatory status, rosuvastatin loading therapy might have a cardioprotective effect,” said lead researcher Josef Veselka, M.D., Ph.D, professor of medicine at Charles University and chief of the department of cardiology at University Hospital Motol in Prague, Czech Republic.

Veselka reported grant and research support from the Ministry of Health, Czech Republic.

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