Pre-PCI Statin Regimen Produces No Significant Effect on Troponin I Release

MIAMI BEACH, FLA.—Negative findings of the TIP 3 study delivered a setback to the strategy of statin loading before PCI. Although most randomized studies suggest that statin loading or reloading helps prevent periprocedural MI due to the effect of statins on plaque stabilization, the therapy remains controversial.

Josef Veselka, MD, PhD, of Motol University Hospital, Prague, Czech Republic, and colleagues randomized patients with troponin-negative stable or unstable angina at four Eastern European centers to rosuvastatin 20 mg 1 day before PCI (n = 220) or no-added rosuvastatin (n = 225). About three quarters of both arms were already on chronic statin therapy. Study and control groups were well matched for baseline characteristics. Periprocedural and angiographic characteristics were also similar.

Post-PCI, there was no difference between groups in rates of troponin I levels greater than 1.5 times the upper limit of normal, the primary endpoint, or in rates of different troponin I elevations (see Figure).

In multivariate analysis, only pretreatment with beta blockers predicted the primary endpoint (OR 0.520; 95% CI 0.294-0.922; P=.03).

A prespecified subgroup analysis of 218 patients with C-reactive protein levels ≥ 2 mg/l (roughly equally divided between rosuvastatin and control patients) also showed no effect of rosuvastatin loading on the incidence of the primary endpoint (12% in the rosuvastatin group vs. 14% in controls; P=.66). However, patients with elevated C-reactive protein showed a decreased release of post-PCI troponin I in the rosuvastatin group (0.032 µg/l vs. 0.056 µg/l; P=.04).

Veselka noted that in the ARMYDA-RECAPTURE trial, chronic statin therapy with up to 80 mg atorvastatin 12 hours before PCI and 40 mg 2 hours before PCI made no difference in the incidence of periprocedural MI (P=.06) or MACE within 30 days (P=.98) in patients with stable angina. However, in the ARMYDA-ACS trial, among ACS patients, atorvastatin pretreatment resulted in a threefold reduction in the incidence of periprocedural MI.

Based on these randomized trials and the current data, Veselka hypothesized that high-dose pre-PCI statin therapy influences post-PCI  troponin I release only in some patients with high procedural risk. Thus, in patients with significant inflammation, rosuvastatin therapy may have a cardioprotective effect, but this possibility requires further prospective study, he said.

In discussion, Germano Di Sciascio, MD, of Campus Bio-Medico University, Rome, Italy, asked Veselka how he views the study results in light of current European Society of Cardiology guidelines recommending statin pre-treatment. “Guidelines are guidelines, and science is science,” Veselka said, adding that he has now performed three randomized studies involving about 1,000 patients and all were negative. “The most plausible explanation is that these patients were really low-risk patients,” he said. “The higher-risk the patient, the higher the potential benefit associated with statin therapy.” 

Another discussant suggested that differences in the solubility of various statins may help explain discordant results.