Effect of rosuvastatin therapy on troponin I release following percutaneous coronary intervention in nonemergency patients (from the TIP 3 study).

Several randomized studies have suggested that pretreatment with statins may reduce a periprocedural biomarker release in patients who underwent percutaneous coronary intervention (PCI); however, results remain controversial. The purpose of this study was to investigate the effect of a 1-day rosuvastatin therapy on troponin I release in patients who underwent nonemergency PCI. A total of 445 patients with angina pectoris were randomly assigned to therapy with rosuvastatin (20 mg 12 hours before coronary angiography + 20 mg immediately before PCI; rosuvastatin group, 220 patients) or PCI without statin therapy (control group, 225 patients). In patients taking statins (73%), rosuvastatin was added to their long-term statin therapy. The primary end point was the incidence of TnI microleak defined as TnI elevation >1.5× upper limit of normal, and the secondary end point was the incidence of post-PCI TnI elevation >3× upper limit of normal. The incidence of primary and secondary end point in the rosuvastatin versus control group was 13.6% versus 12% (p = 0.61) and 8.2% versus 7.1% (p = 0.67), respectively. Patients with C-reactive protein ≥2.0 mg/L had a decreased release of post-PCI TnI in the rosuvastatin group (0.032 [0.010 to 0.143] µg/L vs 0.056 [0.018 to 0.241] µg/L; p = 0.04). In conclusion, 1-day rosuvastatin therapy (20 mg twice a day) did not influence post-PCI TnI release in patients with angina. However, these results suggest that, in patients with an advanced inflammatory status, rosuvastatin loading therapy might have a cardioprotective effect.

Efficacy and safety of transient ulnar artery compression to recanalize acute radial artery occlusion after transradial catheterization.

Radial artery occlusion (RAO) can result from transradial catheterization. We compared the incidence of RAO with 2 heparin dosage regimens after transradial coronary angiography, and we evaluated the efficacy and safety of transient homolateral ulnar artery compression to achieve acute radial artery recanalization. Patients referred for coronary angiography were randomized to very-low-dose heparin (2,000 IU) or low-dose heparin (5,000 IU). On sheath removal, hemostasis was obtained using the TR band with a plethysmography-guided patent hemostasis technique. In the case of RAO as assessed by duplex ultrasonography 3 to 4 hours after hemostasis, immediate 1-hour ulnar artery compression was applied. Hematomas >15 cm(2) were also assessed. We randomized 465 patients, 222 in the 2,000-IU group and 243 in the 5,000-IU group. The baseline and procedural characteristics were comparable in both groups. The incidence of initial RAO was 5.9% in the 2,000-IU group and 2.9% in the 5,000-IU group (p = 0.17), with a compression time of 2.10 ± 0.78 hours and 2.25 ± 0.82 hours, respectively (p = 0.051). After ulnar artery compression, the final incidence of RAO was 4.1% in the 2,000-IU group and 0.8% in the 5,000-IU group (p = 0.03). The incidence of local hematoma was 2.3% and 3.7% in the 2,000- and 5,000-IU groups, respectively (p = 0.42). In conclusion, acute RAO after transradial catheterization can be recanalized by early 1-hour homolateral ulnar artery compression. This simple nonpharmacologic method was effective and safe in patients with very-low- and low-dose heparin. Nevertheless, the incidence of final RAO remained significantly lower after a higher anticoagulation level.