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Abstract:Background: While preprocedural statin treatment for acute coronary syndrome (ACS) is widely regarded as beneficial, there has been no prospective randomized multicenter trial of patients with non-ST elevation ACS in the Japanese population to examine the efficacy of preprocedural aggressive statin use. The aim of this study was to confirm this effect by prospective randomized multicenter design. Methods: Fifty patients who presented with non-ST elevation ACS were enrolled, and randomly assigned to aggressive statin administration before percutaneous coronary intervention (PCI). Troponin-T (TnT), creatine phosphokinase (CK), CK-myocardial band (CK-MB), high-sense Creactive protein (hs-CRP), and brain natriuretic peptide (BNP) were measured at baseline and/ or after procedure. Results: Three days after PCI, the statin group had significantly less CK elevation compared with the nonstatin group (84±17 IU/l versus 180±68 IU/l, respectively, p ¼ 0.02). CK-MB elevation also tended to be lower in the statin group than in the nonstatin group (3.2±1.9 versus. 7.0±3.0, respectively, p ¼ 0.07), as was BNP level (3.2±1.9 versus 7.0±3.0 pg/ml, respectively, p ¼ 0.07). The change of serum LDL cholesterol was significantly correlated with CK (p ¼ 0.01) and TnT (p ¼ 0.02) at 1 day after PCI. Conclusions: Aggressive statin usage before PCI to Japanese patients with non-ST elevation ACS appears to reduce myocardial damage after procedure. The degree of serum lipid level reduction may reflect the vulnerability of atheromatous plaques that could cause cardiac damage after PCI.

Recently, transradial angiography and intervention have been performed with high success rates and low rates of vascular complications. The incidence of compartment syndrome after the transradial approach seems to be very low. However, bleeding in the arm can occur and may lead to the devastating complication of compartment syndrome of the forearm, which if not treated early, can evolve into a disability of the arm. In fact, most cases of such complications are caused by guidewire- or catheter-induced damage to small arterial branches that are considerably proximal to the puncture site. However, we encountered a case of compartment syndrome that was not caused by bleeding or hematoma formation and required urgent fasciotomy for its treatment. The forearm wounds were left open to allow the edema to resolve and closed after 1 week. The patient recovered and was discharged, with full movement of his forearm and hand. We suspect that an arterial spasm induced by the radial sheath or catheter resulted in ischemia of the forearm muscles. To our knowledge, this is the first reported case in which acute compartment syndrome of the forearm occurred after transradial intervention and was not due to bleeding or hematoma formation.