ABSTRACT
AIM: The BASE-ACS trial demonstrated an outcome of titanium-nitride-oxide-coated bioactive stents (BAS) that was statistically non-inferior to that of everolimus-eluting stents (EES) at 12-month follow-up, in patients presenting with acute coronary syndrome (ACS) who underwent early percutaneous coronary intervention (PCI). We explored a post-hoc analysis of the 12-month outcome of the BASE-ACS trial in the subgroup of patients with ST-elevation myocardial infarction (STEMI) versus non-ST-elevation ACS (non-STEACS). METHODS: A total of 827 patients with ACS (321 STEMI) were randomly assigned to receive either BAS or EES. The primary endpoint was a composite of cardiac death, non-fatal myocardial infarction (MI) and ischemia-driven target lesion revascularization (TLR) at 12-month follow-up. RESULTS: The 12-month cumulative incidence of the primary endpoint was similar between the two subgroups (9% versus 9.5%, in STEMI versus non-STEACS patients respectively, P=0.90). The 12-month rate of cardiac death was significantly higher in the STEMI subgroup as compared with the non-STEACS subgroup (2.8 versus 0.6%, respectively, P=0.01). However, the rates of non-fatal MI, ischemia-driven TLR, definite stent thrombosis, and non-cardiac death were all statistically matched between the two subgroups (P>0.05 for all). CONCLUSION: In the current post-hoc analysis of the BASE-ACS trial based on the infarction type, the 12-month outcome of patients who underwent early PCI for ACS was slightly worse in the setting of STEMI as compared with non-STEACS, as reflected by a significantly higher rate of cardiac death.
Subject(s)
Acute Coronary Syndrome/surgery , Drug-Eluting Stents , Multicenter Studies as Topic/statistics & numerical data , Myocardial Infarction/surgery , Percutaneous Coronary Intervention , Sirolimus/analogs & derivatives , Acute Coronary Syndrome/drug therapy , Aged , Anticoagulants/therapeutic use , Coated Materials, Biocompatible , Combined Modality Therapy , Coronary Restenosis/epidemiology , Disease-Free Survival , Everolimus , Female , Follow-Up Studies , Heart Diseases/mortality , Humans , Incidence , Male , Middle Aged , Myocardial Infarction/drug therapy , Myocardial Ischemia/epidemiology , Myocardial Ischemia/surgery , Platelet Aggregation Inhibitors/therapeutic use , Postoperative Complications/mortality , Randomized Controlled Trials as Topic , Sirolimus/administration & dosage , Sirolimus/therapeutic use , Titanium , Treatment OutcomeSubject(s)
Intubation, Intratracheal/adverse effects , Parotitis/etiology , Acute Disease , Fatal Outcome , Humans , MaleABSTRACT
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Subject(s)
Humans , Male , Parotitis/etiology , Intubation, Intratracheal/adverse effects , Myocardial Infarction/surgery , Angioplasty, Balloon, CoronaryABSTRACT
The quantitative capabilities of Western "ligand" blot analysis (LBA) of insulin-like growth factor binding protein have been evaluated using iodine-labeled insulin-like growth factor-II (125I-IGF-II), purified amniotic fluid insulin-like growth factor binding protein-1 (IGFBP-1), and IGFBP-1 in conditioned medium (CM) from Hep-G2 cells. Optimal conditions were evaluated for analysis of IGFBP-1 using IGF-2-II as the ligand. IGFBP-1 ligand blot quantities were measured after autoradiography by one- (1D) and two (2D)-dimensional densitometry. The 2D method was found to exhibit higher linearity (IGF-I, r = 0.993; IGF-II, r = 0.984) over a wider range than the 1D method. Displacement curves for IGF-II against membrane-bound IGFBP-1 measured by LBA were similar to those obtained with IGFBP-1 solutions using antibody precipitation of IGFBP-1. Transfer of IGFBP-1 from sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels to nitrocellulose membranes was linear across the range 3.1-400 ng with both the 0.45- and the 0.2-micron pore sizes tested. The 0.2-micron size, however, showed nearly quantitative binding of IGFBP-1 trapping 20% more of this binding protein than the larger pore size. LBA was used to measure IGFBP-1 in CM from control and des1-3IGF-I (trIGF-I)-treated Hep-G2 cells and the results were compared with those obtained by a specific IGFBP-1 radioimmunoassay. IGFBP-1 concentrations measured by both assays were similar and both demonstrated nearly identical sensitivities. Each assay confirmed the previously noted trIGF-I suppression of IGFBP-1 secretion by Hep-G2 cells.
