First- versus second-generation drug-eluting stents for the treatment of coronary bifurcations

BackgroundRandomized controlled trials have demonstrated that second-generation drug-eluting stents (DESs) for the treatment of obstructive coronary artery disease are associated with comparable, if not improved, clinical outcomes as compared to those of their first-generation counterparts. The aim of this study was to compare the long-term clinical outcomes associated with first- versus second-generation DESs for the treatment of coronary bifurcation lesions.Methods and MaterialsThis was a retrospective study of consecutive de novo bifurcation lesions, excluding those at the left main, treated with either second-generation DES (everolimus-eluting or resolute zotarolimus-eluting stents) between October 2006 and October 2011 (199 bifurcation lesions in 192 patients) or first-generation DES (sirolimus-eluting or paclitaxel-eluting stents) between April 2002 and December 2005 (289 bifurcation lesions in 273 patients).ResultsSecond-generation DES use in this setting was associated with less major adverse cardiac events (MACE) (23.1% vs. 14.4%, p = 0.02) as well as lower target vessel revascularization (TVR) rates (15.5% vs. 8.3%, p = 0.01) at 2-year follow-up. Target lesion revascularization, both per patient (12.6% vs. 7.4%, p = 0.02) and per bifurcation (11.8% vs. 7.0%, p = 0.03), was also improved with second-generation DES over the same follow-up period. Propensity-score adjusted analysis suggested that second-generation DES was associated with a lower incidence of MACE (HR, 0.53; 95% CI, 0.33–0.85; p = 0.01) and TVR (HR, 0.44; 95% CI, 0.24–0.83; p = 0.01).ConclusionsOur results suggest that the use of second-generation DES for the treatment of bifurcation lesions is associated with better clinical outcomes as compared to first-generation DES, largely due to a lower need for repeat revascularization.     

Influence of endothelial nitric oxide synthase gene polymorphisms (G894T, 4a4b, T-786C) and hyperhomocysteinemia on the predisposition to acute coronary syndromes

Background

Nitric oxide is an endothelium-derived relaxing factor that contributes significantly to vascular tone regulation. In this study we investigated the role of endothelial nitric oxide synthase (eNOS) polymorphisms as predisposing factors to acute coronary syndromes (ACS).

Methods

In 477 consecutive patients admitted to the coronary intensive therapy unit of the University of Florence and in 537 unrelated controls, genotypes of eNOS G894T and T-786C polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism analysis and the repeat polymorphism 4a/4b was analyzed by polymerase chain reaction. The genotype distribution was in Hardy-Weinberg equilibrium for all variants.

Results

The multivariate analysis showed that the homozygosity for the eNOS 4a rare variant represented an independent predisposition factor to ACS (odds ratio [OR] 2.5, 95% CI 1.1-5.4, P = .02) and in particular influenced the risk of acute myocardial infarction (OR 3.6, 95% CI 1.2-11.5, P = .03). Subjects carrying the 4a4a/-786CC haplotype showed a higher predisposition to the disease (OR 6.1, 95% CI 1.3-29.6, P = .02). The contemporary presence of hyperhomocysteinemia and homozygosity for the -786C variant influenced the predisposition to ACS (OR 9.1, 95% CI 1.7-46.7, P = .008).

Conclusions

The presence of the eNOS 4a4a genotype represents a predisposing condition to ACS and in particular to acute myocardial infarction. Moreover, our data provide the evidence that the -786CC pattern modulates the susceptibility to ACS in 4a4a homozygotes and in hyperhomocysteinemic patients.