193Special Feature / Cardiovascular Revascularization Medicine 12 (2011) 190–194

patients with smaller vessels treated with XIENCE V from XIENCE VUSA, a large, prospective, real-world study.Methods: The XIENCE V stent used in the study ranged from 2.5 to 4.0 mmin diameter. Baseline and 1-year clinical outcomes were compared betweenpatients who had at least one 2.5-mm stent implanted (the smaller vesselcohort, n=1869) and those who were implanted with stents N2.5 mm indiameter (the non-small vessel cohort, n=2905). Events were adjudicated byan independent committee.Results: A total of 2245 lesions were treated with 2.5-mm stents with amean reference vessel diameter of 2.57 mm in the smaller vessel cohort.Compared to the non-small vessel cohort, the smaller vessel cohortconsisted of more females and presented with more diabetes, hypertension,and recent MI. They also had more bifurcation and chronic total occludedlesions, but less restenotic lesions. There were more lesions treated andmore stents implanted per lesion in the smaller vessel cohort. Table 1 showsthe clinical outcomes.Conclusions: Despite higher prevalence of clinical risk factors and morecomplex lesion characteristics, patients in the smaller vessel cohort hadsimilarly low rates of ST, cardiac death and MI, and TLF at 1 year, ascompared to the non-small vessel cohort. Although the TLR rate is slightlyhigher in the smaller vessel cohort, the rates remained low in both groups.These results demonstrated the safety and effectiveness of small vesseltreatment with XIENCE V in this real-world population.

doi:10.1016/j.carrev.2011.02.010

Genetic deficiency of cystathionine gamma-lyase exacerbatesmyocardial reperfusion injury and is rescued by exogenoushydrogen sulfideShashi Bhushan, Madhav Lavu, Benjamin Predmore, Marah Elston,Juan Pablo Aragon, Saurabh Jha, Susheel Gundewar, David LeferEmory University, Atlanta, GA

Hydrogen sulfide (H2S) is a novel gaseous signaling molecule that up-regulates antioxidants, anti-apoptogens, and promotes cellular survival. Inthe heart, cystathionine gamma-lyase (CSE) is the primary enzyme forendogenous production of H2S. We have previously demonstrated thatCSE transgenic mice or mice treated with H2S are protected againstmyocardial ischemia/reperfusion (MI/R) injury and heart failure. Wehypothesized that CSE knockout mice (KO) would develop increasedinfarct size following MI/R compared to wild-type (WT) mice. CSE KOmice (n=12) and WT mice (n=11) at 12–14 weeks of age were subjectedto 45 min of MI and 24 h of R in vivo, at which time the left ventricular(LV) area at risk (AAR) and infarct size (INF) were determined with

Fig. 1. Myocardial infarct size in WT mice vs. CSE knockout mice with orwithout exogenous sulfide administration.

Evan's blue dye and 2,3,5-triphenyl tetrazolium chloride (TTC) staining(Fig. 1). An additional group of CSE KO mice (n=12) was subjected toMI/R and received Na2S (100 μg/kg) at the time of reperfusion. Westernblotting for basal, cardiac antioxidant enzyme levels was also performedin separate groups of mice (n=6 per group). The results show a significantincrease in the myocardial INF/AAR of CSE KO mice compared to WTmice (62±2% vs. 42±3%, respectively, Pb.001). This exacerbation of MI/R injury was attenuated by 50% following Na2S therapy at reperfusion(29±4% INF/AAR, Pb.001, vs. CSE KO). However, CSE KO mice failedto demonstrate a significant difference (P=NS vs. WT) in myocardialtissue levels of thioredoxin (TRX), superoxide dismutase (SOD), heatshock protein 90 (HSP-90), or hemeoxygenase-1 (HO-1). This studydemonstrates that basal H2S production from CSE is critical for protectingthe heart during ischemia and reperfusion. Future studies will determinethe mechanisms by which CSE KO mice have increased susceptibility toMI/R injury.

doi:10.1016/j.carrev.2011.02.011

High on-treatment platelet reactivity is associated with periproceduralmyocardial infarctionMichael A. Gaglia, Jr., Rebecca Torguson, Rajbabu Pakala,Manuel A. Gonzalez, Itsik Ben-Dor, Gabriel Maluenda,Michael Mahmoudi, Gabriel Sardi, Zhenyi Xue, William O. Suddath,Kenneth M. Kent, Lowell F. Satler, Augusto D. Pichard, Ron WaksmanWashington Hospital Center, Washington, DC, USA

Background: Both high on-treatment platelet reactivity and periproceduralmyocardial infarction (MI) are associated with adverse events followingpercutaneous coronary intervention (PCI). The optimal method ofquantifying platelet reactivity remains controversial.Methods: Ninety-eight patients underwent platelet function testing withVerifyNow P2Y12 at 6 to 24 h following PCI. All patients received 600 mgof clopidogrel before PCI; those presenting with acute MI or baselinetroponin elevation were excluded. Periprocedural MI was defined as peaktroponin > upper limit of normal (0.12 ng/ml), and high on-treatment plateletreactivity (HOPR) as ≥235 platelet reactivity units. Multivariable logisticregression was performed to assess the independent effect of on-treatmentplatelet reactivity upon peak troponin.Results: 25.5% of patients had HOPR following PCI. Peak troponin forpatients with HOPR was 10.1 ng/ml vs. 0.63 ng/ml for patients withoutHOPR. Univariate analysis showed HOPR was associated with periproce-dural MI (P=.04). Following multivariable adjustment, HOPR remainedsignificantly associated with periprocedural MI (Table 1).Conclusion: HOPR as measured by VerifyNow P2Y12 is associated withperiprocedural MI. More aggressive platelet inhibition of such patients mayprevent periprocedural MI.

Table 1Multivariable logistic regression for periprocedural myocardial infarction

Odds ratio forperiprocedural MI

95k confidenceinterval

P value

HOPR (PRU 235) 3.41 1.06–11.0 .04Congestive heart failure 2.69 0.57–12.7 .21Diabetes mellitus 0.28 0.09–0.85 .02Hypertension 0.86 0.15–4.87 .87Chronic renal insufficiency 7.78 1.36–44.6 .02Lesions dilated 1.85 1.04–3.31 .04

doi:10.1016/j.carrev.2011.02.012