090 Preoperative anemia does not increase the risks of early surgical revascularization following myocardial infarction

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Abstracts

that were subjected to perioperative ischemia and reperfusion demonstrated 1.5 fold greater BRCA1 expression compared to those obtained prior to cardiopulmonary bypass and cardioplegic arrest (P ⬍ 0.05). Second, to extend our observations to a model of chronic ischemic heart disease, we obtained ventricular biopsies from patients undergoing open heart surgery. BRCA1 protein levels in ventricular biopsies from patients undergoing valvular surgery without clinical signs and symptoms of ischemia (non-ischemic group, n ⫽ 4) were compared to tissues from patients with documented coronary artery disease undergoing coronary artery bypass surgery (ischemic group, n ⫽ 11). We report that human ventricular tissues from patients with ischemic heart disease demonstrated higher levels of BRCA1 (⬃2.1 fold) compared to those from subjects without ischemic heart disease (P ⬍ 0.05). Lastly, to evaluate whether BRCA1 up-regulation is specific to the developed vs. developing heart, we studied primary cultures of human fetal cardiomyocytes derived from normal hearts after elective pregnancy termination (gestational age 15-20 weeks). We report a significant (P ⬍ 0.05) up-regulation of total and phosphorylated BRCA1 in human fetal cardiomyocytes in response to hypoxia. CONCLUSION: We provide the first evidence that BRCA1 expression is upregulated in response to ischemia or hypoxia in the developed and developing human heart. These data extend the experimental data on the cardioprotective effects of BRCA1 and suggest that strategies aimed at augmenting BRCA1 bioactivity may represent a novel mechanism to limit ischemic cardiomyopathy. Canadian Society of Cardiac Surgeons (CSCS) CSCS002 Poster SURGERY I Sunday, October 23, 2011

090 PREOPERATIVE ANEMIA DOES NOT INCREASE THE RISKS OF EARLY SURGICAL REVASCULARIZATION FOLLOWING MYOCARDIAL INFARCTION L Zhang, B Hiebert, RC Arora Winnipeg, Manitoba BACKGROUND: Recent clinical studies suggest preoperative anemia increases mortality and morbidity following open-heart surgery. The anemic patients with a recent myocardial infarction (MI) are potentially more vulnerable due to potential oxygen delivery compromise and hemodynamic responses to anemia. This study was to investigate the impact of preoperative anemia on short-term outcomes of coronary bypass surgery performed within 21 days of MI. METHODS: Among 655 patients who received an isolated coronary bypass procedure within 21 days of MI between April 2003 and March 2007, 432 patients met the World Health Organization definition of anemia (hemoglobin ⬍ 130 g/L for men and ⬍ 120 g/L for

women). The outcomes of interest were 30-day mortality and major adverse events (MAEs), which included death, MI, stroke, and renal failure requiring hemodialysis. RESULTS: Overall 30-day mortality was 3.8%, whereas the anemic cohort had a mortality of 5.1%, vs 1.3% in the nonanemic patients (P ⫽ 0.02). Moreover, the incidence of MAEs was significantly higher in the anemic cohort (11.6% vs 4.5%, P ⫽ 0.004). After adjustment of other confounding factors by stepwise multivariable regression, however, preoperative anemia was no longer predicting surgical outcomes (mortality: odds ratio ⫽ 1.8, P ⫽ 0.38; MAEs: odds ratio ⫽ 1.13, P ⫽ 0.76). Analysis of preoperative hemoglobin as a continuous variable in the model yielded similar results. A comparison of surgical outcomes between the anemic and nonanemic group using propensity score matching suggested that preoperative anemia was not associated with mortality or major adverse events. CONCLUSION: Preoperative anemia does not directly increase risks of surgical revascularization within 21 days of MI. 091 STATINS PREVENT EXPANSIVE REMODELING IN ARTERIALIZED VEIN GRAFTS B Qiang, J Toma, H Fujii, A Osherov, N Nili, P Fefer, M Samuel, J Butany, H Leong-Poi, B Strauss Toronto, Ontario

Vein grafts (VG) account for more than 70% of conduits used in aortocoronary bypass surgery, but have high failure rates by 10 years. We have previously shown in an experimental model that VG undergo marked expansion by 4 weeks, which was followed by increased total LDL retention at 12 weeks. The objective of this study was to determine whether statin therapy would prevent these expansive remodelling changes. METHODS/RESULTS Reversed jugular vein-to-common carotid artery interposition graft were constructed in 24 cholesterolfed (0.5%) rabbits. Rabbits were randomized to either control or atorvastatin (5 mg/kg/day) groups, starting two weeks prior to vein graft implantation and continuing until sacrifice at 1 or 12 weeks post-surgery. Ultrasound measurements of arterial luminal cross-sectional area (LCSA) were done at day 3 and at 4, 8 and 12 weeks post-surgery. Histomorphometric measurements were performed following sacrifice at 12 weeks. Atorvastatin treatment significantly decreased total plasma cholesterol levels at 12 weeks (6.70 ⫾ 4.19mmol/L vs placebo 38.65 ⫾ 10.55mmol/L, P ⬍ 0.001). Atorvastatin significantly reduced expansive remodelling at all time points, including at 12 weeks (44.6 ⫾ 6.62mm2 vs placebo 77.6 ⫾ 10.68mm2, P ⬍ 0.001). Intimal CSA by histomorphometry was significantly reduced by atorvastatin at 12 weeks (5.59 ⫾ 2.19mm2 vs placebo 9.57 ⫾ 2.43mm2, P ⬍ 0.05). At 1 week, macrophage infiltration was significantly reduced (Ram11 positive intimal staining 0.018 ⫾ 0.019 vs 0.189 ⫾ 0.049, P ⬍ 0.05). Atorvastatin treated samples at 1 week showed reduction in both MMP 2 activity (gelatin zymography) and metalloelastase activity (casein zymography). CONCLUSION: Atorvastatin prevents expansive remodelling in arteri-