Objective: Obese patients are thought to have an increased risk for complications in coronary artery bypass surgery. Several risk stratification systems do not identify obesity as a variable for risk adjustment. The aim of this study is to evaluate the in-hospital and early (one year) mortality and morbidity in obese and non-obese patients after a CABG in the UMC St Radboud. Methods: The data of 1130 patients undergoing a myocardial revascularization from January 2000 to August 2002 were analyzed. Obesity was measured by the body mass index (BMI). A BMI $ 30 kg/m 2 was defined as obese. We compared 206 obese patients with 924 non-obese patients. Uni-and multivariate analysis were used to analyze the results. The 1-year survival was analyzed using Kaplan -Meier methods. Results: There were no significant differences between obese and non-obese patients according to postoperative myocardial infarction, re-operation for bleeding, in-hospital mortality, renal complications, neurological complications, pulmonary complications, gastrointestinal complications, re-intubation, re-admission on intensive care, ventilation time, days on intensive care, days in hospital and late mortality. Only the incidence of postoperative wound infections was increased in obese patients, 8.3% in the obese versus 4.4% in the non-obese ðP ¼ 0:02Þ: Multivariate analysis identified obesity only as risk factor for postoperative for wound infections (P ¼ 0:04; odds ratio: 1.97). Conclusions: Obese patients do not have an increased risk of in-hospital and early (1 year) mortality after CABG. However, obese patients have an increased risk of postoperative wound infections compared to non-obese patients. q

OFU improves the completeness of the follow-up, as expected, but informs superior about mortality and events. That in the NOFU, for 50% of the patients, the information is at the most 78 days postoperative old, let us suppose that a lot of early (6 months) postoperative information is even missed by an NOFU. The establishment of an organized follow-up and feedback of mortality and events after myocardial revascularization becomes indispensable.

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Hexokinase II (HKII) is a glycolytic enzyme that can be bound to mitochondria (mtHKII) or free in the cytosol. Previous studies showed that increased amounts of mtHKII protect the heart against ischemia/reperfusion injury.We hypothesized that reduced mtHKII binding increases ischemia/reperfusion damage by increased respiration and ROS production. Procedures were in accordance with the Institutional Animal Ethical Committee and conform to National Institutes of Health guidelines. Langendorff-perfused rat hearts were exposed to 20 minutes of saline, 1 μ M TAT-only or 200 nM or 1 μ M TAT-HKII, followed by 15 minutes of ischemia and 30 minutes of reperfusion. TAT-HKII translocates HKII from the mitochondria. During the complete protocol, cardiac oxygen consumption (MVO 2), cardiac function (rate pressure product [RPP]), and ROS (DHE fluorescence) were measured. Mitochondrial oxygen tension was measured by using protoporphyrin IX-delayed fluorescence before and after peptide treatment. During reperfusion, necrosis was measured by lactate dehydrogenase (LDH) activity in effluent.In the 1 μ M TAT-HKII hearts, MV−O/RPP was increased and mitochondrial oxygen tension was reduced during peptide treatment. This was not observed after treatment with 200 nM TAT-HKII nor in the control groups. During reperfusion, MVO 2 /RPP was increased in both treatment groups. ROS production increased in both TAT-HKII groups during ischemia and reperfusion. These effects were accompanied by increased LDH activity during reperfusion in both TAT-HKII treated groups. No LDH activity was observed in control groups.Reduction of mtHKII by TAT-HKII treatment turns reversible ischemia into irreversible ischemia. This might be caused by increased ROS production during ischemia and reperfusion, and increased oxygen consumption.