Preoperative oral coenzyme Q(10) therapy in patients undergoing cardiac surgery increases myocardial and cardiac mitochondrial coenzyme Q(10) levels, improves mitochondrial efficiency, and increases myocardial tolerance to in vitro hypoxia-reoxygenation stress.

Open inguinal hernia repair with a nylon darn was equivalent to polypropylene mesh with respect to early measures of postoperative outcome and recurrence at 1 year.

Elevated preoperative TnT highlights a subgroup of cardiac surgical patients who are more likely to have a post-operative course with increased morbidity and mortality.

The efficacy of levosimendan treatment for a low cardiac output status following cardiac surgery has not been established. Here, we review our initial experiences of the perioperative use of levosimendan. This study is a retrospective uncontrolled trial. Nine patients who underwent cardiac surgery, and developed a low cardiac output status resistant to conventional inotropic support, were given levosimendan. The mean preoperative ejection fraction was 35.2+/-3.4%. All patients were on concomitant inotropic agents and had previously undergone intra-aortic balloon pumping. Cardiac index increased immediately from 2.14+/-0.33 l/min/m(2) at baseline to 2.41+/-0.31 (P=0.02) at 1 h, rising to 2.67+/-0.43 (P<0.001) at 4 h after the loading dose was started. Similarly, the systemic vascular resistance index decreased from 2350+/-525 dynes/s/cm(-5)/m(2) at baseline to 1774+/-360 (P=0.002) at 4 h. In the case of all but one of the patients, either the dose of the concomitant inotropic support or the balloon pumping could be weaned down within 24 h after completion of the levosimendan infusion. No withdrawal of levosimendan was required. Levosimendan could constitute a new therapeutic option for postoperative low cardiac output.

With aging of the population, increasing numbers of elderly patients are presenting for cardiac surgery. However, the results in the elderly are inferior to those in the young. A likely contributing factor is an age-related reduction in cellular energy production in the myocardium during surgery, which is known to induce aerobic and ischemic stress. The lipophilic antioxidant and mitochondrial respiratory chain redox coupler, coenzyme Q10 (CoQ10), has the potential to improve energy production in mitochondria by bypassing defective components in the respiratory chain as well as by reducing the effects of oxidative stress. We hypothesized that CoQ10 pretreatment prior to stress could improve the recovery of the myocardium after stress.