ObjectiveDel Nido (DN) cardioplegia solution provides a depolarized hyperkalemic arrest lasting up to 60 minutes, and the addition of lidocaine may limit intracellular calcium influx. Single-dose DN cardioplegia solution may offer an alternative myocardial protection strategy to multi-dose cold whole blood (WB) cardioplegia following acute myocardial infarction (AMI).MethodsWe retrospectively reviewed 88 consecutive patients with AMI undergoing coronary artery bypass (CABG) surgery with cardioplegic arrest between June 2010 to June 2012. Patients exclusively received WB (n = 40, June 2010-July 2011) or DN (n = 48, August 2011-June 2012) cardioplegia. Preoperative and postoperative data were retrospectively reviewed and compared using propensity scoring.ResultsNo significant difference in age, maximum preoperative serum troponin level, ejection fraction, and STS score was present between DN and WB. A single cardioplegia dose was given in 41 DN vs. 0 WB patients (p < 0.001), and retrograde cardioplegia was used 10 DN vs. 31 WB patients (p < 0.001). Mean cardiopulmonary bypass and cross clamp times were significantly shorter in the DN group versus WB group. Tranfusion rate, length of stay, intra-aortic balloon pump requirement, post-operative inotropic support, and 30-day mortality was no different between groups. One patient in the WB group required a mechanical support due to profound cardiogenic shock.ConclusionsDN cardioplegia may provide equivalent myocardial protection to existing cardioplegia without negative inotropic effects in the setting of acute myocardial infarction.Electronic supplementary materialThe online version of this article (doi:10.1186/s13019-014-0141-5) contains supplementary material, which is available to authorized users.

Altogether, these data suggest that increased levels of miR-195 in failing myocardium regulate a novel pathway that involves direct SIRT3 suppression and enzymatic inhibition via increased acetylation of PDH and ATP synthase that are essential for cardiac energy metabolism.

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Following the publication of our article, we became aware of a related publication by Reforgiato and coauthors that described increased de novo ceramide synthesis and inflammation adjacent to the necrotic core area in a mouse model of 30 minutes of ischemia and reperfusion injury (1). Similar to the findings of our study in a chronic model of ischemic cardiomyopathy 3 months following myocardial infarction and in a large cohort of patients with advanced heart failure, Reforgiato et al. found that ceramide accumulation was accompanied by increased levels of serine palmitoyltransferase (SPT), which could be inhibited by administration of myriocin, an inhibitor of SPT. Their study, which was performed in an animal model of acute ischemic injury, independently supports the findings of our systematic lipidomic study in patients with advanced heart failure before and after mechanical unloading and cardiomyopathy as well as Sptlc2-deletion mice. We believe the detailed lipidomic analysis in our study provides an important advance to the field. This analysis allowed the differentiation of various ceramide species, and we related specific ceramide chain lengths to the biologic phenotypes described. Further, we linked ceramide metabolism and de novo ceramide synthesis using various expression plasmids (sptlc1, -2 and -3) in cell culture experiments to changes in ceramide species accumulation and dysregulation of oxidative and glycolytic metabolism as typical for the failing myocardium. Thus, we linked the lipids to changes in their metabolic pathways. Together, these studies highlight a key role of de novo ceramide synthesis of distinct ceramide species and their accumulation following acute ischemic injury and in chronically failing myocardium.