Outcomes of patients receiving clopidogrel prior to cardiac surgery.

BACKGROUND: Clinical impact of the concomitant clopidogrel therapy on clinical outcomes in patients undergoing cardiac surgery is unclear. We aimed to pool and systematically analyze outcomes in clopidogrel-treated patients undergoing cardiac operations to achieve greater statistical power and to define precise effect-estimates. METHODS: PubMed and Central databases were searched for relevant studies published between January 2001 and May 2010. The main outcome measures were the rates of red blood cell (RBC) transfusion, reoperation, myocardial infarction and postoperative mortality. The outcome parameters were pooled with the random-effect model via generic-inverse variance-weighting. RESULTS: Twenty studies comprising a total number of 23,668 patients were analyzed. Pooled analysis revealed that the administration of clopidogrel had a higher risk for postoperative mortality (OR: 1.24; 95% CI: 1.03-1.49, p=0.03) that was consistent among studies. The rates of myocardial infarction were similar between groups. Clopidogrel-exposed patients were associated with a significantly higher rate of RBC transfusion (OR: 1.82; 95% CI: 1.40-2.37; p<0.00001) and reoperation (OR: 2.15; 95% CI: 1.38-3.34; p<0.00001), although there was a marked heterogeneity among studies. According to subgroup analysis the mortality and the rates of transfusions were higher in studies in which clopidogrel was not discontinued 5 days prior to surgery, while the higher risk for reoperation was only apparent in studies published before 2006. CONCLUSION: Meta-analysis of observational studies demonstrated that concomitant treatment with clopidogrel before cardiac surgery is associated with a significant risk of bleeding-related complications and with a higher mortality.

Prolactin-releasing peptide regulates cardiac contractility.

High levels of specific prolactin-releasing peptide (PrRP) binding sites have been found in the myocardium; however, the functional importance of PrRP in the regulation of cardiac function is unknown. In isolated perfused rat hearts, infusion of PrRP (1-100 nM) induced a dose-dependent positive inotropic effect. Inhibition of cAMP catabolism by IBMX, a phosphodiesterase inhibitor, failed to augment the contractile effect of PrRP. The protein phosphatase (PP1/PP2A) inhibitor calyculin A increased the inotropic response to PrRP, whereas the PP2A inhibitor okadaic acid had no effect. Ro32-0432, a protein kinase C alpha (PKC alpha) inhibitor, significantly enhanced the inotropic effect of PrRP as well as the phosphorylation of phospholamban at Ser-16. In conclusion, the present data define a hitherto unrecognized role for PrRP in the regulation of cardiovascular system by showing that PrRP exerts a direct positive inotropic effect. Moreover, our results suggest that the cAMP-independent inotropic response to PrRP is suppressed by concurrent activation of PKC alpha and PP1.

[Pumpless extracorporeal lung assist]. / A minimalizált extracorporális tüdôtámogatás.

The recently introduced pumpless extracorporeal lung assist (PECLA) is a remarkable alternative to the conventional extracorporeal membrane oxygenation in case of severe lung failure. By establishing a shunt between femoral artery and vein using the arterio-venous pressure gradient as a driving force through a low-resistance membrane oxygenator, PECLA provides highly effective gas-exchange by preserved cardiac function. Due to its closed system, reduced priming volume and low heparin demand, the unfavourable effects of extracorporeal membrane oxygenation can be effectively diminished. Hence the small technical, financial and personal input, the PECLA can be ideally used in district hospitals and during transport as well. Our short summary demonstrates the advantages and safety of the system proven over 123 cases.

Direct effects of apelin on cardiomyocyte contractility and electrophysiology.

Apelin, the ligand for the angiotensin receptor like-1, has been implicated in the pathogenesis of atrial fibrillation and heart failure. However, it is unknown if apelin has direct effects on cardiomyocyte contractility and electrophysiology. APJ-like immunoreactivity was localized to T-tubules and intercalated disc area in isolated adult rat ventricular myocytes. Apelin (1 nM) significantly increased sarcomere shortening in normal as well as failing cardiomyocytes. The transient increase in shortening was not accompanied by increased [Ca(2+)] transient amplitude. Apelin significantly activated the sarcolemmal Na(+)/H(+) exchanger (NHE) and increased intracellular pH. Moreover, apelin (10 nM) increased conduction velocity in monolayers of cultured neonatal rat cardiac myocytes. Our results demonstrate for the first time that apelin has direct effects on the propagation of action potential and contractility in cardiomyocytes. One of the mechanisms involved in the inotropic effect may be an increased myofilament sensitivity to Ca(2+) as apelin enhanced the activity of NHE with consequent intracellular alkalinization.