Cardioprotección y anestesia / Anaesthesia and cardioprotection

Junio 10, 2016. No. 2353

Cardioprotección adyuvante en la cirugía cardíaca: actualización. Adjuvant cardioprotection in cardiac surgery: update. Wagner R1, Piler P2, Gabbasov Z3, Maruyama J4, Maruyama K4, Nicovsky J2, Kruzliak P5. Biomed Res Int. 2014;2014:808096. doi: 10.1155/2014/808096. Epub 2014 Aug 19. Abstract Cardiac surgery patients are now more risky in terms of age, comorbidities, and the need for complex procedures. It brings about reperfusion injury, which leads to dysfunction and/or loss of part of the myocardium. These groups of patients have a higher incidence of postoperative complications and mortality. One way of augmenting intraoperative myocardial protection is the phenomenon of myocardial conditioning, elicited with brief nonlethal episodes of ischaemia-reperfusion. In addition, drugs are being tested that mimic ischaemic conditioning. Such cardioprotective techniques are mainly focused on reperfusion injury, a complex response of the organism to the restoration of coronary blood flow in ischaemic tissue, which can lead to cell death. Extensive research over the last three decades has revealed the basic mechanisms of reperfusion injury and myocardial conditioning, suggesting its therapeutic potential. But despite the enormous efforts that have been expended in preclinical studies, almost all cardioprotective therapies have failed in the third phase of clinical trials. One reason is that evolutionary young cellular mechanisms of protection against oxygen handling are not very robust. Ischaemic conditioning, which is among these, is also limited by this. At present, the prevailing belief is that such options of treatment exist, but their full employment will not occur until subquestions and methodological issues with the transfer into clinical practice have been resolved. PDF Cardioproteccción anestésica. Papel de la adenosina Anesthetic cardioprotection: the role of adenosine. Bonney S, Hughes K, Eckle T1. Curr Pharm Des. 2014;20(36):5690-5. Abstract Brief periods of cardiac ischemia and reperfusion exert a protective effect against subsequent longer ischemic periods, a phenomenon coined ischemic preconditioning. Similarly, repeated brief episodes of coronary occlusion and reperfusion at the onset of reperfusion, called post-conditioning, dramatically reduce infarct sizes. Interestingly, both effects can be achieved by the administration of any volatile anesthetic. In fact, cardio-protection by volatile anesthetics is an older phenomenon than ischemic pre- or post-conditioning. Although the mechanism through which anesthetics can mimic ischemic pre- or post-conditioning is still unknown, adenosine generation and signaling are the most redundant triggers in ischemic pre- or post-conditioning. In fact, adenosine signaling has been implicated in isoflurane-mediated cardioprotection. Adenosine acts via four receptors designated as A1, A2a, A2b, and A3. Cardioprotection has been associated with all subtypes, although the role of each remains controversial. Much of the controversy stems from the abundance of receptor agonists and antagonists that are, in fact, capable of interacting with multiple receptor subtypes. Recently, more specific receptor agonists and new genetic animal models have become available paving way towards new discoveries. As such, the adenosine A2b receptor was shown to be the only one of the adenosine receptors whose cardiac expression is induced by ischemia in both mice and humans and whose function is implicated in ischemic pre- or post-conditioning. In the current review, we will focus on adenosine signaling in the context of anesthetic cardioprotection and will highlight new discoveries, which could lead to new therapeutic concepts to treat myocardial ischemia using anesthetic preconditioning. PDF Disfunción diastólica con anestésicos y cardioprotección con halogenados Dr. Carlos Vargas-Trujillo Rev Mex Anestesiología Vol. 35. Supl. 1 Abril-Junio 2012 pp S46-S55 PDF Cursos de Anestesiología en Chile, 2016 Facultad de Medicina. Pontificia Universidad Católica de Chile Información 16th World Congress of Anaesthesiologists 28 August - 2 September 2016  Hong Kong Convention and Exhibition Centre World Federation of Societies of Anaesthesiologists http://wca2016.com/

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Medwave edición Junio 2016

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Condicionamiento isquémico / Ischaemic postconditioning

Junio 9, 2016. No. 2352

El postcondicionamiento isquémico reduce el tamaño del infarto. Revisión sistémica y meta-análisis Ischaemic postconditioning reduces infarct size: systematic review and meta-analysis of randomized controlled trials. Touboul C1, Angoulvant D2, Mewton N3, Ivanes F4, Muntean D5, Prunier F6, Ovize M3, Bejan-Angoulvant T7. Arch Cardiovasc Dis. 2015 Jan;108(1):39-49. doi: 10.1016/j.acvd.2014.08.004. Epub 2014 Nov 13. Abstract BACKGROUND: Infarct size (IS) is a major determinant of patient outcome after acute ST-segment elevation myocardial infarction (STEMI). Interventions aimed at reducing reperfusion injury, such as cardiac ischaemic postconditioning (IPost), may reduce IS and improve clinical outcomes. IPost has been shown to be feasible in patients with STEMI treated by primary percutaneous coronary intervention (PPCI). AIMS: To provide an updated summary of the efficacy of IPost, assessed by analysing accurate surrogate markers of IS. METHODS: We performed a meta-analysis of randomized controlled trials that evaluated the efficacy of IPost in STEMI patients undergoing PPCI. The main outcome was area under the curve of serum creatine kinase release (CK-AUC). Secondary outcomes were other surrogate biomarkers of IS, complete ST-segment resolution, direct measurement of IS by single-photon emission computed tomography and estimation of IS by cardiac magnetic resonance (CMR-IS). RESULTS: Eleven studies were retrieved, including 1313 STEMI patients undergoing PPCI with or without IPost. Compared with controls, we observed a significant reduction in CK-AUC (standard mean difference [SMD] -2.84 IU/L, 95% CI -5.43 to -0.25 IU/L; P=0.03). Other surrogate markers, such as CMR-IS (SMD -0.36, 95% CI -0.88 to 0.15; P=0.16), showed a non-significant IS reduction in the IPost group. CONCLUSIONS: This meta-analysis, dealing with accurate surrogate markers of IS, suggests that IPost reduces IS. However, results should be interpreted cautiously because of limited sample sizes and significant heterogeneity. Whether this translates into improvements in cardiac function and patient prognosis still needs to be demonstrated in larger prospective randomized controlled studies that are powered sufficiently. PDF Señalización postcondicionamiento en el corazón: mecanismos y traducibilidad. Postconditioning signalling in the heart: mechanisms and translatability. Bice JS1, Baxter GF. Br J Pharmacol. 2015 Apr;172(8):1933-46. doi: 10.1111/bph.12976. Epub 2014 Dec 15. Abstract The protective effect of ischaemic postconditioning (short cycles of reperfusion and reocclusion of a previously occluded vessel) was identified over a decade ago commanding intense interest as an approach for modifying reperfusion injury which contributes to infarct size in acute myocardial infarction. Elucidation of the major mechanisms of postconditioning has identified potential pharmacological targets for limitation of reperfusion injury. These include ligands for membrane-associated receptors, activators of phosphokinase survival signalling pathways and inhibitors of the mitochondrial permeability transition pore. In experimental models, numerous agents that target these mechanisms have shown promise as postconditioning mimetics. Nevertheless, clinical studies of ischaemic postconditioning and pharmacological postcondition in gmimetics are equivocal. The majority of experimental research is conducted in animal models which do not fully portray the complexity of risk factors and comorbidities with which patients present and which we now know modify the signalling pathways recruited in postconditioning. Cohort size and power, patient selection, and deficiencies in clinical infarct size estimation may all represent major obstacles to assessing the therapeutic efficacy of postconditioning. Furthermore, chronic treatment of these patients with drugs like ACE inhibitors, statins and nitrates may modify signalling, inhibiting the protective effect of postconditioning mimetics, or conversely induce a maximally protected state wherein no further benefit can be demonstrated. Arguably, successful translation of postconditioning cannot occur until all of these issues are addressed, that is, experimental investigation requires more complex models that better reflect the clinical setting, while clinical investigation requires bigger trials with appropriate patient selection and standardization of clinical infarct size measurements. PDF Cursos de Anestesiología en Chile, 2016 Facultad de Medicina. Pontificia Universidad Católica de Chile Información

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