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Adjuvant cardioprotection in cardiac surgery: update
R. Wagner, P. Piler, Z. Gabbasov, J. Maruyama, K. Maruyama, J. Nicovsky, P. Kruzliak,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
NLK
Free Medical Journals
od 2013
PubMed Central
od 2013
Europe PubMed Central
od 2013
ProQuest Central
od 2013
Open Access Digital Library
od 2001-01-01
Open Access Digital Library
od 2012-12-04
Open Access Digital Library
od 2013-01-01
CINAHL Plus with Full Text (EBSCOhost)
od 2013-01-01
Medline Complete (EBSCOhost)
od 2013-01-01
Health & Medicine (ProQuest)
od 2013
Wiley-Blackwell Open Access Titles
od 2001
ROAD: Directory of Open Access Scholarly Resources
od 2013
PubMed
25215293
DOI
10.1155/2014/808096
Knihovny.cz E-zdroje
- MeSH
- adjuvancia farmaceutická terapeutické užití MeSH
- ischemický postconditioning MeSH
- kardiochirurgické výkony * škodlivé účinky MeSH
- kardiotonika terapeutické užití MeSH
- klinické zkoušky jako téma MeSH
- lidé MeSH
- výsledek terapie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
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.
Citace poskytuje Crossref.org
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- $a Wagner, Robert $u Department of Cardiovascular Anesthesiology, Centre of Cardiovascular and Transplant Surgery, Pekarska 53, 656 91 Brno, Czech Republic ; Department of Cardiovascular Diseases, International Clinical Research Center, St. Anne's University Hospital and Masaryk University, Pekarska 53, 656 91 Brno, Czech Republic.
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- $a 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.
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