Document Detail

Modulation of individual susceptibility to the no-reflow phenomenon after acute myocardial infarction.
MedLine Citation:
PMID:  23270556     Owner:  NLM     Status:  Publisher    
Coronary reperfusion using primary percutaneous coronary intervention (PCI) dramatically reduces morbidity and mortality among patients with acute myocardial infarction (AMI). Nevertheless, inadequate myocardial perfusion, known as the "no-reflow" phenomenon, is observed in approximately 15% of patients and is associated with poor outcomes. No-reflow is caused not only by mechanical occlusion of the microvasculature due to thromboembolism but also by myocardial injury. Transmural myocardial damage before PCI and the size of the associated area are major factors in the development of no-reflow. There is evidence indicating that inflammation, oxidative injury, morphological changes of endothelial cells, hyperglycemia, and absence of ischemic preconditioning also contribute to the development of no-reflow. Several strategies have been attempted to counteract these risk factors. To prevent microembolization related to PCI, thrombus aspiration appears promising, but distal protection devices have failed to demonstrate the expected results among patients with AMI. Most cardioprotective agents developed to modify the risk factors for no-reflow have been effective in animal experiments but have disappointed in clinical trials. Adjunctive treatments using statins, adenosine, atrial natriuretic peptide, nicorandil, or glycoprotein IIb/IIIa antagonists have been effective in reducing the infarct size or improving outcomes after AMI in clinical studies, although some have shown inconsistent results. It is probable that the relevance of each component associated with no-reflow is different for individual patients, and therefore the attempt to indiscriminately apply one treatment to all patients will not be as successful as expected. Individual susceptibility has to be evaluated when selecting an appropriate adjunctive treatment to prevent no-reflow in patients with AMI.
Katsuomi Iwakura
Related Documents :
11045426 - Cardiac functional improvement by a human bcl-2 transgene in a mouse model of ischemia/...
2407376 - Mechanisms and therapy of myocardial reperfusion injury.
9401816 - Protection of rat myocardium by mitogenic and non-mitogenic fibroblast growth factor du...
6252586 - Studies on myocardial mitochondria in ischemic dog hearts by electron spin resonance (e...
1104166 - Applications of echocardiography in acute myocardial infarction.
17055466 - The dietary flavonoid quercetin activates bkca currents in coronary arteries via produc...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-12-21
Journal Detail:
Title:  Current pharmaceutical design     Volume:  -     ISSN:  1873-4286     ISO Abbreviation:  Curr. Pharm. Des.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-28     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9602487     Medline TA:  Curr Pharm Des     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Division of Cardiology, Sakurabashi Watanabe Hospital 2-4-32, Umeda, Kita-ku, Osaka 530000, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Protecting the heart: Biological targets and Clinical Strategies.
Next Document:  Uneven chances of breastfeeding in Spain.