title: [Coronary perfusion, necrosis area, pumping function of the myocardium, and cardiac electrical stability following revascularisation of infarction-affected myocardium].
abstract: Analysing the literature data suggests that coronary angioplasty in acute myocardial infarction (AMI) fails to completely remove the focus of ischaemia, even in case of successful recanalization of the infarction-related artery. Inadequate post-angioplasty reperfusion of the infarction-stunned myocardium is mainly caused by the so-called <<no reflow>> phenomenon. Primary coronary angioplasty is capable of decreasing the size of the necrosis focus, being however incapable of completely removing myocardial infarction. Such a situation results from death of a considerable number of cardiomyocytes in the area of ischaemia, to have occurred long before coronary reperfusion is restored. An endovascular intervention in AMI may improve the impaired myocardial contractile performance and save the life of the patients sustaining the cardiogenic shock. However, coronary angioplasty does not preclude the development of cardiac insufficiency in all the patients suffering from acute myocardial infarction, which is a consequence of inadequate cardiac reperfusion and a result of necrotic death of a considerable segment of the heart muscle. Currently, there is no evidence regarding the effect of primary angioplasty on the risk of sudden cardiac death following AMI. An endovascular intervention on the infarction-related artery cannot prevent the development of the postmyocardial-infarction cardiac remodelling, which is a consequence of incompletely restored coronary blood flow within the area of infarction.
authors.affiliation: Federal Facility Research Institute of Cardiology, Tomsk Scientific Centre, Siberian Branch of the Russian Academy of Medical Sciences, Tomsk, Russia. maslov@cardio.tsu.ru
authors.forename: L N
authors.initials: LN
authors.lastname: Maslov
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D005464:Fluorobenzenes / Q000627:therapeutic use; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology* / Q000628:therapy*; D015425:Myocardial Reperfusion / Q000379:methods*; D009204:Myocardial Revascularization / Q000379:methods*; D009336:Necrosis / Q000473:pathology*; D011743:Pyrimidines / Q000627:therapeutic use; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000627:therapeutic use; D042461:Vascular Endothelial Growth Factor A / Q000097:blood; D014664:Vasodilation / Q000502:physiology
chemical_list: D000924:Anticholesteremic Agents; D005464:Fluorobenzenes; D011743:Pyrimidines; D013449:Sulfonamides; D042461:Vascular Endothelial Growth Factor A; D000068718:Rosuvastatin Calcium; D002097:C-Reactive Protein