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Published Online First: 17 March 2006. doi:10.1136/hrt.2005.086959
Heart 2006;92:1559-1562
Copyright © 2006 BMJ Publishing Group Ltd & British Cardiovascular Society

MINI-SYMPOSIUM

The pathophysiology of myocardial reperfusion: a pathologist’s perspective

C Basso, G Thiene

Institute of Pathological Anatomy, University of Padua Medical School, Padua, Italy

Correspondence to:
Dr Cristina Basso
Institute of Pathological Anatomy, University of Padua Medical School, Via A. Gabelli, 61, 35100 Padova, Italy; cristina.basso@unipd.it

Keywords: acute myocardial infarction; microcirculation; pathology; percutaneous coronary interventions; thrombolysis

The first 150 words of the full text of this article appear below.

Coronary artery thrombosis, caused either by fissuring or erosion of atherosclerotic plaques, is the usual cause of acute myocardial infarction.1 If a coronary occlusion persists for more than 30 minutes, irreversible damage to the myocardium occurs. Persistent coronary occlusion results in a progressive increase of the infarct size with a wave-front transmural extension from the endocardium towards the epicardium.2,3 Although reperfusion can occur spontaneously, thrombotic coronary artery occlusion persists in the majority of patients suffering an acute myocardial infarction. Thus, timely coronary artery recanalisation and myocardial reperfusion, either by thrombolytic therapy or primary angioplasty and/or stenting, represents the most effective way of restoring the balance between myocardial oxygen supply and demand. Prevention of myocardial cell necrosis by the restoration of blood flow depends on the severity and duration of pre-existing myocardial ischaemia. Experimental and clinical data indicate that the recovery of systolic and diastolic function and the reduction in overall . . . [Full text of this article]


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  • Leopold, J. A. (2008). Does Thrombolytic Therapy Facilitate or Foil Primary PCI?. NEJM 358: 2277-2279 [Full Text]  

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