In recent years numerous reports have appeared demonstrating that even in the absence of previous myocardial infarction, patients with coronary artery disease often present with chronic regional wall motion abnormalities that are reversible spontaneously1 after coronary revascularization2, angioplasty3,4, thrombosis5, and chelation therapy.6 This regional dysfunction, in the absence of infarction, is postulated to result from either prolonged postischemic dysfunction (stunning) or adaptation to chronic hypoperfusion (hibernation). Hibernation myocardium has been defined as a state of persistently impaired left ventricular function at rest that is due to reduced coronary blood flow.7 In contrast, stunned myocardium is defined as postischemic left ventricular dysfunction.8,9 Myocardial stunning and hibernation have been reported to last for months to years.1,2,10,11,12 It has now been established that the time sequence for return of functional integrity to hibernating myocardial tissue can be independent of correcting the mechanical obstruction of flow.2,3,13,14,15 Stunned myocardial cells are postulated to be a temporary phenomenon and the term simply refers to the unexplained delay in return of optimal function of cellular activity after flow has been restored. Myocyte hibernation appears to be much more difficult to explain. All reports to date have involved myocardial myocytes.
- Chelation Therapy
- Stun Myocardium
- Impaired Left Ventricular Function
- Anterior Infarction
- Hibernation Myocardium
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