Heart 1998;80:218-222 ( September )
Review
Myocardial hibernation and stunning: from physiological principles to clinical practice
a Department
of Cardiology, St Thomas' Hospital, London, UK, b Cattedra di Cardiologia,
Universitá degli Studi di Brescia, Brescia, Italy
Correspondence to: Dr Michael S Marber, The Rayne Institute, Department of Cardiology, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK.
Accepted for publication 13 May 1998
| The first 150 words of the full text of this article appear below. |
 |
Introduction |
|---|
In
patients with coronary artery disease, one of the most powerful
determinants of prognosis is left ventricular
function.1,2 Thus, if we assume that the prognostic
benefit of revascularisation is mediated through an effect on left
ventricular function, two mechanisms might explain this benefit. First,
coronary artery bypass surgery or angioplasty could reduce the impact
of coronary artery disease on the attrition of left ventricular
function
in other words, left ventricular function deteriorates more
slowly following revascularisation. Second, revascularisation could
improve left ventricular function per se; this mechanism assumes that there must be areas of the heart that are alive but not contracting properly, and that revascularisation will improve this contractile dysfunction. Thus impairment of left ventricular function does not
necessarily mean that the myocardium is dead, but rather that it may be
alive though with reduced function. This has stimulated much research
into the mechanisms of reversible left ventricular dysfunction
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