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J Thorac Cardiovasc Surg 2008;136:1405-1412
© 2008 The American Association for Thoracic Surgery
Expert Commentary |
Centre Cardio-Thoracique de Monaco, Monte Carlo, Monaco
Received for publication April 22, 2008; accepted for publication July 31, 2008. * Address for reprints: Vincent Dor, MD, Centre Cardio-Thoracique de Monaco, 11 bis, Avenue d'Ostende, Cedex MC 98004, Monte Carlo, Monaco. (Email: vdor@ccm.mc).
| The first 300 words of the full text of this article appear below. |
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Introduction |
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An operative procedure can be precise and perfect only if it is based upon the surgeon's profound knowledge of anatomy, his understanding of the alteration of this normal anatomy by the pathology with which he is dealing and his ability to use the anatomic information in organizing and affecting his surgical procedure.J. W. Kirklin 1
Magnetic resonance imaging (MRI), with its ability to precisely define myocardial anatomy, echoes the teachings of one of cardiac surgery's most distinguished pioneers. Since the 1990s, several studies have demonstrated the preeminence of cardiac magnetic resonance (CMR) for analysis of wall motion abnormalities after myocardial infarction (MI).2,3
Both cine-MRI to determine precise scar location and the late enhancement technique to assess the transmural extension of infarcted myocardium illustrate the utility of CMR. CMR is the preeminent method of assessing left ventricular remodeling and aneurysmal progression after MI. Moreover, thrombus formation; the site, depth, and extension of the scarred myocardial wall; precise localization of asynergic areas; disorganization of the mitral apparatus; and estimation of left ventricular volume and performance are all circumstances in which CMR has proved more accurate than other techniques.4 In our opinion, a complete MRI evaluation of cardiac function is paramount before deciding how to appropriately treat patients after MI.
The core problem with ischemic congestive heart failure (CHF) is the undue demand put on the residual viable left ventricular myocardium. As noted by Klein and colleagues5 more than 40 years ago, "When the myocardium in the aneurismal area functions improperly, or has been replaced by fibrosis in 20%–25% of the surface area of the left ventricle, the extent of shortening required of the remaining functioning heart begins to exceed physiological limits." This was later confirmed by McKay and associates,6 who showed that left ventricular dilatation occurs when the asynergic (dyskinetic or akinetic)
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