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  • Title: Physiologic compensation is supranormal in compensated aortic stenosis: does it return to normal after aortic valve replacement or is it blunted by coexistent coronary artery disease? An intramyocardial magnetic resonance imaging study.
    Author: Biederman RW, Doyle M, Yamrozik J, Williams RB, Rathi VK, Vido D, Caruppannan K, Osman N, Bress V, Rayarao G, Biederman CM, Mankad S, Magovern JA, Reichek N.
    Journal: Circulation; 2005 Aug 30; 112(9 Suppl):I429-36. PubMed ID: 16159858.
    Abstract:
    BACKGROUND: In compensated aortic stenosis (AS), cardiac performance measured at the ventricular chamber is typically supranormal, whereas measurements at the myocardium are often impaired. We investigated intramyocardial mechanics after aortic valve replacement (AVR) and the effects relative to the presence or absence of coronary artery disease (CAD+ or CAD-), respectively. METHODS AND RESULTS: Twenty-nine patients (46 to 91 years, 10 female) with late but not decompensated AS underwent cardiovascular MRI before AVR (PRE), with follow-up at 6+/-1 (EARLY) and 13+/-2 months (LATE) to determine radiofrequency tissue-tagged left ventricle (LV) transmural circumferential strain, torsion, structure, and function. At the myocardial level, concentric LV hypertrophy regressed 18% LATE (93+/-22 versus 77+/-17 g/m2; P<0.0001), whereas at the LV chamber level, ejection fraction was supranormal PRE, 67+/-6% (ranging as high as 83%) decreasing to 59+/-6% LATE (P<0.05), representing not dysfunction but a return to more normal LV physiology. Between the CAD+ and CAD- groups, intramyocardial strain was similar PRE (19+/-10 versus 20+/-10) but different LATE, with dichotomization specifically related to the CAD state. In the CAD- patients, strain increased to 23+/-10% (+20%), whereas in CAD+ patients it fell to 16+/-11% (-26%), representing a nearly 50% decline after AVR (P<0.05). This was particularly evident at the apex, where CAD- strain LATE improved 17%, whereas for CAD+ it decreased 2.5-fold. Transmural strain and myocardial torsion followed a similar pattern, critically dependent on CAD. AVR impacted LV geometry and mitral apparatus, resulting in decreased mitral regurgitation, negating the double valve consideration. CONCLUSIONS: In AS patients after AVR, reverse remodeling of the supranormal systolic function parallels improvement in cardiovascular MRI-derived regression of LV hypertrophy and LV intramyocardial strain. However, discordant effects are evident after AVR, driven by CAD status, suggesting that the typical AVR benefits are experienced disproportionately by those without CAD and not by those obliged to undergo concomitant coronary artery bypass grafting/AVR.
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