Valve replacement for aortic stenosis normalizes subendocardial function in patients with normal ejection fraction.
2010 (English)In: European Journal of Echocardiography, ISSN 1525-2167, E-ISSN 1532-2114Article in journal (Refereed) Published
AIMS: Long-standing aortic stenosis (AS) causes various degrees of left ventricular (LV) dysfunction, which may improve after valve replacement. The aim of this study was to assess the nature of LV subendocardial abnormalities in AS and their response to valve replacement (AVR). METHODS AND RESULTS: We studied 41 consecutive symptomatic patients (age 64 +/- 13 years) with severe AS, normal LV ejection fraction (EF), but no obstructive coronary artery disease before, a week after AVR, and 6 months after AVR. LV subendocardial function was studied from recordings of long-axis M-mode (amplitude), tissue-Doppler (myocardial velocities) and speckle tracking (myocardial strain) echocardiographic techniques. Results were compared with those from 20 age- and gender-matched controls. In patients, LV dimensions and markers of asynchrony, total isovolumic time (t-IVT), and Tei index were not different from controls before AVR and remained unchanged afterwards. LV lateral long-axis amplitude, as well as lateral and septal systolic velocities and strain, were reduced (P < 0.001 for all) and E/E' was modestly raised. Lateral long-axis amplitude, systolic and diastolic velocities normalized within a week of AVR but strain lagged behind until 6 months later. The reduced septal long-axis amplitude remained permanently unchanged (NS) despite the early normalization of its systolic velocities (P < 0.001) and strain (P < 0.001). LV mass normalized at 6 months after AVR (P < 0.005). CONCLUSIONS: In patients with severe AS and maintained LV ejection fraction, subendocardial function is globally abnormal showing reduced amplitude of motion, velocities, and strain. The different response of its components suggests an evidence for differential reverse remodelling, irrespective of myocardial mass regression.
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IdentifiersURN: urn:nbn:se:umu:diva-34737DOI: 10.1093/ejechocard/jeq026ISI: 000280704100013PubMedID: 20219771OAI: oai:DiVA.org:umu-34737DiVA: diva2:324406
Advance Access published March 10, 2010; Received 3 December 2009; accepted after revision 11 February 20102010-06-152010-06-152011-10-17Bibliographically approved