Abstract 13796: Global Longitudinal Strain (GLS) Predicts Progression to Severe Aortic Stenosis (AS) in Patients With Normal or Minimally Dysfunctional Bicuspid Aortic Valve (BAV)
Background: While prior research has documented the rate of progression of BAV to severe AS, myocardial function factors have received less attention. We hypothesized that reduced GLS might conceivably identify a high risk subset of BAV patients, as it has in other instances of severe valvular heart disease, such as chronic severe aortic regurgitation.
Methods: We computed GLS (apical 2-, 3-, and 4-chamber views, Arena Software,TomTec) on baseline studies in two groups of pts with BAV. All had (1) EF ≥ 50%, (2) were free of wall motion abnormality and (3) were free of any significant valve dysfunction. Pts were followed for mean of 70 ± 18 months. In group 1 (STABLE) the BAV remained hemodynamically non-significant (absent or mild aortic regurgitation or stenosis) throughout follow-up and in group 2 (PROGRESS) the disease progressed from no or mild aortic disease to severe AS.
Results: 21 patients were included, 11 STABLE patients and 10 PROGRESS patients. Baseline characteristics were similar for the two groups (Table 1). All patients in PROGRESS had abnormal GLS (< -18%), whereas STABLE patients had GLS greater than -18%. GLS was significantly impaired in PROGRESS compared to STABLE (-15.9% vs -21.2%, p = 0.0001).
Summary: 1. Baseline GLS was impaired in patients who progressed from normal or mild aortic disease to severe aortic stenosis.
2. Baseline GLS was grossly within normal limits in those in whom the bicuspid aortic valve remained normal or minimally dysfunctional.
Conclusions: A normal baseline GLS appears to predict a more benign course for patients with normal or minimally dysfunctional BAV, whereas a reduced GLS might identify a group at high risk for progression. Whether reduced baseline GLS relates to abnormalities in load or contractility, or signifies a ‘myocardial factor’ which is related to the BAV syndrome all remain to be elucidated.
Author Disclosures: A. Iskandar: None. L. Pape: None. D. Tighe: None. G.P. Aurigemma: None.
- © 2015 by American Heart Association, Inc.