Abstract 17131: Diastolic Dysfunction in Asymptomatic Patients With Moderate to Severe Aortic Regurgitation is Strongly Related to Increased Longitudinal Fiber Stress and Subsequent Non-uniform Myocardial Relaxation
Introduction: Diastolic dysfunction in aortic regurgitation (AR) is present at an early stage of the disease. Yet, the mechanisms are not clearly understood.
Hypothesis: We hypothesized that diastolic dysfunction in AR patients is caused by increased longitudinal (meridional) fiber stress and subsequent impaired relaxation of the corresponding subendocardial (longitudinal) fibers.
Methods: Thirty asymptomatic patients with moderate to severe aortic regurgitation (AR) and 17 age matched healthy controls (C) where analyzed (32 ± 7 and 35 ± 4 (SD) years, respectively, p=NS) with 3D speckle tracking echocardiography. We measured early diastolic longitudinal- (LSRe) and circumferential (CSRe) strain rate (1/s) as the time derivative of strain (%) and the peak difference (LSRe – CSRe) during isovolumic relaxation (IVR). Early diastolic flow rate (sec-1) was estimated as the time derivative of the LV volume curve normalized to end-diastolic volume (EDV). Finally, we calculated end-systolic meridional fiber stress (mmHg).
Results: LV ejection fraction in C and AR was 61 ± 2 and 62 ± 3 %, respectively (p=NS). AR patients had signs of impaired LV filling with lower early diastolic flow rate (Table 1). During IVR, the strain rate curves consistently departed (Figure 1, arrow), indicating a non-homogenous relaxation. A negative correlation was shown between meridional fiber stress and the IVR strain rate gradient (y= -0.0123x + 1.0921, r=0.61, p<0.001).
Conclusions: We have demonstrated a non-homogenous relaxation of subendocardial- relative to circumferential fibers in AR patients that strongly correlated with longitudinal fiber stress, suggesting a causal relationship.
Author Disclosures: S. Urheim: None. K. Broch: None. G. Kunszt: None. R. Massey: None. S. Aakhus: None. L. Gullestad: None.
- © 2014 by American Heart Association, Inc.