Left ventricular (LV) filling following atrial contraction generates LV myocardial stretch that propagates from base to apex with a speed proportional to myocardial elasticity. The aim of this study was to test the hypothesis that intrinsic velocity propagation of myocardial stretch (iVP) would be altered in patients with valvular disease and chronic LV pressure overload or volume overload, which may adversely affect mechanical properties of the LV tissue. A second aim was to compare iVP with flow propagation velocity in the chamber.Methods
Sixty subjects were prospectively recruited: 20 with severe aortic stenosis (AS), 20 with severe degenerative mitral regurgitation (MR), and 20 normal control subjects. LV iVP was measured using ultrahigh–frame rate tissue Doppler (350–460 frames/sec) and flow propagation velocity by color flow M-mode imaging. Follow-up data (up to 2 years) were retrieved from medical records.Results
iVP was highest in patients with AS (2.2 ± 0.7 m/sec), intermediate in those with MR (1.6 ± 0.5 m/sec), and lowest in control subjects (1.4 ± 0.2 m/sec; P < .0001). Fourteen patients with AS and eight with MR had iVP > 1.8 m/sec. Overall, iVP correlated with age, LV morphology, severity of aortic valve obstruction, and measures of LV preload and afterload. At follow-up, patients with high iVP had lower survival free of major adverse cardiac events (P = .002). Flow propagation velocity was similar between groups and correlated poorly with iVP (r = 0.26, P = .10).Conclusions
A significant number of patients with severe AS and severe MR had rapid transmission of myocardial stretch, indicating increased myocardial stiffness. This information was not conveyed by measurement of flow propagation. Larger studies are needed to investigate the clinical utility of this novel measurement.