Abstract 2548: Velocity Vector Imaging Reveals the Cause of Prolongation of Isovolumic Relaxation Time During Myocardial Ischemia
Background: Isovolumic relaxation time (IRT) prolongs during myocardial ischemia because of slow deceleration of left ventricular (LV) pressure decay. Postsystolic shortening is a sensitive marker of myocardial ischemia; however, the influence on LV relaxation is still unclear. Velocity vector imaging (VVI) demonstrates regional wall motion speed without angle-dependency. Therefore, we sought to investigate the influence of postsystolic shortening derived from VVI on IRT.
Methods: LV short-axis images were acquired using a Sequoia ultrasound system (Siemens) in 15 dogs at baseline and 15 seconds after occlusion of the left circumflex artery. The risk area was determined by myocardial contrast echocardiography. To assess postsystolic shortening, radial velocities at the mitral valve opening (MVO) were analyzed in the center of the risk area at baseline and during ischemia by VVI. IRT was measured from pulsed-wave Doppler recordings of aortic and mitral flow.
Results: IRT increased significantly during ischemia (from 64.6±12.5 to 93.7±14.4 ms, p<0.0001). VVI demonstrated that the vectors at MVO in the risk area were directed inward during ischemia, characterized as positive value of postsystolic shortening. In an ischemic model, the inward motion velocity in the longer IRT group was faster than that in the shorter IRT, although the size of the risk area was not different significantly. Excellent linear correlation was shown between radial velocity at MVO and IRT (r=0.80, p<0.05, figure⇓).
Conclusion: VVI is a useful method for detecting LV dyssynchronous relaxation. Dyssynchrony caused by postsystolic shortening results in the prolongation of IRT during ischemia.