Abstract 966: Biphasic Tissue Velocity Waves prior to and after Ejection Caused by Valve Closure
Background: Normal left ventricular (LV) myocardium demonstrates marked biphasic velocity waves prior to and at the end of LV ejection. We hypothesize that they are due to early-systolic shortening and late-systolic lengthening that are interrupted by mitral (MVC) and aortic valve closure (AVC), respectively, as illustrated in the figure⇓.
Methods and Results: In 11 anesthetized dogs timing of valve closure was determined by pressure variables and LV dimensions by sonomicrometry. Myocardial shortening started 20±10 ms (±SD, p<0.01) prior to MVC, and was interrupted at the time of MVC (time difference (TD) =4±7 ms). Similarly, myocardial lengthening started 31±15 ms (p<0.01) prior to AVC, and was interrupted at the time of AVC (TD = 0±3 ms). Prevention of mitral (n=4) and aortic valve (n=4) closure by stenting the valves abolished the pre- and post-ejection biphasic velocity waves, respectively. The alternative hypothesis that the atrial contraction and relaxation sequence causes the LV pre-ejection biphasic velocity wave was investigated in 10 patients with atrial fibrillation. Atrial fibrillation did not remove the pre-ejection biphasic velocity wave which occurred 28±16 ms prior to MVC and had a peak velocity of 31±12 mm/s.
Conclusion: This study supports the hypothesis that normal LV pre- and post-ejection velocity spikes are attributed to valve closures that interrupt early systolic shortening and late systolic lengthening, respectively.