Mechanisms of Preejection and Postejection Velocity Spikes in Left Ventricular Myocardium

Abstract

Background-Normal left ventricular myocardium demonstrates distinct spikes in the velocity trace before and after left ventricular ejection. We tested the hypothesis that the preejection and postejection velocity spikes reflect early systolic shortening and late systolic lengthening that are interrupted by mitral and aortic valve closure, respectively. Methods and Results-In 11 anesthetized dogs, timing of valve closure was determined by pressure variables; left ventricular dimensions were determined by sonomicrometry. Myocardial shortening started 20Ϯ10 ms (meanϮSD; PϽ0.001) before mitral valve closure and was interrupted at the time of mitral valve closure (time difference, 4Ϯ7 ms). Similarly, myocardial lengthening started 31Ϯ15 ms (PϽ0.001) before aortic valve closure and was interrupted at the time of aortic valve closure (time difference, 0Ϯ3 ms). Prevention of mitral (nϭ4) and aortic (nϭ4) valve closure by stenting the valves abolished the preejection and postejection velocity spikes, respectively. Echocardiographic measurements of patients (nϭ15) with severe mitral regurgitation showed that the preejection velocity spike was reduced after prosthetic valve replacement (43Ϯ25 versus 32Ϯ15 mm/s; Pϭ0.036), indicating that preejection shortening was larger with a leaking valve. Similarly, late systolic lengthening was reduced in patients (nϭ15) with severe aortic regurgitation after prosthetic valve replacement; minimum postejection velocity spike was increased from Ϫ32Ϯ11 to Ϫ17Ϯ11 mm/s; Pϭ0.0003). Asynchronous onset of contraction/ relaxation and atrioventricular interaction were investigated as alternative mechanisms of the velocity spikes in dogs and patient groups but were found implausible. Conclusions-This

Response to Letter Regarding Article, “Mechanisms of Preejection and Postejection Velocity Spikes in Left Ventricular Myocardium: Interaction Between Wall Deformation and Valve Events”

“…1 Our aim was to understand what causes the pre-and postejection velocity spikes. The main focus of Sengupta et al is to understand why the spikes sometimes cross the zero line, a phenomenon that they name biphasic spikes, as it denotes both a shortening phase (positive velocity) and a lengthening phase (negative velocity).…”

Letter by Sengupta et al Regarding Article, “Mechanisms of Preejection and Postejection Velocity Spikes in Left Ventricular Myocardium: Interaction Between Wall Deformation and Valve Events”

“…In our opinion, although the experimental and clinical work by Remme et al 1 shows an interesting and important association between the preejection and postejection phases and velocity spikes, the presented observations have a limited ability to explain the mechanism of biphasic configuration of the velocity spikes, especially when the prestretch component is considered.…”

“…We read with great interest the article by Remme et al 1 Although the study implies a strong association between the preejection and postejection phases and velocity spikes, we believe there are several aspects of heterogeneity in myocardial mechanics that merit further discussion.…”

“…3 During preejection, flow accelerates towards the LV outflow region and a wake vortex is formed in the submitral region. According to the hypothesis and pictorial depiction by Remme et al, 1 volume shifts and flow acceleration would cease with mitral valve closure. However, closure of the mitral valve does not halt LV flow acceleration or LV deformation.…”

Tissue Doppler Imaging-Derived Myocardial Acceleration During Isovolumetric Contraction Predicts Pulmonary Capillary Wedge Pressure in Patients With Reduced Ejection Fraction

“…Remme et al explained this biphasic motion as an early systolic shortening that is interrupted by the longitudinal motion produced by mitral valve closure; and added that myocardial deformation does not occur during IC. 16 In our study, both IVV and IVA correlated with a´ only in patients with EF <55% (r=0.35, 0.55, P=0.017, <0.0001, respectively), suggesting that IVV may be related to the elastic potential energy of a´, which favors the findings by Remme et al However, this does not seem enough to explain the correlations noticed in our study, especially that, again, both IVV and IVA lost such correlation with a´ in patients with EF ≥55% (r=0.043, 0.15, P=0.784, 0.338, respectively). IC was, however, reported in other studies to be dynamic in terms of thickening because of subendocardial fiber shortening, which, because of subepicardial sheet extension and negative angle formation, is kept within the isovolumetric constraint.…”