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”
To the Editor:
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.
In the experiments, the creation of acute mitral regurgitation reduced the preejection spike. However, left ventricular (LV) pressure was also reduced (eg, from >80 mm Hg to about <40 mm Hg, as shown in Figure 1 of the article by Remme et al). Therefore, the marked reduction in the preejection velocity spike may reflect reduction in preejection pressure development and altered stress-strain relationship. This observation associates the velocity spikes with the preejection phase but does not explain why the spike is biphasic.
In contrast to the animal experiments, the preejection velocity in patients with chronic mitral regurgitation was higher when compared with that in healthy controls. This may reflect the difference in LV hemodynamics in acute and chronic mitral regurgitation settings. Similarly, changes in LV afterload may explain the reduction in LV preejection velocities after mitral valve replacement.
The presence of a biphasic pattern suggests 2 opposite patterns of deformation: an initial shortening deformation followed by lengthening in preejection2,3 and vice versa in postejection. The study by Remme et al1 does not offer an explanation for lengthening during preejection or shortening during postejection. The presence of prestretch and lengthening wave during preejection has been previously established.2–4
Transmural deformation of myocardial layers and segmental shortening in an apex-to-base direction are not synchronous during the preejection and postejection phases, as has been extensively documented by other investigators.2–4 The synchronicity analysis of LV deformation is therefore incomplete in the current study and would have been more appropriately addressed by evaluating detailed segmental and transmural strain and strain rates.
A previous investigation suggested that preejection shortening in one direction is accompanied by a stretch in the other direction.5 Such deformation changes may have important roles in explaining the observed biphasic velocity spikes. In the discussion, the authors1 present a picture of LV flow showing that apical flow displacement during preejection closes the mitral valve. This depiction is not representative of current in vivo observations.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. Flow acceleration continues accompanied by LV shape changes in which simultaneous shortening and stretch occur within the isovolumic intervals.
In our opinion, although the experimental and clinical work by Remme et al1 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.
Dr Belohlavek’s research is supported in part by GE Healthcare. The other authors report no conflicts.
Remme EW, Lyseggen E, Helle-Valle T, Opdahl A, Pettersen E, Vartdal T, Ragnarsson A, Ljosland M, Ihlen H, Edvardsen T, Smiseth OA. Mechanisms of preejection and postejection velocity spikes in left ventricular myocardium: interaction between wall deformation and valve events. Circulation. 2008; 118: 373–380.
Coppola BA, Covell JW, McCulloch AD, Omens JH. Asynchrony of ventricular activation affects magnitude and timing of fiber stretch in late-activated regions of the canine heart. Am J Physiol Heart Circ Physiol. 2007; 293: H754–H761.
Goetz WA, Lansac E, Lim HS, Weber PA, Duran CM. Left ventricular endocardial longitudinal and transverse changes during isovolumic contraction and relaxation: a challenge. Am J Physiol Heart Circ Physiol. 2005; 289: H196–H201.