Response to Letter Regarding Article, “Mechanisms of Preejection and Postejection Velocity Spikes in Left Ventricular Myocardium: Interaction Between Wall Deformation and Valve Events”
We thank Drs Sengupta and colleagues for their interest in our work.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). This is an interesting topic, but it was outside the scope of our study.1 The preejection velocity has a spike shape, ie, an upstroke and a downstroke. The upstroke from zero reflects the start of shortening, which pushes blood toward the valve plane and closes the mitral valve. Mitral valve closure then restrains further shortening and the velocity is reduced (downstroke). Because each part of the myocardium is tethered to neighboring regions, there will be mechanical interactions. As long as the myocardial properties are not 100% homogenous, stronger segments will lengthen the weaker ones during the isovolumic phases. Lengthened segments will exhibit negative velocities (their downstroke crosses the zero line). This mechanism may account for the lengthening that is sometimes seen after mitral valve closure. A similar mechanism may explain positive postsystolic velocities. Thus, a biphasic configuration of a spike may be caused by a tug-of-war between weak and strong segments.
Sengupta et al note that there is a transmural activation delay. However, our data1 demonstrated essentially simultaneous shortening of the long- and short-axis diameters, which were measured from apex to equator and in the equatorial plane, respectively. This suggests that both longitudinal and circumferential fibers shortened and contributed to the volume reduction before mitral valve closure and that transmural activation delay did not seem to play a major role in generation of the spike. We agree with Sengupta et al that prestretch is often present, particularly close to the valve region. The basal left ventricular region is known to be activated last. We believe that possible stretching of basal segments together with ballooning of the valve plane may account for the volume shift from apex to base. This mechanism may explain why Goetz et al2 experienced prestretch between an ultrasonic crystal placed at the apex and crystals placed in the valve plane.
Previous work by Sengupta et al3 shows blood flow toward the mitral valve as it closes, which supports Figure 8 in our work,1 which schematically illustrates the shift of blood volume from the more apical region toward the valve plane during mitral valve closure. Regional vortices within the volume shift are of less importance for our hypothesis. Mitral valve leaflet motion into the left atrium is stopped by tensing of the chordae tendineae. When this leaflet motion is stopped during early systole, it introduces a new restraint on both myocardial deformation (shortening) and blood flow. Blood volume displacement in this direction must cease, but it may take other directions. Similarly, the initial shortening motion of the myocardium cannot continue in the same manner and shortening is decelerated. Myocardial deformation may still take place by mechanisms such as tug-of-war between the different myocardial segments and left ventricular twist. Total removal of the valve restraint in our study1 by stenting the valve allowed shortening to continue uninterrupted into ejection; ie, the myocardial velocity component represented by the preejection spike was not reduced but was merged with the S-wave as downstroke of the spike was reduced or abolished altogether. This is consistent with the measurements from the mitral regurgitation patients, which showed continued shortening (ie, positive velocities) during isovolumic contraction before valve replacement.
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.
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.
Sengupta PP, Khandheria BK, Korinek J, Jahangir A, Yoshifuku S, Milosevic I, Belohlavek M. Left ventricular isovolumic flow sequence during sinus and paced rhythms: new insights from use of high-resolution Doppler and ultrasonic digital particle imaging velocimetry. J Am Coll Cardiol. 2007; 49: 899–908.