Mitral Chordal-Leaflet-Myocardial Interactions in Mitral Valve Prolapse

Abstract

The submitral apparatus maintains annular-papillary continuity and myocardial geometry. In mitral valve prolapse (MVP), elongated chords and redundant leaflets can interact at the region of myocardial attachment, leading to apparent discordant motion of the basal inferolateral wall. The aim of this study was to test the hypothesis that basal inferolateral wall inward motion would occur later in MVP and that this delay is associated with MVP severity. Thirty consecutive patients with MVP and matched controls underwent stress echocardiography. Time to peak transverse displacement (TPD) of the inferolateral wall compared with the anteroseptal wall was measured using speckle-tracking echocardiography. The time difference was analyzed as raw data, normalized to the RR interval, and as a percentage of the time to maximal displacement of the anteroseptal segment(s). Compared with controls, TPD was delayed in patients with MVP both at rest and at peak stress, when evaluating basal segments or basal-mid segments as a unit, both in real time and, more importantly, when correcting for anteroseptal TPD. In patients compared with controls, observed delay at rest and at peak stress was 50 ± 90 versus -30 ± 90 msec (P= .006) and 70 ± 80 versus -30 ± 60 msec (P < .0001), respectively; relative to TPD of the anteroseptal segment, the observed delay at rest and at peak stress was 117 ± 24% versus 97 ± 22% (P= .007) and 144 ± 68% versus 95 ± 21% (P= .003), respectively. Similar significant findings were observed in basal-mid segments. TPD results were not statistically significant when stratified by prolapse severity. Intraclass correlation coefficients were 0.88 and 0.93, and two-tailed t tests indicated good interobserver and intraobserver variability. Inferolateral wall TPD is delayed in MVP. TPD is a novel method to characterize chordal-leaflet-myocardial interactions in patients with MVP. Prolapse severity does not predict TPD, likely because of the timing of prolapse and dynamic loading conditions. Implications of this observation include attribution of a perceived wall motion abnormality in MVP during stress echocardiography to a physiologic state and new mechanistic insights into mitral valve physiology.