Systolic longitudinal global and segmental myocardial mechanics in symptomatic isolated left ventricular non-compaction cardiomyopathy.

Abstract

Left ventricular (LV) non-compaction cardiomyopathy (LV-NC) is rare, and data of segmental myocardial mechanics are largely lacking. We investigated myocardial longitudinal mechanics in adults with symptomatic LV-NC (n=30) versus individuals with healthy hearts (n=150). The contribution of compacted and non-compacted myocardial layer to systolic LV function has to be determined. Seven parameters derived from speckle tracking echocardiography were evaluated and documented utilizing polar-diagrams to obtain overviews of myocardial mechanics of the entire LV. According to embryonal myocardial development, non-compacted myocardium was mostly located in mid-ventricular and apical segments of the free LV wall. LV ejection fraction was reduced in LV-NC (34±15%, healthy 63±5%, P<.0001). The compact wall layer in LV-NC demonstrated increasing systolic radial thickness (diastolic 5.6±1.4, systolic 6.5±1.4mm, P=.016), whereas the non-compacted layer remained unchanged or tended to decrease in thickness (diastolic 17.6±5.3, systolic 16.0±4.6mm, P=.22). Compared with heart-healthy individuals in LV-NC peak systolic longitudinal strain (healthy -21.1% vs. LV-NC -8.8, P<.0001), peak systolic longitudinal strain-rate (-1.23%/s vs. -0.64, P<.0001), and peak longitudinal displacement (12.1 vs. 5.6mm, P<.0001) were reduced, while pre-systolic stretch index (1.31% vs. 3.2%, P<.0001) and post-systolic index (2.5% vs. 15.9%, P<.0001) increased. Time-to-peak longitudinal strain (371 vs. 389ms, P=.065) and time-to-peak longitudinal strain rate (181 vs. 200ms, P=.0677) did not differ significantly. In LV-NC, there were no significant differences between analyses using an interpolated endocardial border along the edges of the recesses and the endocardial edge of the compact wall layer. Hence, LV function appeared to depend only on the thin compact wall layer. In LV-NC, myocardial efficiency is severely diminished compared with healthy controls and LV function seemed to depend mainly on the compact myocardial wall layer.