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Published on: February 16, 2016
Systolic longitudinal global and segmental myocardial mechanics in symptomatic isolated left ventricular
Nikola Bogunovic1, Martin Farr1, Lukas Pirl2
1Clinic for General and Interventional Cardiology/Angiology, Herz- und Diabeteszentrum NRW, Ruhr Universität Bochum, Bad Oeynhausen, Germany.
Insights
Left ventricular non-compaction cardiomyopathy (LV-NC) severely diminishes myocardial efficiency. In LV-NC patients, heart function relies primarily on the compact myocardial layer, not the non-compacted segments.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Myocardial Mechanics
Background:
- Left ventricular non-compaction cardiomyopathy (LV-NC) is a rare condition with limited data on segmental myocardial mechanics.
- Understanding the contribution of compacted and non-compacted myocardial layers to systolic function in LV-NC is crucial.
Purpose of the Study:
- To investigate and characterize myocardial longitudinal mechanics in adults with symptomatic LV-NC.
- To compare segmental myocardial mechanics between patients with LV-NC and healthy individuals.
Main Methods:
- Speckle tracking echocardiography was used to evaluate seven parameters of myocardial mechanics.
- Polar-diagrams were utilized to visualize and analyze the mechanics of the entire left ventricle.
- Segmental analysis focused on the contributions of both compacted and non-compacted myocardial layers.
Main Results:
- LV ejection fraction was significantly reduced in LV-NC patients (34%) compared to healthy controls (63%).
- While the compact layer showed increased systolic radial thickness, the non-compacted layer thickness remained unchanged or decreased.
- Key longitudinal mechanics parameters, including peak systolic longitudinal strain and strain rate, were significantly reduced in LV-NC patients.
Conclusions:
- Myocardial efficiency is severely diminished in LV-NC compared to healthy individuals.
- Left ventricular function in LV-NC appears to depend predominantly on the compact myocardial wall layer.
Background:
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.
Methods:
Seven parameters derived from speckle tracking echocardiography were evaluated and documented utilizing polar-diagrams to obtain overviews of myocardial mechanics of the entire LV.
Results:
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. 5.6 mm, 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. 389 ms, P = .065) and time-to-peak longitudinal strain rate (181 vs. 200 ms, 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.
Conclusion:
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.
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