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Mechanical Control of Relaxation Using Intact Cardiac Trabeculae
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Excessive trabeculations in noncompaction do not have the embryonic identity
Bjarke Jensen1, Allard C van der Wal2, Antoon F M Moorman1
1Department of Anatomy, Embryology & Physiology, Academic Medical Center, University of Amsterdam, The Netherlands.
International Journal of Cardiology
|November 14, 2016
Summary
Excessive trabeculations in ventricular noncompaction do not originate from embryonic tissue. This suggests noncompaction arises from compact wall growth, not failed compaction.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Pathology
Background:
- Ventricular noncompaction is a heart condition marked by excessive trabeculations, linked to heart failure.
- It is hypothesized to stem from incomplete embryonic compaction, retaining primitive trabeculations.
Purpose of the Study:
- To investigate the cellular identity of trabeculations in noncompaction.
- To test the hypothesis that noncompaction results from retained embryonic trabeculations.
Main Methods:
- Immunohistochemistry was used to analyze cardiac sections.
- Samples included a control embryo, 3 fetal noncompaction cases, and 3 control fetal hearts.
Main Results:
- Embryonic trabeculations expressed ANF/NPPA; fetal trabeculations (both noncompaction and control) were largely ANF-negative and wider.
- Noncompaction hearts showed excessively thick trabeculations, but these did not match the embryonic trabeculation identity.
- Both fetal compact and noncompaction myocardium were vascularized, unlike embryonic trabeculations.
Conclusions:
- Excessive trabeculations in noncompaction are not embryonic in origin.
- Noncompaction is unlikely due to failed compaction; a new hypothesis suggests compact wall growth into the lumen.
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