This review highlights the developmental origins of isolated left ventricular non-compaction, linking it to disrupted embryonic ventriculogenesis.
Should not yet change practice for ventricular non-compaction; leaves open human validation of candidate transcription factors.
Isolated ventricular non-compaction is an increasingly commonly diagnosed myocardial disorder characterised by excessive and prominent trabeculation of the morphologically left, and occasionally the right, ventricle. This is associated with high rates of thromboembolism, cardiac failure, and cardiac arrhythmia. Recent improvements in understanding the embryonic processes underlying ventricular formation have led to the hypothesis that ventricular non-compaction is due to a failure of normal ventriculogenesis, leading to abnormal myocardium which may present clinically many years later. Experimental work in animal models provides several candidate transcription factors and signalling molecules that could, in theory, cause ventricular non-compaction if disrupted.
No takes yet. Share an insight, caveat, or question.
Breckenridge et al. (2007) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: