Keywords:
Cardiac, MR, Diagnostic procedure, Dilatation
Authors:
O. Larina, E. A. Mershina, V. Sinitsyn, M. Kharlap, R. Miasnikov; Moscow/RU
Purpose
Left ventricular non-compaction cardiomyopathy (LV NC CMP) is a rare condition characterised by numerous excessively prominent left ventricular trabeculation and deep intertrabecular recesses communicating with the ventricular cavity and severely altering myocardial structure [1–4].
It is supposed that LV NC CMP can be caused by arrest of normal embryogenesis of the endocardium and myocardium.
It is known that LV NC CMP can be associated with other congenital cardiac defects,
but it is also seen in the absence of other cardiac anomalies.
During early embryonic development,
the myocardium is a loose network of interwoven fibers separated by deep recesses that link the myocardium with the left ventricular cavity.
Gradual “compaction” of this spongy meshwork of fibers and intertrabecular recesses,
or “sinusoids,” occurs between weeks 5 and 8 of embryonic life,
proceeding from the epicardium to endocardium and from the base of the heart to the apex (Fig.1)[4].
Clinical manifestations are highly variable,
ranging from no symptoms to disabling congestive heart failure,
arrhythmias,
and systemic thromboemboli.
The purpose of our study was to evaluate the relationship between volumetric parameters,
myocardial mass (MM) and systolic dysfunction of left ventricle (LV) in patients with non-compacted cardiomyopathy (NC CMP).