We should first ask whether left ventricular NVM could be the consequence of DOMV. In the other words, could left ventricular NVM present as an acquired disease caused by DOMV?
The cause and pathogenesis of acquired left ventricular NVM remains unknown, but several speculations can be raised to explain its occurrence [14, 15]:(1) left ventricular NVM represents an insufficient, compensatory attempt of hypertrophy of the impaired left ventricular myocardium.(2) left ventricular NVM results from an attempt to enlarge the endocardial surface to move large stroke volumes with reduced contractility and to maintain a sufficient cardiac output/stroke volume in volume overload.(3) left ventricular NVM results from a "dissection" of the impaired myocardium because of reduced adhesion of cardiomyocytes and malfunction of gap junctions particularly at the most demanded regions of the myocardium with consecutive transformation to a meshwork of trabeculations. However, in the present case, it seems that the above-mentioned speculations can not explain its occurrence because the volume load is mild and there are not other overloads. Therefore, left ventricular NVM could not present as an acquired disease.
In addition, the question must be posed as to whether DOMV and left ventricular NVM are both the consequence of an additional undetermined cause?
The formation of the mitral valve begins in the fourth week of gestation and continues to the sixth month. The primitive mitral leaflets are formed from endomyocardial cushions, and the papillary muscle and chordae are formed by primitive trabeculation in the left ventricle and the endomyocardial cushions. The trabeculations continue to fuse until the 24th week, by which time they have formed the two distinct papillary muscles. By the sixth month, the muscular tissue of the chordae is replaced with thin, delicate collagenous tissue, completing the connection between the now well-formed papillary muscles and leaflets [11]. Similar to the tricuspid valve, the mitral valve is formed from endocardial cushion tissue and from ventricular myocardium, separated from the ventricular wall by undermining and diverticulation [13]. In the other words, the mitral valve and its apparatus originate from the endomyocardium, which is thought to be origin of noncompacted myocardium. Although the coexistence of NVM and DOMV could be a coincidence, we believe that both defects were probably caused by a developmental arrest of the left ventricular myocardium in the present case.