Acquired left ventricular hypertrabeculation/noncompaction in myotonic dystrophy type 1

A possible diagnosis of isolated right ventricular hypertrabeculation /noncompaction in an elderly man by three-dimensional echocardiography

“…Although there is no established criteria for HVM/NVM in the right ventricle, right ventricle HVM/NVM has been reported in some cases [6][7][8][9][10][11][12] in whom the diagnosis of right ventricle HVM/NVM were pretty dependent on 2DE. The morphological assessment of the right ventricle is often difficult in adult patients by 2DE and 2DE image quality is operator dependent.…”

“…The persistence of HVM/ NVM is usually associated with congenital left or right ventricular outflow tract obstruction. However, it may not be associated with any factor that could explain the arrest of the development of the myocardial structure (isolated HVM/ NVM) [3], and it has been also reported of the possibility that HVM/NVM could present as an acquired disease [4][5][6][7][8][9].…”

Cardiac magnetic resonance imaging characteristics of isolated left ventricular noncompaction in a Chinese adult Han population

“…The etiology and the pathogenetic background are not clear in adult IVNC. Both congenital and acquired cases have been reported [1,3,4,19,20]. It is widely thought that the basic mechanism involved in IVNC may be an arrest of the normal myocardial compaction during 5-8 weeks of gestation.…”

Acquired noncompaction associated with coronary heart disease and myopathy

“…[4][5][6][7] The pathogenetic background of acquired LVHT is unknown, but it is speculated that acquired LVHT results from 1) an insufficient attempt of hypertrophy in compensation of the impaired left ventricular myocardium; 2) an attempt to enlarge the endocardial surface to move large stroke volumes with reduced contractility and to maintain a sufficient cardiac output/stroke volume; 3) a ''dissection'' of an 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; 4) hypervascularization of the subendocardial layer in the regions mechanically and metabolically most demanded during systole; 5) transformation of microinfarcts caused by impaired metabolism or impaired microvascular supply; or 6) misinterpretation as a falsepositive finding, visualized only after unfolding of the noncompacted layer as in an accordion. 8 To date, there are few data available to support these speculations.…”