Finsterer Josef, Stöllberger Claudia, Feichtinger Hans
Department of Neurology, Krankenanstalt Rudolfstiftung, Vienna, Austria.
Cardiology. 2006;105(4):223-5. doi: 10.1159/000091738. Epub 2006 Feb 27.
The histological workup of the myocardium of a patient with Duchenne muscular dystrophy and left ventricular hypertrabeculation/noncompaction (LVHT) revealed an extremely thin left ventricular wall and a noncompacted layer double in size compared to the compacted layer. Within the compacted layer islets of fibrous tissue predominated, surrounded by areas of myxoid appearance hardly producing collagen, and occasionally normal or dystrophic cardiomyocytes. The noncompacted layer consisted largely of intact cardiomyocytes rarely intermingled with collagen-producing, fibrous tissue. This variant appearance of the compacted and noncompacted layer was found in all areas of noncompaction. These histopathological findings suggest that LVHT represents a compensatory attempt to overcome the failing compacted but dystrophic myocardium.
对一名患有杜氏肌营养不良症和左心室小梁增多/心肌致密化不全（LVHT）患者的心肌进行组织学检查发现，左心室壁极薄，心肌致密化不全层的大小是致密层的两倍。在致密层内，纤维组织小岛占主导，周围是几乎不产生胶原蛋白的黏液样区域，偶尔还有正常或营养不良的心肌细胞。心肌致密化不全层主要由完整的心肌细胞组成，很少与产生胶原蛋白的纤维组织混合。在心肌致密化不全的所有区域均发现致密层和非致密层的这种变异外观。这些组织病理学发现表明，LVHT代表了一种代偿性尝试，以克服功能衰竭但营养不良的致密心肌。
