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Normal papillary muscles are typified by a cellular architecture in which myocytes are arranged in orderly arrays, whose alignment is approximately parallel to the lines of tension within the muscle. To examine the contribution of directed tensile force to the maintenance of myocyte architecture within the papillary muscle, we studied the histologic effects of abrupt disruption of tension on the myocytes of the left ventricular papillary muscles in 84 patients who died after mitral valve replacement. Focal contraction band necrosis or coagulation necrosis was seen in 57 cases (68%) and fibrosis in 71 cases (85%). Zonal lesions sarcoplasmic condensations adjacent to intercalated discs were present in 49 cases (58%) and correlated negatively with survival time. Myocyte disarray in 26 cases (31%) was more frequent with longer survival and became an interconnecting random network of myocytes. All 10 patients who survived more than 1 year had disarray, as did eight of 10 patients who survived 1 month to 1 year. Myocyte atrophy in 19 cases (23%) correlated with the degree of acquired disarray. Multivariate regression analysis of these five histologic features showed significant prediction of survival time by myocyte disarray only. This finding demonstrates that the development and progression of disarray is not significantly associated with any of the other lesions studied. Since surgical disruption of normal lines of tension causes papillary muscles to function in a setting that approaches idealized isotonic contraction, it appears that myocyte disarray may be acquired over time in such a physical state. The findings support the concept that while myocyte orientation usually arises during development as a direct consequence of force distribution within the myocardium, disarray may also be acquired postnatally in regions of myocardium in which force distribution is altered.

Myocyte disarray develops in papillary muscles released from normal tension after mitral valve replacement.