LVH Case Study

Recently a large cohort of naturally-occurring LVH cases and SD in captive rhesus macaques was identified by antemortem and postmortem evaluation. These monkeys present clinical and pathologic entities resembling HCM in humans.[101, 102] In addition, case reports of LVH-related SD have been documented in other non-human primates such as owl monkeys (aotus spp.), captive western lowland gorillas (Gorilla gorilla gorilla), and captive chimpanzees (Pan troglodytes). In the cohort of rhesus macaques with LVH, several sires had multiple affected offspring, suggesting that LVH is inherited within the colony. Further inspection of the pedigrees has suggested that the LVH in this colony is dominated by founder effects, although the pattern of inheritance …show more content…
Interestingly, the histologic lesions of LVH in rhesus macaques, unlike human and feline HCM, does not show obvious myocyte disarray, interstitial fibrosis, medial hypertrophy in intramural coronary arteries. These changes with disorganized myocyte architecture and expanded collagenous matrix have been associated with development of arrhythmias and SD in humans, implying that the pathologic and genetic entity of LVH in rhesus macaques might be different from HCM in humans.[37] However, in humans with HCM, disorganized myocardial architecture is not confined to the regions of the left ventricle and can be seen in regions with normal to mild thickening.[104] This pattern challenges the theory that the degree of hypertrophy is related to the degree of architectural disorganization. Indeed, as in human patients with HCM, SD remains the primary clinical manifestation of LVH in rhesus macaques. These findings suggest that rhesus macaques with LVH may be useful in unraveling these associations, where hypertrophy is seen in the absence of overt architectural disorganization or clear vascular