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Spontaneous Cardiomyopathy in Cynomolgus Monkeys (Macaca Fascicularis)

Roche Pharmaceuticals, Pathology Department, Non-clinical safety, Palo Alto, CA 94304 USA

Correspondence: Tanja S. Zabka, Roche Pharmaceuticals, 340 Kingsland St., Bldg. 100, Nutley, NJ 07110, USA; phone: (973) 235-6894; e-mail:tanja.zabka{at}roche.com.

A previously undescribed spontaneous cardiomyopathy was identified by routine light microscopic examination of the heart from four clinically healthy purpose-bred cynomolgus monkeys that ranged from four to nine years of age and included 2 males and 2 females. Special stains of Sirius red, Masson’s trichrome, and Mallory’s phosphotungstic acid hematoxylin (PTAH); and immunohistochemistry using anti-CD68, troponin-I, and desmin antibodies were used to facilitate lesion characterization and assess cardiomyocyte viability. Microscopically, the apical to mid-ventricular myocardium to subendocardium had foci of cardiomyocyte disarray with cytoplasmic pallor to stippling and karyomegaly, vacuolization of the perimyseal connective tissue, a meshwork of fibrous tissue that concentrated around medium-sized blood vessels and dissected between or less often replaced affected cardiomyocytes; and a minimal, predominantly macrophage infiltrate. The disrupted cardiomyocytes were immunoreactive to desmin and troponin-I antibodies and had a normal cross-striation pattern by PTAH, indicating the chronic cardiomyopathy was not associated with active cardiomyocyte damage. The consistent distribution and morphology of the cardiomyopathy suggested a common etiology and pathogenesis. The features were reminiscent of chronic catecholamine-induced experimental cardiomyopathy and stress cardiomyopathy in monkeys and humans, respectively. This report documents another spontaneous heart lesion in clinically healthy monkeys for consideration during interpretation of toxicology studies.

Key Words: background • desmin • immunohistochemistry • heart • monkey • special stains • troponin

This version was published on October 1, 2009

Toxicologic Pathology, Vol. 37, No. 6, 814-818 (2009)
DOI: 10.1177/0192623309345692


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