Naturally occurring left ventricular hyperplasia is a rare but lethal disease. There are very few reports of this cardiac disease in captive nonhuman primates. In a colony of Macaca mulatta (Rhesus monkey) at California National Primate Research Center, a large number of rhesus macaques were diagnosed by autopsy with naturally occurring left ventricular hypertrophy without obvious underlying diseases over a 22-year period. The confirmatory diagnosis of ventricular hypertrophy was based on findings of notable left ventricular concentric hypertrophy with reduced left ventricular lumen, which is very similar to human ventricular hypertrophy cases. This report discusses an 11-year-old Macaca fascicularis monkey (Cynomolgus monkey, crab-eating macaque), weighing 2.95 kg, that was presented for enrollment in a pharmacokinetic (PK) study. During the PK experiment, the monkey died following a sudden decrease in percutaneous oxygen saturation and heart rate. Gross and histological examinations of the heart were performed. On gross pathology, the left ventricular wall was thickened, and the chamber lumen was reduced. In histopathological examination using hematoxylin- eosin and Masson-trichrome stains, fibrosis and myocyte disarray were not observed, but an increased cell density, compared to the normal heart, was confirmed. The autopsy results confirmed left ventricular hyperplasia as the major cause of death.

This study aimed to examine the effect of a mild elevation in serum cholesterol level in a porcine coronary overstretch restenosis model using a balloon angioplasty catheter or drug-eluting coronary stent. Pigs were divided into two groups and were fed a commercial normal diet (CND, n = 4) or a high-fat diet (HFD, n = 4) for 5 weeks. Coronary overstretch injury by balloon angioplasty or stent implantation was induced in the left anterior descending and left circumflex artery after 1 week of feeding. Histopathological analysis was performed at 4 weeks after coronary injury. During the experiment, the total cholesterol level in the HFD group increased by approximately 44.9% (from 65.9 ± 3.21 mg/dL at baseline to 95.5 ± 9.94 mg/dL at 5 weeks). The lumen area in the CND group was reduced in comparison with that in the HFD group after balloon angioplasty. After stent implantation, the injury score showed no significant difference. There were significant differences in the neointimal area (2.7 ± 0.33 mm2 in the CND group vs. 3.3 ± 0.34 mm2 in the HFD group, p<0.05), lumen area (2.6 ± 0.54 mm2 in the CND group vs. 2.0 ± 0.33 mm2 in the HFD group, p<0.05), and percent area stenosis (52.0 ± 7.96% in the CND group vs. 62.4 ± 5.15% in the HFD group, p<0.05). Body weight change was not different between the two groups. Increased serum cholesterol level activated vascular smooth muscle cell proliferation in the porcine coronary overstretch model.