* Compensatory changes
valvular thickening (fibrosis)
microscopic coronary arteriosclerosis
microscopic intramural myocardial infarction (MIMIs)
myocardial hypertrophy *
lipofuscin accumulation in myocyte cytoplasm
Myocardial amyloid deposition.
Lipofuscin accumulation in myocyte cytoplasm increases with age in the dog, and starts
at about 7 years of age. It is not known whether it has any adverse effect on myocyte
Cardiac amyloidosis is a frequent finding at post-mortem examination in geriatric
humans (50% of people over 65 years, and 84% of people over 90 years), but in one
study of dogs only 0.6% (all over 10 years of age) had this change at routine autopsy.
In one report valvular endocardiosis lesions increased in incidence and severity
with increasing age, and were present in all dogs over 13 years of age (Whitney 1974).