Hypertrophic cardiomyopathy is the most common form of heart disease in cats. Multiple genetic mutations have been identified in humans with HCM; however, to date, a myosin-binding protein C mutation in Maine Coon cats and Ragdoll cats is the only gene mutation identified in association with HCM in felids.1–4 However, a genetic basis of this disease is suspected in cats affected with HCM.
Although genetic factors may predispose cats to the development of HCM, the interaction between genetics and environmental factors may also play a role in the development or manifestation of the HCM phenotype. Environmental factors such as diet and growth patterns may influence disease severity and the time of onset for this condition. Such a link between cardiac function, early growth, and diet has been determined in other species. For example, mice that express a mutant β-myosin heavy chain have significantly depressed cardiac contractile function when fed a soy-rich diet, compared with the effect of being fed a casein-rich diet.5 This change in cardiac function is especially pronounced in male mice.5 In hamsters, environmental stress such as exercise has also been found to affect the development of cardiomyopathy.6 By increasing the amount of exercise during infancy, both the expression of β-myosin heavy-chain mRNA and the degree of degenerative mitochondrial changes in cardiomyocytes were decreased.6 Among humans, individuals with fast early growth and those who are fed high-nutrient diets as infants will later develop higher adult body weight, higher adult blood pressure, and a predisposition for the development of cardiovascular diseases than other individuals.7–11 In utero nutritional conditions may also play a role; studies12–14 in sheep have revealed that maternal nutrient restriction results in left ventricular hypertrophy in the offspring. This is thought to be related to increased circulating IGF-1 activity, but could also be the result of increased blood angiotensin-II concentration or upregulation of myocardial genes for α-cardiac actin, caveolin-1, and titin.13–15 Therefore, in cats, it seems plausible that dietary intake during early developmental stages that results in faster growth may be a determinant in the severity of HCM; if this proves to be true, then dietary manipulations may be able to alter the disease progression or phenotypic expression of HCM in cats.
In a previous study,16 cats with HCM had significantly higher concentrations of serum growth hormone, compared with concentrations in healthy control cats. Growth hormone secretion is pulsatile, and a single measurement might not provide a complete assessment of growth hormone secretion. Because IGF-1 is the mediator of the growth-promoting effects of growth hormone, measurement of serum IGF-1 concentration may be a better method of assessment for growth hormone status. Insulin-like growth factor is also of interest because of its correlation with body size and nutritional status.17
Typically, the heart size of a dog or cat will vary proportionally with the animal's body size or vertebral length.18,19 In contrast, cats with HCM have higher heart-to-body weight ratios20 and larger heart dimensions for their body sizes.21 To our knowledge, no other morphometric measurements have been assessed in cats with HCM. The purpose of the study reported here was to compare morphometric measurements and serum IGF-1 concentration in cats with and without HCM. Dietary history was also assessed. Our hypothesis was that cats with HCM would have larger body size and skeletal features and higher serum IGF-1 concentrations than healthy cats.
Body condition score
Insulin-like growth factor-1
Length of the fourth thoracic vertebra
Length of the 12th thoracic vertebra
Vertebral heart score
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