Page 378 - Feline Cardiology

396 Section N: Endocrine Diseases Affecting the Heart

mass (Skelton and Sonnenblink 1974). The reversibility 132.0 ± 1.62 mm Hg, respectively) (Kobayashi et al.
of such changes was also appreciated at this time, with 1990). More recently, a study of 39 cats examined
complete regression of thickening in cats allowed to before and 30–60 days after treatment did not identify a
recover for 12 months. When naturally occurring feline significant difference in systolic blood pressure values
hyperthyroidism first was documented in the early 1980s, (Stepien et al. 2003). A small but significant decrease
left ventricular thickening was a prominent feature of the (from 144.9 ± 16.8 mm Hg to 139.8 ± 21.3 mm Hg)
disease (Liu et al. 1984) but prevalence information was did occur in 100 hyperthyroid cats treated with carbima-
not available. Shortly thereafter, an echocardiographic zole or thyroidectomy, but euthyroidism was then asso-
study identified left ventricular free wall hypertrophy in ciated with the appearance of systemic hypertension in
72% of hyperthyroid cats and interventricular septal 9/40 (22.5%) previously normotensive cats (Syme and
hypertrophy in 40% (Bond 1988). A more recent study Elliott 2003). This change suggested an unmasking of
of 91 hyperthyroid cats has shown that 37% of hyperthy- concurrent chronic kidney disease or other hypertensive
roid cats have an echocardiographically demonstrable factors. Overall, while few hyperthyroid cats appear to
cardiac lesion, and for the most part these are mild experience a dramatic lowering of blood pressure with
lesions. Therefore, while the prevalence of gross cardiac the return of euthyroidism, some experience a new onset
changes approaches 40% in the current population of of systemic hypertension. This finding justifies the
hyperthyroid cats, the clinical impact of these changes ongoing measurement of blood pressure in hyperthy-
appears to be minimal and, in many cases, negligible. roid cats that are receiving or have received antithyroid
The prevalence of systemic hypertension in hyperthy- therapy.
roid cats ranges widely. One study has documented 19%
of hyperthyroid cats with systolic blood pressure mea- Etiology, Pathophysiology, and
surements ≥160 mm Hg when assessed with standard Gross Pathology
Doppler ultrasonic sphygmomanometry (Stepien et al. Mechanism of Hyperthyroidism
2003) whereas another study also using Doppler mea- In cats, hyperthyroidism is caused by primary hyperse-
surements identified 85% of hyperthyroid cats as having cretion of thyroid hormone from the thyroid gland. The
systolic blood pressure >2 standard deviations above cause of excessive hormone synthesis and secretion is a
control subjects (Kobayashi et al. 1990). This extremely functional neoplasm of the thyroid gland that has been
broad range can be better understood based on the chro- given many different names (adenoma, thyroid adeno-
nology of the studies: the higher prevalence was identi- matous goiter, adenomatous hyperplasia, and others)
fied in a study of 39 cats evaluated in a report published and that affects both thyroid lobes in most (70%) feline
in 1990, whereas the lower prevalence was identified in cases.
an abstract published 13 years later. As will be discussed Thyroid hormone is not indispensable for cardiac
below, newer case series of feline hyperthyroidism function, but its presence—and its excess—can greatly
describe abnormalities that are less severe, likely due to influence the cardiovascular system (Dillman 2002). The
an earlier recognition of the disease compared to origi- actions of thyroid hormone on the cardiovascular system
Endocrine Diseases hyperthyroidism (1980s). Furthermore, the lower preva- least four broad categories of effects: 1) myocardial
nal reports from the first decade of emergence of feline
are manyfold, and thyroid hormone excess can exert at
lence noted in the more recent study identified higher
hypertrophy, 2) increased systolic and diastolic function,
blood pressure readings in another group of hyperthy-
3) vasodilation and increased circulating blood volume,
roid cats that was no different clinically, but in which
and 4) alterations in heart rate and rhythm (Figure
blood pressure was measured in a busy clinical environ-
ment by operators with varying amounts of training. 26.1). The clinical repercussions of hyperthyroidism on
the heart and vasculature are the result of the interplay
Therefore, at the present time, if the blood pressure of of these actions and other factors, a process that can
hyperthyroid cats is measured by an experienced opera- change frequently from day to day and over the extended
tor using the Doppler technique in an environment that course of the disease.
minimizes external stressors, the true prevalence of sys- Myocardial hypertrophy is likely mediated at least in
temic hypertension in feline hyperthyroidism likely part by an increase in the synthesis of myosin.
approaches the lower value of 19%. Triiodothyronine (T3, the metabolically active form of
The prevalence of systemic hypertension in feline thyroid hormone in all cells that is created from mainly
hyperthyroidism may or may not change with antithy- hepatic monodeiodination of thyroxine, T4) activates
roid treatment. An early report identified a significant transcription of the α-myosin heavy chain (V1) (Klein
change from pre- to 2–3-month post-treatment values and Ojamaa 2001; Dillman 2002). This mechanism has
in 7 hyperthyroid cats (from 159.5 ± 15.4 mm Hg to a greater impact in animals, where the α-myosin (V1)