Page 377 - Feline Cardiology

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Endocrine Diseases Affecting the Heart

Key Points

• In cats, hyperthyroidism produces concentric ventricular hypertrophy (thickening) and systemic hypertension as its primary
cardiovascular effects.
• Reversion to euthyroidism can cause complete or partial reversal of these changes in many cases. Initial reports of feline
hyperthyroidism (1980s) described lesions that were often more dramatic and severe than those observed today; possible
explanations include earlier recognition of cases at present and the emergence of milder forms of feline hyperthyroidism.
• A small proportion of hyperthyroid cats may be affected with idiopathic hypertrophic cardiomyopathy simultaneously.
The presence of the two concurrent disorders is confirmed retrospectively, when antithyroid treatment brings long-term
euthyroidism but cardiovascular abnormalities (e.g., left ventricular hypertrophy) persist.
• The cardiovascular implications of hyperthyroidism are mild for the most part, and with the exception of acute severe
decompensation (“thyroid storm”), are infrequently responsible for morbidity or mortality in affected cats.

HYPERTHYROIDISM cardiomyopathy is now known to be a type of idiopathic
or inherited myocardial protein defect that causes ven-
Introduction tricular thickening in the absence of any intracardiac or
The seminal report that first detailed cardiovascular systemic causes. Therefore, the cardiac changes caused
changes in spontaneously hyperthyroid cats appeared in by hyperthyroidism are correctly referred to as thyrotoxic
1984 (Liu et al. 1984). Additional milestones have heart disease or hyperthyroid heart disease, not hypertro-
included investigation of electrocardiographic features phic cardiomyopathy. The distinction is a clinically
of feline hyperthyroidism (Peterson et al. 1982), echo- important one, since thyrotoxic heart disease presents
cardiographic features (Bond et al. 1988; Peterson et al. the opportunity for normalization of cardiovascular
1993), the cardiac effects of a return to the euthyroid structure and function with antithyroid treatment,
state (Peterson et al. 1993; Weichselbaum et al. 2005), whereas with hypertrophic cardiomyopathy, no treat-
the evolution of hyperthyroidism itself over time ment is available that returns cardiac structure to normal.
(Broussard et al. 1995; Edinboro et al. 2004), and an
exploration of etiologic factors (Kass et al. 1999; Prevalence of Cardiovascular Abnormalities
Edinboro et al. 2004; Martin et al. 2000). in Hyperthyroid Cats
Although much of our current understanding of The recognition that elevated circulating thyroid
hyperthyroidism can be traced back to early reports (Liu hormone levels in cats cause structural cardiac changes
et al. 1984; Holzworth et al. 1980), some confusion occa- predates the emergence of clinical feline hyperthyroidism
sionally persists regarding nomenclature. Original by several years. Experimental hyperthyroidism induced
descriptions of “hypertrophic cardiomyopathy caused in cats in the early 1970s via daily intraperitoneal injec-
by hyperthyroidism” (Liu et al. 1984) are no longer accu- tions of l-thyroxine for 10 months produced massive
rate and may seem misleading, because hypertrophic biventricular hypertrophy, with near-doubling of cardiac

Feline Cardiology, First Edition. Etienne Côté, Kristin A. MacDonald, Kathryn M. Meurs, Meg M. Sleeper.
© 2011 John Wiley & Sons, Inc. Published 2011 by John Wiley & Sons, Inc.

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