Page 387 - Feline Cardiology

Chapter 26: Endocrine Diseases 405

the typical diabetic patient (Peterson et al. 1990). diabetes mellitus (Maggio et al. 2000) and diabetes is
Abdominal organomegaly, stertor due to excess growth therefore considered to not be a clinically significant
of pharyngeal tissues, and broadening and flattening of cause of systemic hypertension in cats (Brown et al.
the forehead are other physical features of acromegaly 2007).
in cats (Peterson et al. 1990; Feldman and Nelson 2000;
Berg et al. 2007; Niessen et al. 2007). Other anabolic Hyperadrenocorticism
effects of growth hormone may explain cardiovascular Hyperadrenocorticism, a disease of glucocorticoid
physical examination abnormalities, notably systolic excess, is rare in the cat. Feline hyperadrenocorticism is
heart murmurs in 9/14 (64%) of cats and signs of con- caused by a functional pituitary tumor in approximately
gestive heart failure in 6/14 (43%) (Peterson et al. 1990). 50% of cases and a functional adrenal tumor in the
In one case series of acromegalic cats, congestive heart remaining 50% (Feldman and Nelson 2000). Due to the
failure manifested with ascites in 2/6 cats, in addition to insulin-antagonistic effects of glucocorticoids, the clini-
pulmonary edema (5/6) and pleural effusion (1/6) cal presentation is typically that of insulin-resistant dia-
(Peterson et al. 1990). Thoracic radiographs revealed betes mellitus. Historical, physical exam findings, and
mild to moderate cardiomegaly in a majority (12/14, diagnostic test results are not remarkable with respect to
86%) of cats, and echocardiography demonstrated left the cardiovascular system. Abnormalities should be
ventricular concentric hypertrophy, with septal thicken- viewed with skepticism in terms of causality, and
ing in 7/8 cats and left ventricular free wall thickening common, independent disorders (e.g., hypertrophic car-
in 5/8 cats (Peterson et al. 1990). Systemic hypertension diomyopathy if left ventricular concentric hypertrophy
and electrocardiographic abnormalities do not appear is noted echocardiographically, or chronic kidney disease
to be a common feature of feline acromegaly (Niessen or the white coat effect if the patient is hypertensive)
et al. 2007), both having been detected in zero of 17 occurring concurrently with hyperadrenocorticism
acromegalic cats. Despite treatment with pituitary should be considered a likely explanation for such
gland irradiation and/or the somatostatin analog octreo- findings.
tide, 5/14 cats in one series developed congestive heart
failure, which contributed to euthanasia or death in 4. Hyperaldosteronism
Necropsy results in 10 cats included “hypertrophic car- Excessive synthesis and systemic release of mineralocor-
diomyopathy” (likely left ventricular concentric hyper- ticoids produces the syndrome of hyperaldosteronism, a
trophy) in 7 and “dilated cardiomyopathy” (possibly rare endocrinopathy of cats. The cause is almost invari-
growth hormone–associated myocardial failure) in 1. ably a primary adrenal neoplasm (Ash et al. 2005).
Nevertheless, the clinical relevance of acromegaly in The pathophysiologic nexus is systemic sodium reten-
feline cardiology remains that it may cause left ventricu- tion and severe potassium wasting caused by excessive
lar concentric hypertrophy and subsequent congestive activity of the aldosterone-driven sodium-potassium
heart failure, and that such disorders may be addressed exchanger pump in the distal renal tubule. Accordingly,
most effectively through therapies that treat the endo- history and physical exam typically describe weakness
crinopathy, in addition to treatment for congestive heart due to hypokalemia-associated decreased skeletal muscle
failure should it be present. tone, inappetence, and other nonspecific signs. A minor-
ity of patients (2/13 in one case series) presents with Endocrine Diseases
Diabetes Mellitus acute vision loss due to intraocular hemorrhage and
Diabetes mellitus in humans is an important risk factor retinal detachment. Diagnostic testing typically reveals
for heart disease, but this association does not hold true profound hypokalemia (may be <2.5 mEq/l) that is typi-
in cats. Most likely this difference is due to the different cally refractory to standard supplementation alone. This
underlying substrate of heart disease: the most common hypokalemia predisposes hyperaldosteronemic cats to
heart disease of humans in industrialized nations is ventricular ectopy, which may resolve with correction of
coronary artery atherosclerosis, and this disease is serum potassium concentration. However, the feline
potentiated by diabetes mellitus. Fortunately for cats, ECG is notable for the rare occurrence of U waves with
the feline species does not sustain coronary artery ath- profound hypokalemia, in contrast to humans. Systemic
erosclerosis to any clinically meaningful degree, either in hypertension due to aldosterone-mediated sodium
diabetic or nondiabetic states. retention is present in many cats, including some with
Diabetic humans also have an increased incidence of target-organ damage (e.g., fundic lesions) that may or
systemic hypertension. This cardiovascular problem, may not have led to overt organ dysfunction (i.e., some
likewise, is virtually unknown in diabetic cats: 2 cases of cats with hypertensive fundic lesions are still visual,
systemic hypertension have been recorded in cats with while others present due to acute blindness) (Ash et al.