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Left ventricular abnormalities in dogs with hyperadrenocorticism | VETgirl Veterinary Continuing Education Podcasts

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In today’s VETgirl veterinary continuing education podcast, we review echocardiographic findings in dogs with hyperadrenocorticism. Hyperadrenocorticism (e.g., “Cushing’s disease”) is common in middle to older aged dogs and results in a state of chronic hypercortisolemia. Resultant systemic sequelae of this disease state include renal/urinary disease, diabetes mellitus, pulmonary thrombembolism (due to hypercoagulability), and systemic hypertension, among others. (Hence, one of the reasons why it’s so important that we treat this endocrine disease in dogs!). In humans with hyperadrenocorticism, increases in left ventricular wall thickness have been detected echocardiographically. So, Takano et al out of Japan wanted to evaluate myocardial structure and function in dogs with hyperadrenocorticism.

In a prospective study, the authors evaluated 22 dogs with previously diagnosed hyperadrenocorticism and 6 control dogs free of systemic disease. In this study, the authors chose to match controls to the study group with respect to the incidence of chronic valvular heart disease and pulmonary hypertension because of the predisposing signalment (e.g., middle-older age, small breed dogs) shared by both hyperadrenocorticism and chronic valvular heart disease and pulmonary hypertension.

In the affected dogs, the diagnosis of hyperadrenocorticism was based on clinical signs, abdominal ultrasound, chemistry profile, ACTH-stimulation testing (e.g., a cortisol post-ACTH > 20 ug/dL), or a low-dose dexamethasone suppression test (e.g., cortisol > 1 ug/dL at 8 hr post dexamethasone administration). All of the dogs received complete echocardiograms and blood pressure monitoring (via Doppler, with systemic hypertension defined as > 160 mm Hg). In addition to standard measurements of chamber size and wall thicknesses, these values were normalized to body weight. Left ventricular mass and left ventricular mass index (to body surface area) was also calculated in this study.

Overall, 15 of the 22 dogs had pituitary-dependent hyperadrenocorticism, while 7 dogs had functional adrenal tumors. 91% (20/22) of the dogs hyperadrenocorticism had diagnosed via ACTH-stimulating test, while the remaining (9%) were diagnosed based on a low-dose dexamethasone suppression test. Overall, there was no significant difference in the incidence of concurrent cardiovascular disorders.

In this study, 5 of the dogs with hyperadrenocorticism had systemic hypertension, as compared to 0 in the control group. Thirteen of the hyperadrenocorticism dogs were treated with trilostane, while 9 were untreated at the time of the study. 1 dog had a right adrenalectomy performed 18 months prior to the study. 68% (15/22) of the dogs with hyperadrenocorticism had significant increases in the normalized left ventricular and septal wall thicknesses and left ventricular mass index. There was no difference in the two dimensional wall thickness measurements among treated versus untreated dogs within the hyperadrenocorticism group, but dogs in the untreated group did have increased left ventricular mass and left ventricular mass index measurements compared with the treated dogs. Lastly, 30% (6/20) of the dogs with hyperadrenocorticism had an abnormal relaxation pattern (based on a Doppler-derived echocardiogram parameter of diastolic function); this was not seen in any of the control dogs (however, this wasn’t statistically significant).

So, what do we take from this VETgirl podcast? The majority of dogs with hyperadrenocorticism (68%) had increased left ventricular wall thickness and mass as compared to the control dogs. This is similar to human studies documenting concentric left ventricle remodeling in 62% of participants. This is the first published report of left ventricular hypertrophy secondary to hyperadrenocorticism in dogs. In dogs with concurrent systemic hypertension, the systemic hypertension is presumed to be a significant contributing etiology to the left ventricular hypertrophy. However, most dogs in this study with left ventricular hypertrophy (n=11/15) did not have systemic hypertension and the two are not necessarily associated in humans with hyperadrenocorticism, as well. The mechanism for left ventricular hypertrophy in systemic hypertension is independent of hyperadrenocorticism and is not well understood. One suggested mechanism in humans with hyperadrenocorticism is activation of mineralocorticoid receptors within the diseased myocardium by the circulating cortisol, which then causes myocardial remodeling and fibrosis). The identification of a difference in left ventricular mass and left ventricular mass index between treated and untreated dogs with hyperadrenocorticism suggests that the myocardial changes may be reversible to some degree with treatment (which has been demonstrated in humans following adrenalectomy).

Overall, this was a small but interesting study in a confined group of dogs with hyperadrenocorticism. If nothing else, it was good in that it was the first step in formally identifying that myocardial changes do occur in dogs with hyperadrenocorticism. What impact this truly has on myocardial function in these dogs remains to be seen. Although an abnormal relaxation pattern was reported in dogs with hyperadrenocorticism, this was not statistically significant and its important to know that these abnormal relaxation patterns also occur very commonly simply with aging (in both dogs and humans). The limitation of this study was that the number of dogs in both the hyperadrenocorticism and control group was very small, so its hard to make any judgments as to whether or not the abnormal relaxation is specific to the left ventricular hypertrophy from hyperadrenocorticism, or simply a function of shared predisposition because of advancing age. Clinically, isolated left ventricular hypertrophy in a dog with hyperadrenocorticism is not likely to result in cardiovascular consequences that would PRECEDE the more common clinical signs of hyperadrenocorticism (and thus its detection and treatment). In a dog with preexisting valvular or myocardial disease who then develops hyperadrenocorticism and secondary left ventricular hypertrophy, the left ventricular hypertrophy (and any possible effect on left ventricular function) could be amplified, however.

So, in conclusion, left ventricular hypertrophy appears to be associated with hyperadrenocorticism in dogs, with a suspected causal relationship. The impact of this hypertrophy on myocardial function and clinical signs remains to be seen. Preliminary results suggest that the myocardial hypertrophy may be reversible with treatment of the hyperadrenocorticism but further studies are needed.

References:
1. Takano H, Kokobu A, Sugimoto K, et al. Left ventricular structural and functional abnormalities in dogs with hyperadrenocorticism. J Vet Cardiol 2015:17;173-181.

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