Avaliação eletrocardiográfica Holter de cães submetidos ao teste de estimulação com hormônio adrenocorticotrófico

Abstract

Hyperadrenocorticism (HC) is an endocrine disorder frequently diagnosed in dogs, resulting from chronic exposure to elevated glucocorticoid levels, a condition that triggers important metabolic alterations. Definitive diagnosis is established through specific hormonal tests, such as the adrenocorticotropic hormone (ACTH) stimulation test (ACTHst), which is also widely used for therapeutic monitoring. Scientific evidence indicates that glucocorticoids exert a direct influence on the sympatho-adrenomedullary system, stimulating the synthesis and release of catecholamines by the adrenal glands. In addition, these hormones prolong the effects of catecholamines at neuromuscular junctions, increase cardiovascular responsiveness, and enhance the affinity of β-adrenergic receptors in smooth muscle cells. This interaction between glucocorticoids and catecholamines may significantly affect hemodynamic parameters, considering that catecholamines play a central role in the regulation of cardiac output, blood pressure, and the physiological stress response. Considering this relationship, the present study aimed to evaluate the effects of ACTH on cardiac electrical activity and blood pressure in dogs subjected to the ACTHst and to placebo with saline solution, through continuous electrocardiography and blood pressure measurement. A total of 18 dogs were analyzed, of which 77.8% were females and 22.2% males, with a mean body weight of 10.4 ± 6.9 kg and a mean age of 10 ± 2.7 years. Eight dogs (44.4%) had a previous diagnosis of HC and underwent the ACTHst for therapeutic monitoring. Ten animals (55.6%) were evaluated due to clinical suspicion, resulting in four confirmed diagnoses (22.2%) while six cases (33.3%) remained inconclusive. No significant electrocardiographic or hemodynamic alterations were observed during the hormonal test, suggesting that the administration of ACTH, at the dose and route standardized for the ACTHst, is not capable of inducing an increase in cardiac sympathetic tone or promoting relevant hemodynamic changes in dogs.