No evidence of ectopic lipid accumulation in the pathophysiology of the acromegalic cardiomyopathy

Abstract

Results: AlthoughMYCLtended to be lower, HCL was significantly lower in ACRO-active compared with CON (HCL: 1.2%± 1.2% vs 4.3%± 3.5% of 1H-magnetic resonance spectroscopy signal, P< .02). Parameters of systolic function and hypertrophy were significantly increased in ACRO-active compared with CON, as were insulin secretion and resistance. After the control of GH excess, HCL and MYCL remained unchanged, but pericardial fat was increased in the patients in whom GH excess was controlled (from 11.6± 5.5 to 14.7± 6.2 cm2, P= .02). Context: Patients with acromegaly frequently display disturbances of glucose and lipid metabolism, which might contribute to their increased cardiovascular risk. Because insulin resistance and increased lipolysis have been linked to ectopic lipid deposition, altered lipid accumulation in the liver and the myocardium might contribute to metabolic and cardiac complications in these patients. Objective: The aim of this study was to investigate myocardial (MYCL) and hepatic lipid content (HCL), insulin sensitivity, and cardiac function in active acromegaly and after control of GH excess through transsphenoidal surgery. Patients: Ten patients with newly diagnosed acromegaly (ACRO-active) were compared with 12 healthy controls (CON), matched for age, body mass index, and gender. In seven patientsGHexcess was controlled, and they were compared with their active state. Methods: MYCLandHCLwere assessed by 1H-magnetic resonance spectroscopy, pericardial fat and cardiac function by 1H-magnetic resonance imaging, and insulin sensitivity and secretion by an oral glucose tolerance test. Conclusion: Acromegaly represents a unique condition characterized by low myocardial and hepatic lipid content despite decreased insulin sensitivity, hyperinsulinemia, and hyperglycemia. Hence, ectopic lipid accumulation does not appear to contribute to cardiac morbidity, and increased lipid oxidation might counteract ectopic lipid accumulation inGHexcess.