Abstract
Context Growth hormone excess and growth hormone deficiency (GHD) are both associated with increased cardiovascular morbidity. A specific acromegaly-related cardiomyopathy has been described, characterized in part by increased left ventricular mass (LVM). Growth hormone deficiency is associated with reduced LVM. Following cure of acromegaly with surgery or radiation therapy, GHD may develop; however, its effects on cardiac morphology and function in this population are not established. Objective We hypothesized that the development of GHD in patients with prior acromegaly would be associated with cardiac morphologic and functional changes that differ from those in patients who are GH sufficient following cure of acromegaly. Design A cross-sectional study was conducted in a Clinical Research Center. Study participants consisted of three groups of subjects ( n = 34): I. Cured acromegaly with GHD ( n = 15), II. Cured acromegaly with GH sufficiency ( n = 8), and III. Active acromegaly ( n = 11). Main outcome measures included cardiac morphology and function, using echocardiography parameters. Results Mean age and BMI, 44.6 ± 2.3 years (SEM) and 30.7 ± 1.3 kg/m 2, respectively, were not different among the three groups. Mean peak GH values were: I. 2.8 ± 0.4 ng/ml; II. 30.1 ± 9.1 ng/ml ( p = 0.0002.) In group I, left ventricular mass, indexed to body surface area (LVMi), was within the normal range in all patients; moreover, left ventricular (LV) geometry was normal. At least 50% of patients in groups II and III had elevated LVMi, and in 50% of patients, LV geometry was abnormal, indicating pathologic hypertrophy. Ejection fraction was similar between all three groups. There were no significant differences in diastolic function. Conclusions Patients who develop GHD following cure of acromegaly do not demonstrate elevated LV mass, in contrast to patients with a history of acromegaly but normal GH levels or to patients with active acromegaly. This suggests that GH status after treatment of acromegaly correlates with LV mass, and that, in GH sufficient patients, reversal of remodeling may be slower than previously thought. These data suggest that it will be important to determine whether GH replacement alters left ventricular morphology over time.
Highlights
Cardiovascular (CV) disease is a leading cause of death in acromegaly
Patients who develop growth hormone deficiency (GHD) following cure of acromegaly do not demonstrate elevated left ventricular (LV) mass, in contrast to patients with a history of acromegaly but normal GH levels or to patients with active acromegaly. This suggests that GH status after treatment of acromegaly correlates with LV mass, and that, in GH sufficient patients, reversal of remodeling may be slower than previously thought
These data suggest that it will be important to determine whether GH replacement alters left ventricular morphology over time
Summary
Cardiovascular (CV) disease is a leading cause of death in acromegaly. Overall survival is reduced by an average of ten years in active acromegaly [1], and persistent disease following surgical intervention carries a 2 to 3.5-fold increased relative mortality risk per year [2,3,4]. The sequelae of growth hormone excess include structural and functional cardiac changes, as well as inflammatory and metabolic effects [5]. A distinct entity of cardiac hypertrophy associated with acromegaly has been described [6,7], independent of the hypertension often seen in these patients [8,9]. Morphological cardiac changes include increased left ventricular mass (LVM) [8,10,11,12], which appears to reflect interstitial fibrosis as well as increased myocyte size [13,14]. Structural changes may occur before any clinical signs of cardiac dysfunction [6]; left ventricular (LV) hypertrophy is seen even in younger patients with shorter durations of disease [12,15]
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