Supraphysiological Doses of GH Induce Rapid Changes in Cardiac Morphology & Function
Supraphysiological Doses of GH Induce Rapid Changes in Cardiac Morphology and Function -- Cittadini et al. 87 (4): 1654 -- Journal of Clinical Endocrinology & Metabolism
The observation that a mere 4 wk of GH treatment at high doses induces a significant increase of LV mass associated with a high cardiac output state has relevant clinical implications. In fact, although there are no published statistics for obvious reasons, GH abuse probably lasts for years (2). Such continued exposure to high GH/IGF-I levels may lead to the development of an acromegalic syndrome. In addition to the attendant risk of malignancy, peripheral neuropathy, and glucose intolerance, the negative reverberations of chronic GH excess on the cardiovascular system have been extensively characterized: systemic hypertension, LV hypertrophy with marked histological changes, arrhythmias, abnormal LV diastolic filling, and systolic function (7). These alterations, particularly LV hypertrophy, observed after only 4 wk of GH administration in our high-dose group, and cardiac arrhythmias, in turn, are known to predispose to heart failure and sudden death (30). It must also be stressed that small increments in LV mass, as those reported in the current investigation, have been found to be associated with increased risk for sudden death in the Framingham population (31), particularly when associated with LV concentric remodeling (32). In addition, even though the high cardiac output state observed in our high-dose group may augment exercise capacity, it may be detrimental in the long term because of the attendant increase of oxygen consumption and, therefore, of cardiac energy requirements.
In a realistic scenario, the possibility of concomitant abuse of GH and anabolic steroids should be taken into account. Indeed, anabolic steroids are commonly employed among athletes and body builders and are associated with increased LV mass and altered diastolic filling (33, 34). It appears likely that the actions of both prohibited substances may be additive or even synergistic on myocardial growth, and possibly responsible for functional derangements. This speculation is supported by the recent observation that nandrolone decanoate per se increases IGF-I mRNA in rat respiratory muscles (35).
Besides the rapid cardiac structural and functional changes observed in our study, almost half of the subjects in the active treatment group developed significant side effects, compared with 12% in the placebo group. It may be anticipated that such a percentage would increase under a chronic exposure to GH/IGF-I excess.
In conclusion, short-term administration of supraphysiological doses of GH to healthy, moderately trained subjects is associated with increased LV mass and a high cardiac output state.
Supraphysiological Doses of GH Induce Rapid Changes in Cardiac Morphology and Function -- Cittadini et al. 87 (4): 1654 -- Journal of Clinical Endocrinology & Metabolism
The observation that a mere 4 wk of GH treatment at high doses induces a significant increase of LV mass associated with a high cardiac output state has relevant clinical implications. In fact, although there are no published statistics for obvious reasons, GH abuse probably lasts for years (2). Such continued exposure to high GH/IGF-I levels may lead to the development of an acromegalic syndrome. In addition to the attendant risk of malignancy, peripheral neuropathy, and glucose intolerance, the negative reverberations of chronic GH excess on the cardiovascular system have been extensively characterized: systemic hypertension, LV hypertrophy with marked histological changes, arrhythmias, abnormal LV diastolic filling, and systolic function (7). These alterations, particularly LV hypertrophy, observed after only 4 wk of GH administration in our high-dose group, and cardiac arrhythmias, in turn, are known to predispose to heart failure and sudden death (30). It must also be stressed that small increments in LV mass, as those reported in the current investigation, have been found to be associated with increased risk for sudden death in the Framingham population (31), particularly when associated with LV concentric remodeling (32). In addition, even though the high cardiac output state observed in our high-dose group may augment exercise capacity, it may be detrimental in the long term because of the attendant increase of oxygen consumption and, therefore, of cardiac energy requirements.
In a realistic scenario, the possibility of concomitant abuse of GH and anabolic steroids should be taken into account. Indeed, anabolic steroids are commonly employed among athletes and body builders and are associated with increased LV mass and altered diastolic filling (33, 34). It appears likely that the actions of both prohibited substances may be additive or even synergistic on myocardial growth, and possibly responsible for functional derangements. This speculation is supported by the recent observation that nandrolone decanoate per se increases IGF-I mRNA in rat respiratory muscles (35).
Besides the rapid cardiac structural and functional changes observed in our study, almost half of the subjects in the active treatment group developed significant side effects, compared with 12% in the placebo group. It may be anticipated that such a percentage would increase under a chronic exposure to GH/IGF-I excess.
In conclusion, short-term administration of supraphysiological doses of GH to healthy, moderately trained subjects is associated with increased LV mass and a high cardiac output state.