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Published on: March 8, 2017
The heart: an end-organ of GH action
A Colao1, G Vitale, R Pivonello
1Department of Molecular and Clinical Endocrinology and Oncology, 'Federico II' University, via S. Pansini 5, 80131 Naples, Italy. colao@unina.it
Insights
Growth hormone (GH) and IGF-I significantly impact heart health. GH deficiency causes cardiac issues, while excess GH in acromegaly leads to specific heart conditions, both potentially reversible with treatment.
Area of Science:
- Endocrinology
- Cardiology
- Physiology
Background:
- The heart is recognized as a target organ for growth hormone (GH) action.
- Growth hormone deficiency (GHD) in children and adults is linked to cardiac abnormalities.
- Acromegaly, characterized by GH and IGF-I overproduction, results in a distinct cardiomyopathy.
Purpose of the Study:
- To elucidate the role of GH and IGF-I in cardiac structure and function.
- To investigate the cardiac consequences of GH deficiency and excess.
- To examine the effects of GH/IGF-I modulation on cardiovascular health.
Main Methods:
- Review of experimental and clinical studies on GH/IGF-I and the heart.
- Analysis of cardiac structure and function in patients with GHD and acromegaly.
- Evaluation of the impact of GH replacement therapy and acromegaly treatment on cardiac parameters.
Main Results:
- GHD is associated with reduced cardiac mass, impaired diastolic filling, and diminished exercise response.
- Acromegaly presents with concentric cardiac hypertrophy, diastolic dysfunction, and potentially systolic dysfunction and heart failure.
- Treatment of GHD can partially reverse cardiac abnormalities; successful acromegaly control reduces cardiac mass and improves function.
Conclusions:
- GH and IGF-I are critical regulators of cardiac development and performance.
- Both deficiency and excess of GH/IGF-I significantly affect cardiovascular health.
- Therapeutic interventions targeting GH/IGF-I levels can positively influence cardiac outcomes.
Abstract:
Several experimental and clinical studies have indicate that the heart is an end-organ of GH action. Patients with either childhood- or adulthood-onset GH deficiency (GHD) have abnormalities of cardiac structure and function, such as reduced cardiac mass, impaired diastolic filling and reduced left ventricular response at peak exercise. These cardiovascular abnormalities can be reversed, at least partially, after GH replacement therapy. On the other hand, the chronic overproduction of GH and IGF-I in acromegaly leads to the development of a specific cardiomyopathy. Concentric cardiac hypertrophy occurs in more than two-thirds of patients at diagnosis and is commonly associated with diastolic dysfunction. In later stages, impaired systolic function ending in heart failure can occur if GH/IGF-I excess is not controlled. Additionally, acromegalic cardiomyopathy is complicated by abnormalities of cardiac rhythm and cardiac valves. Successful control of acromegaly is accompanied by a decrease of the left ventricular mass and improvement of cardiac function. These beneficial effects appear earlier in young patients with short disease duration than in elderly patients. In conclusion, GH and IGF-I play a main role in the regulation of cardiac development and performance.
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