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Related Experiment Videos

Cardiovascular function in acromegaly.

R N Clayton1

  • 1School of Medicine, Keele University, Stoke-on-Trent, Staffordshire, ST4 7QB, United Kingdom. r.n.clayton@keele.ac.uk

Endocrine Reviews
|June 6, 2003
PubMed
Summary
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Acromegaly significantly increases mortality due to vascular disease, linked to prolonged excess growth hormone (GH) exposure. Effective treatment normalizing GH and IGF-I levels improves survival by addressing cardiac and endothelial dysfunction.

Area of Science:

  • Cardiology
  • Endocrinology
  • Vascular Medicine

Background:

  • Acromegaly, caused by excess growth hormone (GH), is linked to a 2-3 fold increase in mortality, primarily from vascular disease.
  • Long-term exposure to elevated GH before diagnosis contributes to tissue damage and increased mortality.
  • Effective treatment normalizing GH and Insulin-like Growth Factor I (IGF-I) levels is crucial for improving patient outcomes and survival.

Purpose of the Study:

  • To investigate the specific structural and functional cardiac and endothelial changes in acromegaly.
  • To explore the contribution of these changes to increased vascular mortality in acromegaly.
  • To assess the potential for treatment to reverse these detrimental effects and improve prognosis.

Main Methods:

  • Review of existing evidence on cardiac structure and function in acromegaly, including left ventricular hypertrophy and diastolic dysfunction.

Related Experiment Videos

  • Assessment of endothelial function, specifically flow-mediated dilatation, as a marker of atherosclerosis.
  • Evaluation of arterial structural changes, such as intima-media thickness.
  • Analysis of the impact of GH-lowering treatment on these parameters.
  • Main Results:

    • Acromegaly is associated with myocardial structural changes (myocyte hypertrophy, fibrosis) and common left ventricular hypertrophy, even in early disease stages.
    • Impaired left ventricular diastolic function and reduced exercise tolerance are prevalent, with partial improvement post-treatment.
    • Endothelial dysfunction and early arterial structural changes are observed in active acromegaly and may improve with effective treatment.
    • Increased risk of ventricular arrhythmias may be linked to altered left ventricular architecture.

    Conclusions:

    • Impaired cardiac and endothelial structure and function are significant risk factors for vascular mortality in acromegaly.
    • These cardiovascular alterations should be considered legitimate therapeutic targets in acromegaly management.
    • Effective treatment aimed at normalizing GH and IGF-I levels can potentially reverse some cardiac and vascular abnormalities, improving long-term survival.