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Altered hypothalamic-pituitary-adrenal axis activity in patients with chronic heart failure

E V Sivukhina1, A S Poskrebysheva, Iu V Smurova

  • 1Department of Anatomy II, Friedrich-Schiller University, Jena, Germany.

Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|June 23, 2009
PubMed

Insights

Chronic heart failure patients show altered neuroendocrine signaling, with increased hypothalamic-pituitary-adrenal axis activity despite normal cortisol levels. Structural adrenal changes suggest relative glucocorticoid deficiency contributing to this neuroendocrine dysregulation.

Area of Science:

  • Endocrinology
  • Cardiology
  • Neuroscience

Background:

  • Neuroendocrine factors are crucial in chronic heart failure (CHF) pathogenesis.
  • The precise role of the hypothalamic-pituitary-adrenal (HPA) axis and glucocorticoids in CHF remains unclear.
  • This study investigates HPA axis activity and morphology in CHF patients.

Purpose of the Study:

  • To assess plasma cortisol concentrations in CHF patients across different functional classes.
  • To examine the morphological changes in the HPA axis components in deceased CHF patients.
  • To correlate HPA axis neurohormone expression with CHF severity and adrenal structure.

Main Methods:

  • Plasma cortisol levels were measured in 74 CHF patients (NYHA classes I-IV) and 17 controls.
  • Immunohistochemistry and quantitative analysis were used to study hypothalamic neurohormones (CRH, vasopressin) and pituitary ACTH.
  • Histological examination of adrenal cortex was performed on tissue from 8 deceased CHF patients and 9 controls.

Main Results:

  • Plasma cortisol levels did not differ between CHF patients and controls, or with disease severity.
  • A two-fold increase in CRH-immunoreactive neurons and CRH/vasopressin co-expressing neurons was observed in the hypothalamus of CHF patients.
  • An increased density of ACTH-immunoreactive cells in the pituitary and significant thinning/dystrophic changes in the adrenal zona fasciculata were found in CHF patients.

Conclusions:

  • Despite normal plasma cortisol, CHF patients exhibit HPA axis upregulation at the hypothalamic and pituitary levels.
  • Adrenal cortex structural changes suggest relative glucocorticoid deficiency in CHF.
  • This relative deficiency may drive the observed neuroendocrine adaptations in the HPA axis in chronic heart failure.

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