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Adrenergic mechanisms in congestive heart failure
Acta Medica Scandinavica. Supplementum
|January 1, 1986
Summary
In heart failure, increased sympathetic nervous system activity does not rely on circulating noradrenaline. Elevated plasma noradrenaline levels in heart failure patients predict mortality, offering a better prognostic guide.
Area of Science:
- Cardiovascular Physiology
- Neuroendocrinology
- Heart Failure Pathophysiology
Background:
- Congestive heart failure disrupts normal cardiovascular control by the sympathetic nervous system.
- Increased sympathetic activity in heart failure may elevate plasma noradrenaline levels.
Purpose of the Study:
- To investigate the role of sympathetic nervous system activity and noradrenaline in heart failure.
- To explore the relationship between plasma noradrenaline, beta-adrenoceptor density, and prognosis in heart failure.
Main Methods:
- Analysis of sympathetic nervous system activity and plasma noradrenaline levels in heart failure patients.
- Assessment of beta-adrenoceptor density in the failing human heart.
- Correlation of plasma noradrenaline concentrations with ventricular function and mortality.
Main Results:
- Plasma noradrenaline levels in heart failure are generally insufficient to activate adrenergic systems directly.
- A decrease in myocardial beta-adrenoceptor density correlates with reduced ventricular function.
- Reduced beta-adrenoceptor density suggests high local noradrenaline exposure, leading to receptor downregulation despite depleted stores.
Conclusions:
- Cardiovascular effects of increased sympathetic activity in heart failure are not mediated by circulating noradrenaline.
- Decreased beta-adrenoceptor density indicates myocardial noradrenaline exposure and contributes to cardiac dysfunction.
- Plasma noradrenaline concentration is a strong predictor of mortality in heart failure, surpassing other cardiac performance indexes.