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Neurohumoral profile in congestive heart failure: response to beta-blockade
1Division of Cardiology, Ohio State University, Columbus 43210.
Insights
Beta-blockade in heart failure impacts neurohormones. Increased catecholamines post-dosing may signal compensatory responses, helping identify patients at risk for adverse hemodynamic effects.
Area of Science:
- Cardiology
- Pharmacology
- Neuroendocrinology
Background:
- Congestive heart failure (CHF) exhibits abnormal neurohumoral profiles.
- Beta-blockade may offer hemodynamic benefits in CHF by modulating these profiles.
Purpose of the Study:
- To investigate the relationship between neurohumoral profiles and hemodynamic responses to beta-blockade in CHF patients.
- To identify predictors of adverse hemodynamic effects from beta-blocker therapy.
Main Methods:
- Measured neurohumoral and hemodynamic variables in 10 subjects with congestive cardiomyopathy.
- Administered the beta-blocker pindolol and re-assessed variables.
- Analyzed correlations between baseline and post-dosing neurohumoral and hemodynamic parameters.
Main Results:
- Baseline stroke index inversely correlated with plasma norepinephrine and renin.
- Pulmonary vascular resistance directly correlated with plasma norepinephrine.
- Post-dosing catecholamine increases, particularly norepinephrine, coincided with decreased stroke volume index.
Conclusions:
- Elevated catecholamines after beta-blocker dosing may indicate a compensatory response to adverse hemodynamic effects.
- Neurohumoral profiles and their relation to hemodynamic parameters can help identify CHF patients at risk for negative beta-blockade responses.
Abstract:
Beta-blockade has been reported to have beneficial hemodynamic effects in chronic congestive heart failure that may be related to alterations in the abnormal neurohumoral profile characteristic of this population. To determine the relationship of the neurohumoral profile to the hemodynamic response to beta-blockade in patients with chronic congestive heart failure, neurohumoral and hemodynamic variables were measured in 10 subjects having congestive cardiomyopathy at baseline and after administration of the beta-blocker pindolol. Baseline stroke index was noted to have an inverse curvilinear relation with plasma norepinephrine (r = -0.69) and renin (r = -0.71) concentration. Pulmonary vascular resistance demonstrated a direct logarithmic relation with plasma norepinephrine concentration (r = 0.68). Increases in norepinephrine, dopamine, and epinephrine concentrations after dosing were noted, with the most marked increase in norepinephrine concentration being coincident with a significant decline in stroke volume index. Two patients not tolerating beta-blockade were characterized by having baseline norepinephrine concentrations 3 SD higher than those of the remaining patients, more marked increases in epinephrine concentration after dosing, and the most profoundly decompensated heart failure at baseline, as defined by the relationship between neurohumoral and hemodynamic variables. These observations suggest that increases in catecholamines after dosing reflect a compensatory response to the adverse hemodynamic-inotropic effects of beta-blockade in congestive heart failure. The neurohumoral profile and the relationship of neuroendocrine to hemodynamic parameters may be useful in delineating patients at risk for adverse hemodynamic effects of beta-blockade.