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Effects of digoxin on chemoreflex in patients with chronic heart failure
F Paganelli1, J M Maixent, R Gélisse
1Service de Cardiologie, H pital Nord Marseille, CHU Nord, Chemin des Bourrelly, Marseille, France. Fpaganelli@mail.ap-hm.fr
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Digoxin therapy in chronic heart failure patients improved hemodynamic function and blood gas levels. This treatment appeared to inactivate the chemoreflex, suggesting a potential new therapeutic avenue for heart failure management.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Digitalis effects on baroreflexes in heart failure are known.
- Chemoregulation remains functional in cardiac failure.
- The impact of digoxin on chemoreflexes requires investigation.
Purpose of the Study:
- To evaluate chronic digoxin administration effects on chemoreflexes in chronic heart failure.
- To assess changes in hemodynamic and blood gas parameters.
- To determine if digoxin alters chemoreflex activation.
Main Methods:
- Assessed hemodynamic and blood gas parameters in 7 chronic congestive heart failure patients.
- Administered digoxin (0.25 mg daily) for 10 days.
- Measured parameters at baseline and after 30 min of pure O2 inhalation to inhibit chemoreflexes.
Main Results:
- Digoxin therapy increased cardiac output, stroke volume, and PaO2.
- Digoxin therapy decreased heart rate, systemic resistance, and pulmonary wedge pressure.
- Post-digoxin, O2 inhalation did not alter heart rate or hemodynamics, indicating chemoreflex inactivation.
Conclusions:
- Chronic digoxin therapy appears to inactivate the chemoreflex in heart failure patients.
- This inactivation may stem from digoxin's sympatho-inhibitory and positive inotropic effects.
- Improved hemodynamics and blood gases likely contribute to reflex inactivation.
Abstract:
The effects of digitalis on the baroreflexes in human chronic heart failure have been well studied. Similarly, since it has been recently shown that chemoregulation remains generally effective during cardiac failure, the goal of this study was to evaluate the effects of a chronic administration of digoxin on the chemoreflexes. Hemodynamic and blood gas parameters were assessed in 7 patients with chronic congestive heart failure before and after chronic administration for 10 days of digoxin therapy (0.25 mg daily). In both situations measurements were performed 1/ in baseline conditions at room air and, 2/ after inhalation of pure O2 for 30 min, in order to inhibit the activation of the chemoreflexes. At room air, acute O2 inhalation resulted in a significant decrease in heart rate and cardiac output. After digoxin therapy, comparatively to pre-treatment values, cardiac output, stroke volume and PaO2 were significantly higher while heart rate, systemic resistance and pulmonary wedge pressure were lower. Furthermore, acute O2 inhalation did not modify heart rate or any hemodynamic variables. These results suggest that after digoxin therapy chemoreflex was no more activated in these patients. This effect may be related to the sympatho-inhibitory and to the positive inotropic effects of digoxin: improving hemodynamic and blood gas parameters may result in the inactivation of the reflex.