Induction of a reduction in haemoglobin concentration by enalapril in stable, moderate heart failure: a double blind study
- PMID: 1931347
- PMCID: PMC1024644
- DOI: 10.1136/hrt.66.3.199
Induction of a reduction in haemoglobin concentration by enalapril in stable, moderate heart failure: a double blind study
Abstract
Objective: To study the long term effects (12 weeks) of enalapril on central haemodynamic function and on arterial oxygen content and its determinants--haemoglobin concentration and oxygen saturation--in patients with stable moderate heart failure.
Design: Double blind placebo controlled randomised study.
Patients: 17 patients with stable moderate heart failure caused by dilated cardiomyopathy which was treated with diuretics and digoxin.
Methods: Central haemodynamic function, arterial oxygen content, arterial haemoglobin concentration, and arterial oxygen saturation were measured at rest and during submaximal exercise. Plasma volume and total body haemoglobin were determined at rest.
Results: With enalapril treatment heart rate, pulmonary capillary wedge pressure, mean arterial pressure, and systemic vascular resistance decreased significantly both at rest and during submaximal exercise. Cardiac output did not change at rest but tended to increase (p = 0.06) during submaximal exercise. Arterial oxygen saturation remained unchanged while haemoglobin concentration and arterial oxygen content were significantly reduced. Total body haemoglobin was significantly reduced but the plasma volume remained unchanged. At rest, the reduction in arterial oxygen content resulted in a significantly reduced mixed venous oxygen content. However, during submaximal exercise the increase in cardiac output fully compensated for the reduction in arterial oxygen content and this effect was indicated by the unaltered mixed venous oxygen content. No changes were found in the placebo group after twelve weeks.
Conclusions: Enalapril unloads the heart and reduces haemoglobin concentration. During submaximal exercise, the improvement in systemic blood flow was counterbalanced by this negative effect on the oxygen carrying capacity and systemic oxygen delivery was unchanged.
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