A better selection of patients referred for cardiac transplantation should lead to better surgical results. The presence of severe and irreversible pulmonary hypertension is an important factor and its pretransplantation assessment requires pharmacodynamic testing with vasodilators and dobutamine. The aim of this study of 10 patients in congestive cardiac failure referred for cardiac transplantation was to evaluate enoximone in this indication by comparing it with sodium nitroprussiate (3 micrograms/kg/mn). Intravenous enoximone (total dose of 1.5 mg/kg) increased the cardiac index (+49%; p less than 0.01), slightly reduced the mean systemic blood pressure (-8%; p less than 0.05) whilst inducing a greater reduction in systemic arterial resistances (-36%; p less than 0.01); the fall in mean blood pressure was less than with sodium nitroprussiate (-23%; p less than 0.01). Myocardial oxygen consumption (rate-pressure product) did not increase in contrast to the effect of dobutamine (+21%; p less than 0.01). There was a significant reduction in pulmonary arteriolar resistances (p less than 0.01) with all three drugs but the interpretation of this response and its prognostic significance in patients with a low cardiac output and persistent pulmonary hypertension are discutable even when pulmonary arteriolar resistances are less than 6 Wood units. The value of using an inotropic agent such as Dobutamine or Enoximone is to unmask fixed pulmonary hypertension which may be missed in patients with low cardiac output even with vasodilator drugs, and also to mimic the haemodynamic result of transplantation. In this indication Enoximone may be used like Dobutamine but with the advantage of not increasing myocardial oxygen consumption and being probably less arrhythmogenic.
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J Clin Invest
January 2025
Department of Medicine, University of California San Francisco, San Francisco, United States of America.
Hypoxia is a major cause of pulmonary hypertension (PH) worldwide, and it is likely that interstitial pulmonary macrophages contribute to this vascular pathology. We observed in hypoxia-exposed mice an increase in resident interstitial macrophages, which expanded through proliferation and expressed the monocyte recruitment ligand CCL2. We also observed an increase in CCR2+ macrophages through recruitment, which express the protein thrombospondin-1 that functionally activates TGF-beta to cause vascular disease.
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