title: High-dose enoximone to evaluate reversibility of pulmonary hypertension: is there a diagnostic value of neurohormonal measurements?
abstract: BACKGROUND
  Heart transplantation is associated with a reduction of the neurohumoral activation seen in patients with severe congestive heart failure. In this study, we investigated whether pharmacologically induced complex hemodynamic improvement during assessment of reversibility of pulmonary hypertension with a phosphodiesterase inhibitor is able to induce neurohormonal changes of diagnostic importance.
  
  
  RESULTS
  Twenty-one patients with New York Heart Association class III-IV heart failure underwent infusion of 3 mg/kg enoximone over a period of 30 minutes. Before and after drug infusion, we determined the plasma concentrations of atrial natriuretic peptide, endothelin-I, angiotensin-II, aldosterone, norepinephrine, epinephrine, and angiotensin-converting enzyme activity sampled from a peripheral vein and the pulmonary artery. In addition to the expected significant reduction of pulmonary hypertension and enhancement of cardiac output, increased levels of the vasoconstrictors endothelin-I, angiotensin-II, and norepinephrine were observed. Aldosterone fell after enoximone infusion; a higher baseline aldosterone level correlated to the degree of reduction of the pulmonary arteriolar resistance by enoximone. Baseline atrial natriuretic peptide levels correlated with parameters, indicating the severity of heart failure. However, the plasma concentration of this peptide did not change significantly after enoximone infusion.
  
  
  CONCLUSIONS
  Acute hemodynamic improvement after enoximone bolus in candidates for heart transplantation is not accompanied by a reduction of the enhanced neurohumoral activity in these patients. The reaction of the investigated hormones cannot predict the individual degree of reversibility of pulmonary hypertension.
authors.affiliation: Department of Cardiology and Cardiosurgery, Kerckhoff-Clinic, Max Planck Society, Germany.
authors.forename: O
authors.initials: O
authors.lastname: Schulz
authors.forename: V
authors.initials: V
authors.lastname: Mitrovic
authors.forename: M
authors.initials: M
authors.lastname: Schönburg
authors.forename: J
authors.initials: J
authors.lastname: Thormann
mesh_terms: D000804:Angiotensin II / Q000097:blood; D009320:Atrial Natriuretic Factor / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D006328:Cardiac Catheterization; D002395:Catecholamines / Q000097:blood; D019332:Endothelin-1 / Q000097:blood; D017335:Enoximone / Q000008:administration & dosage*; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000150:complications / Q000188:drug therapy; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood* / Q000188:drug therapy / Q000209:etiology; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D010726:Phosphodiesterase Inhibitors / Q000008:administration & dosage*; D011379:Prognosis; D011651:Pulmonary Artery; D011667:Pulmonary Veins; D012720:Severity of Illness Index
chemical_list: D015415:Biomarkers; D002395:Catecholamines; D019332:Endothelin-1; D010726:Phosphodiesterase Inhibitors; D000804:Angiotensin II; D009320:Atrial Natriuretic Factor; D017335:Enoximone; D007703:Peptidyl-Dipeptidase A