title: Impaired vasoreactivity in end-stage heart failure patients on intravenous inotropic support.
abstract: BACKGROUND
  Vasoreactivity is known to be impaired in heart failure patients; however, it has not been determined whether standard medical therapy for end-stage heart failure patients (ES-HF) ameliorates this impairment. Therefore, we sought to investigate flow-mediated dilation (FMD) responses in ES-HF with normal or near normal cardiac indices from continuous inotropic support.
  
  
  RESULTS
  Vascular ultrasound was used to assess FMD responses to isometric exercise and cuff occlusion in 15 ES-HF patients and 5 control subjects (C). ES-HF patients had significant hyperemic response to maximal exercise (P < .05), which was blunted relative to C (ES-HF; 84 +/- 21 mL/min versus C; 299 +/- 85 mL/min, P < .05). ES-HF patients did not show a significant hyperemic response to submaximal exercise. C had a significant increase in arterial diameter that exceeded ES-HF after both maximal (C; 8 +/- 1% versus. ES-HF; -0.9 +/- 0.86%, P < .05) and submaximal exercise (C; 6 +/- 1% versus ES-HF; 0.57 +/- 1%, P < .05). FMD responses at similar absolute workloads showed that both the mean hyperemic response and the change in arterial diameter were significantly greater in C. After cuff occlusion, the mean hyperemic response for ES-HF was again significantly blunted compared with C (ES-HF; 117 +/- 26% versus C; 352 +/- 86%, P < .05). After cuff occlusion, arterial diameter in C significantly increased in response to hyperemia, whereas ES-HF patients had a paradoxical vasoconstrictive response (C; 10.7 +/- 1.1% versus ES-HF; -5.3 +/- 1.5%, P < .05).
  
  
  CONCLUSIONS
  Peripheral vasoreactivity in response to either maximal exercise, submaximal exercise, or hyperemic stimuli is impaired in ES-HF patients with normal resting cardiac outputs.
authors.affiliation: Cardiovascular Research Center, Temple University, Philadelphia, Pennsylvania, USA.
authors.forename: Abigail S
authors.initials: AS
authors.lastname: Dean
authors.forename: Kenneth B
authors.initials: KB
authors.lastname: Margulies
authors.forename: John J
authors.initials: JJ
authors.lastname: Nicholas
authors.forename: Sharon
authors.initials: S
authors.lastname: Rubin
authors.forename: John P
authors.initials: JP
authors.lastname: Gaughan
authors.forename: Joseph R
authors.initials: JR
authors.lastname: Libonati
mesh_terms: D001783:Blood Flow Velocity / Q000187:drug effects; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology*; D006328:Cardiac Catheterization; D002316:Cardiotonic Agents / Q000008:administration & dosage* / Q000627:therapeutic use; D004280:Dobutamine / Q000008:administration & dosage / Q000627:therapeutic use; D004452:Echocardiography; D005080:Exercise Test; D005500:Follow-Up Studies; D005542:Forearm / Q000098:blood supply / Q000502:physiology; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D007275:Injections, Intravenous; D007537:Isometric Contraction / Q000502:physiology; D008297:Male; D008875:Middle Aged; D020105:Milrinone / Q000008:administration & dosage / Q000627:therapeutic use; D012720:Severity of Illness Index; D016896:Treatment Outcome; D018608:Ultrasonography, Doppler; D014661:Vasoconstriction / Q000187:drug effects*; D016278:Ventricular Function, Right / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D004280:Dobutamine; D020105:Milrinone