title: Echocardiographic predictors of an adverse response to a nifedipine trial in primary pulmonary hypertension: diminished left ventricular size and leftward ventricular septal bowing.
abstract: BACKGROUND
  The clinical course in primary pulmonary hypertension (PPH) is improved by calcium channel blocker therapy in those with a favorable hemodynamic response during a trial of high-dose oral nifedipine. Although trials of nifedipine are performed only in patients who demonstrate pulmonary vasodilator reserve to short-acting agents, this response does not predict the safety of nifedipine treatment, which can result in severe first-dose hypotension and death.
  
  
  OBJECTIVE
  To identify echocardiographic parameters that predict first-dose nifedipine-induced hypotension in patients with PPH.
  
  
  METHODS
  The pretrial echocardiograms of 23 consecutive PPH patients (mean age, 42.3 +/- 13 years; 77% female) undergoing evaluation of pulmonary vasodilator reserve with nifedipine were analyzed. Patients were classified as those who suffered first-dose nifedipine hypotension (group 1) and those who did not (group 2). Echocardiographic measures of chamber size and septal geometry in the two groups were compared.
  
  
  RESULTS
  Five measures reflecting diminished left ventricular (LV) size and leftward ventricular septal bowing were found to be associated with nifedipine hypotension: LV transverse diameter in systole (LVDs; p = 0.007), LV transverse diameter in diastole (LVDd; p = 0.05), LV area in systole (LVAs; p = 0.009), LV area in diastole (LVAd; p = 0.03), the ratio of RV to LVAs (p = 0. 02), and leftward ventricular septal bowing (p = 0.01). The LV dimensions found to best predict nifedipine-induced hypotension were LVDs < 2.7 cm, LVDd < 4.0 cm, LVAs < 15.5 cm(2), and LVAd < 20.0 cm(2).
  
  
  CONCLUSIONS
  Readily available echocardiographic parameters in patients with PPH are predictive of nifedipine-induced hypotension, and can be used to select patients in whom a trial of nifedipine should be avoided.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: Ricciardi
authors.forename: E
authors.initials: E
authors.lastname: Bossone
authors.forename: D S
authors.initials: DS
authors.lastname: Bach
authors.forename: W F
authors.initials: WF
authors.lastname: Armstrong
authors.forename: M
authors.initials: M
authors.lastname: Rubenfire
mesh_terms: D000284:Administration, Oral; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000008:administration & dosage / Q000009:adverse effects*; D004452:Echocardiography; D005260:Female; D006346:Heart Septum / Q000000981:diagnostic imaging* / Q000187:drug effects; D006352:Heart Ventricles / Q000000981:diagnostic imaging* / Q000187:drug effects; D006801:Humans; D006976:Hypertension, Pulmonary / Q000000981:diagnostic imaging / Q000188:drug therapy*; D007022:Hypotension / Q000139:chemically induced* / Q000000981:diagnostic imaging; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009543:Nifedipine / Q000008:administration & dosage / Q000009:adverse effects*; D011237:Predictive Value of Tests; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects; D014694:Ventricular Outflow Obstruction / Q000139:chemically induced / Q000000981:diagnostic imaging
chemical_list: D002121:Calcium Channel Blockers; D009543:Nifedipine