Acute vasodilator testing in primary and secondary pulmonary hypertension

Citation
P. Schenk et al., Acute vasodilator testing in primary and secondary pulmonary hypertension, WIEN KLIN W, 113(13-14), 2001, pp. 496-503
Citations number
27
Categorie Soggetti
General & Internal Medicine
Journal title
WIENER KLINISCHE WOCHENSCHRIFT
ISSN journal
00435325 → ACNP
Volume
113
Issue
13-14
Year of publication
2001
Pages
496 - 503
Database
ISI
SICI code
0043-5325(20010716)113:13-14<496:AVTIPA>2.0.ZU;2-U
Abstract
Background: Pulmonary vasoconstriction is an important pathophysiological f eature of pulmonary hypertension. Acute vasodilator testing is essential fo r making therapeutic decisions and provides an outlook on prognosis. Aims: To evaluate retrospectively the haemodynamics, gas exchange response, practical feasibility and safety of acute vasodilator trials with nifedipi ne, diltiazem, prostacyclin, and nitric oxide in patients with pulmonary hy pertension. Methods: From 1993 to January 2001, 37 patients with precapillary pulmonary hypertension (23 with primary and 14 with secondary pulmonary hypertension ) were tested after insertion of a pulmonary artery and arterial catheter. Peroral nifedipine (10 mg) or diltiazem (60 mg) was given on an hourly basi s, intravenous prostacyclin was increased in steps of 2 ng/kg.min, and nitr ic oxide (20 ppm) was inhaled for 15 minutes. A positive vasodilator respon se was defined as a > 20% reduction in mean pulmonary artery pressure (PAPm ) and pulmonary vascular resistance (PVR). Results: Of 6 patients who received nifedipine or diltiazem, 2 were respond ers (mean change of PAPm: -24% and PVR: -42%), 3 were unfavorable responder s (with serious side effects) and 1 had mild side effects. Of 4 patients re ceiving prostacyclin, 1 was a responder (change of PAPm: -31% and PVR: -48% ), 1 a resistance responder (fall of PVR > 20% without a significant reduct ion in PAPm), 1 a non-responder with mild side effects, and 1 an unfavorabl e responder with serious side effects. Of 27 patients tested with inhaled n itric oxide, 7 (26%) were responders (mean change of PAPm:-35% and PVR: -46 %), 3 were resistance responders and 17 were nonresponders; no side effects occurred. Arterial oxygen saturation increased during nitric oxide inhalat ion (from 93 +/- 3% to 95 +/- 3%, p < 0.01), whereas it worsened under calc ium channel blockers (from 94.5 +/- 4% to 90 +/- 5%, p < 0.05) and prostacy clin (from 95 +/- 2% to 90 +/- 2%, p < 0.05). Three patients developed cath eter-associated complications (pneumothorax, n = 2, temporary Horner's tria s, n = 1) Conclusion: Inhaled nitric oxide is a safe tool for acute vasodilator testi ng in pulmonary hypertension and should be given preference over nifedipine , diltiazem, and prostacyclin.