G M Domenighetti1, V G Saglini. 1. Dipartimento di Medicina Interna dell' Ospedale Distrettuale La Carità di Locarno, Switzerland.
Abstract
STUDY OBJECTIVE: The present study was undertaken to evaluate at rest the short- and long-term effects of oral nifedipine (N) in patients with pulmonary hypertension (PH). DESIGN AND SETTING: A prospective study with ten consecutive cases during two years in a setting of a district acute hospital. PATIENTS OR PARTICIPANTS: Seven patients with advanced COPD and three with severe lung fibrosis (LF) during a period of stable condition. Three patients with COPD were eligible for the long-term investigation. INTERVENTIONS: Right heart catheterization with a 7F Swan-Ganz triple-lumen thermodilution catheter and radial cannulation with a 3F arterial catheter. MEASUREMENTS AND RESULTS: Measurement of CO, MAP, RAP, PAP, PWP, HR, and ABG and calculation of CI, TSR, PAR, and DO2 before and after 20 mg of N sublingually at rest. For the group as a whole, N induced a reduction in MAP and TSR, with a significant increase in CI and DO2. There were no significant changes in PAP, PAR (magnitude of the reduction: -10 percent), HR, and PaO2. The individual analysis of the driving pressures (PAP-PWP) in function of the cardiac output demonstrated that a real vasodilating effect in the pulmonary circulation occurred in only three COPD patients (magnitude of the PAR reduction: -43 percent), while in the three patients with LF, N induced a deleterious increase in PAP and PAR. After long-term treatment (10 mg of N daily every 4 h; average 12 months) in the former, despite a persistent beneficial hemodynamic effect (magnitude of the PAR reduction: -36 percent), there was the usually expected clinical worsening. CONCLUSIONS: N in small doses may be able in some patients with severe COPD to induce a beneficial short- and long-term hemodynamic effect on the pulmonary circulation when PH is present. On the other hand, N should not be used in patients with PH and advanced LF.
STUDY OBJECTIVE: The present study was undertaken to evaluate at rest the short- and long-term effects of oral nifedipine (N) in patients with pulmonary hypertension (PH). DESIGN AND SETTING: A prospective study with ten consecutive cases during two years in a setting of a district acute hospital. PATIENTS OR PARTICIPANTS: Seven patients with advanced COPD and three with severe lung fibrosis (LF) during a period of stable condition. Three patients with COPD were eligible for the long-term investigation. INTERVENTIONS: Right heart catheterization with a 7F Swan-Ganz triple-lumen thermodilution catheter and radial cannulation with a 3F arterial catheter. MEASUREMENTS AND RESULTS: Measurement of CO, MAP, RAP, PAP, PWP, HR, and ABG and calculation of CI, TSR, PAR, and DO2 before and after 20 mg of N sublingually at rest. For the group as a whole, N induced a reduction in MAP and TSR, with a significant increase in CI and DO2. There were no significant changes in PAP, PAR (magnitude of the reduction: -10 percent), HR, and PaO2. The individual analysis of the driving pressures (PAP-PWP) in function of the cardiac output demonstrated that a real vasodilating effect in the pulmonary circulation occurred in only three COPDpatients (magnitude of the PAR reduction: -43 percent), while in the three patients with LF, N induced a deleterious increase in PAP and PAR. After long-term treatment (10 mg of N daily every 4 h; average 12 months) in the former, despite a persistent beneficial hemodynamic effect (magnitude of the PAR reduction: -36 percent), there was the usually expected clinical worsening. CONCLUSIONS: N in small doses may be able in some patients with severe COPD to induce a beneficial short- and long-term hemodynamic effect on the pulmonary circulation when PH is present. On the other hand, N should not be used in patients with PH and advanced LF.