Pulmonary Arterial Hypertension-Specific Drug Therapy in COPD Patients with Severe Pulmonary Hypertension and Mild-to-Moderate Airflow Limitation.
BACKGROUND
Patients with severe pulmonary hypertension (PH) associated with chronic obstructive pulmonary disease (COPD) present a poor outcome. Specific PH treatment could improve the clinical and hemodynamic status of these patients but may worsen arterial blood gases.


OBJECTIVE
Our study retrospectively included 28 patients with severe precapillary PH (mean pulmonary arterial pressure >35 mm Hg) associated with mild-to-moderate COPD [forced expiratory volume in 1 s (FEV1) >50% predicted]. All patients underwent specific pulmonary arterial hypertension (PAH) treatment as mono-, bi- or triple therapy.


METHODS
Our single-center study was conducted based on retrospective data of 537 right heart catheterizations (RHCs) performed on patients with COPD from January 2004 to June 2014. An echocardiography, comprehensive blood tests, pulmonary function tests, and a high-resolution computed tomography were performed before the RHCs. All patients underwent RHC with a Swan-Ganz catheter.


RESULTS
Compared to baseline, patients treated with specific PAH drugs showed a significant increase in cardiac index at long term (2.5 ± 0.7 liters/min/m2 at baseline vs. 3.2 ± 0.6 liters/min/m2 at 6/12 months; p = 0.003) as well as a decrease in pulmonary vascular resistance in the long term (8.4 ± 4.2 Wood units at baseline vs. 5 ± 1.7 Wood units at 6/12 months; p = 0.008). There was a slight decrease in arterial oxygen tension (PaO2) after 3 months of treatment (-2.4 ± 7.21 mm Hg; p = 0.066). During a median follow-up of 3 years, 12 patients (42.8%) died (including all causes of death).


CONCLUSIONS
This preliminary report suggests that the use of specific PH therapy in severe PH associated with mild-to-moderate COPD can improve pulmonary hemodynamic parameters, with worsening of PaO2, which had no clinical significance and did not lead to specific PAH therapy withdrawal in any patient.
Service de Pneumologie, Nouvel Hx00F4;pital Civil, Universitx00E9; de Strasbourg, Strasbourg, France.
George
G
Calcaianu
Matthieu
M
Canuet
Armelle
A
Schuller
Irina
I
Enache
Ari
A
Chaouat
Romain
R
Kessler
D000368:Aged; D000369:Aged, 80 and over; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001784:Blood Gas Analysis; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D002245:Carbon Dioxide / Q000097:blood; D065128:Endothelin Receptor Antagonists / Q000627:therapeutic use*; D011464:Epoprostenol / Q000627:therapeutic use; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D016285:Iloprost / Q000627:therapeutic use; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D010313:Partial Pressure; D058986:Phosphodiesterase 5 Inhibitors / Q000627:therapeutic use*; D016016:Proportional Hazards Models; D011653:Pulmonary Diffusing Capacity; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D012189:Retrospective Studies; D012720:Severity of Illness Index; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000627:therapeutic use*; D014797:Vital Capacity
D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D065128:Endothelin Receptor Antagonists; D058986:Phosphodiesterase 5 Inhibitors; D014665:Vasodilator Agents; D002245:Carbon Dioxide; D011464:Epoprostenol; D016285:Iloprost