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. Objectives: 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.

Acute respiratory distress syndrome (ARDS) is a diffuse lung injury that leads to a severe acute respiratory failure. Traditional diagnostic criteria for pulmonary hypertension (PH), in this situation, may be unreliable due to the effects of positive pressure ventilation and vasoactive agents. The aim of this study is to describe the hemodynamic characteristics of PH secondary to ARDS, in relation with respiratory parameters. We assessed the hemodynamic, respiratory function, and ventilator parameters in a cohort of 38 individuals with ARDS-associated PH defined by mean pulmonary arterial pressure (mPAP) ≥ 25 mmHg. Individual characteristics: PaO2/FiO2 = 110 ± 60 mmHg, alveolar-arterial oxygen gradient (A-aO2) = 549 ± 148.9 mmHg, positive end-expiratory pressure (PEEP) = 8.7 ± 3.5 cmH2O, pulmonary static compliance (Cstat) = 30 ± 12.1 L*cmH2O-1, mPAP = 35.4 ±6.6 mmHg, pulmonary artery wedge pressure (PAWP) = 15.6 ± 5.5 mmHg, cardiac index (CI) = 3.4 ± 1.2 L/min/m2, pulmonary vascular resistance (PVR) = 3.3 ± 1.6 Wood units (WU), right atrial pressure (RAP) = 13.4 ± 5.4 mmHg, diastolic pulmonary gradient (DPG) = 12.6 ± 6.5 mmHg, and trans-pulmonary gradient (TPG) = 19.7 ± 7.7 mmHg. The composite marker—DPG >7 mmHg and PVR > 3 WU—is associated with lower CI (P = 0.016), higher mPAP (P = 0.003), and lower pulmonary static compliance (P = 0.028). We confirmed a poor prognosis of ARDS associated with PH, with a 50% survival rate after 17 days. We observed that the survival rate at 28 days was better in the case of improvement in the PaO2/FiO2 ratio in the first 24 h (log rank P = 0.003). ARDS associated with PH is a severe condition with a very poor survival rate. The composite marker DPG > 7 mmHg and PVR > 3 WU seemed to better describe the hemodynamic and respiratory dysfunction. The improvement in PaO2/FiO2 ratio in the first 24 h defined a better survival in our cohort of patients.

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Once initiated for pulmonary arterial hypertension (PAH), epoprostenol treatment usually needs to be delivered for an indefinite duration. It is possible that some participants could be transitioned from epoprostenol to oral therapies. We retrospectively evaluated eight PAH participants transitioned from epoprostenol to PAH oral drugs. The criteria for epoprostenol withdrawal were: (1) persistent improvement of clinic and hemodynamic status; (2) stable dose of epoprostenol for the last three months; and (3) the participant's preference for oral therapy after evaluation of risk-benefit. We evaluated the clinical, functional, and hemodynamic status at baseline, at withdrawal, and after the transition to oral PAH therapy. The transition was completed in all eight participants. Four participants had a complete successful transition (CT) with a stable clinical and hemodynamic course and four participants had a partial successful transition (PT) remaining stable clinically, with a mild hemodynamic worsening, but without need to re-initiate epoprostenol therapy. The four CT participants were treated with epoprostenol for a shorter period of time (CT group: 35 AE 30 versus PT group: 79 AE 49 months, P ¼ 0.08). Mean epoprostenol dosage was lower in the CT group (CT group: 15 AE 1.5 ng/kg/min versus PT group: 24 AE 11 ng/kg/min, P ¼ 0.09). Safe withdrawal of epoprostenol treatment and transition to oral PAH therapy was possible in a small and highly selected group of participants. The majority of these participants had a portopulmonary PAH or PAH associated to HIV infection.

Once initiated for pulmonary arterial hypertension (PAH), epoprostenol treatment usually needs to be delivered for an indefinite duration. It is possible that some participants could be transitioned from epoprostenol to oral therapies. We retrospectively evaluated eight PAH participants transitioned from epoprostenol to PAH oral drugs. The criteria for epoprostenol withdrawal were: (1) persistent improvement of clinic and hemodynamic status; (2) stable dose of epoprostenol for the last three months; and (3) the participant’s preference for oral therapy after evaluation of risk-benefit. We evaluated the clinical, functional, and hemodynamic status at baseline, at withdrawal, and after the transition to oral PAH therapy. The transition was completed in all eight participants. Four participants had a complete successful transition (CT) with a stable clinical and hemodynamic course and four participants had a partial successful transition (PT) remaining stable clinically, with a mild hemodynamic worsening, but without need to re-initiate epoprostenol therapy. The four CT participants were treated with epoprostenol for a shorter period of time (CT group: 35 ± 30 versus PT group: 79 ± 49 months, P = 0.08). Mean epoprostenol dosage was lower in the CT group (CT group: 15 ± 1.5 ng/kg/min versus PT group: 24 ± 11 ng/kg/min, P = 0.09). Safe withdrawal of epoprostenol treatment and transition to oral PAH therapy was possible in a small and highly selected group of participants. The majority of these participants had a porto-pulmonary PAH or PAH associated to HIV infection.

Background Obstructive sleep apnea (OSA) is a potential cardiovascular risk factor. However, there is currently no prominent screening strategy for its diagnosis in patients with acute coronary syndrome (ACS). The aim of this study was to establish the impact of apneic events in case of OSA associated with ACS. Methods Between January 1st and June 30th, fifty-three subjects with ACS (first acute myocardial infarction) were prospectively evaluated for OSA. Each patient was evaluated by polysomnography (PSG) two months after the ACS. Results Mean age of 59±9,6 years, 81,1% males, BMI at 28,5±4,2 kg/m2, neck circumference of 42,5±12,6 cm, and waist circumference os 102,5±16,5 cm. The majority of patients (73,6%) had moderate to severe OSA (apnea-hypopnea index (AHI) ≥ 15/h and arousal index ≥ 10/h). We defined the apneic coefficient (AC) as the ratio between apnea index (AI) and AHI. We chose as cut-off the median value of apnea coefficient in our population which was at 37%. The patients with a higher AC (AC ≥ 37% versus AC < 37%) had higher levels of Troponin-I (63,4±63,2 versus 29,7±36,1 ng/mL, p=0,016), higher levels of NT-proBNP (1879,8±2141,8 versus 480±621,3 pg/mL, p=0,001), higher SYNTAX score (15,8±11,5 versus 10,2±5,9, p=0,049), and lower left ventricle ejection fraction (LVEF 53,3±11,4 versus 59,4±6,4%, p=0,023) and were more likely to have a STEMI (21 patients (77,7%) vesus 14 patients (53,8%), p=0,031). Conclusion An apneic coefficient (AI/AHI) ≥ 37% is correlated with more severe cardiac impairment, as well as higher hypoxemia and arousal index.

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