Pulmonary arterial wall disease in COPD and interstitial lung diseases candidates for lung transplantation.

BACKGROUND: Pulmonary hypertension (PH) associated with lung disease has the worst prognosis of all types of PH. Pulmonary arterial vasculopathy is an early event in the natural history of chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD). The present study characterized the alterations in the structure and function of the pulmonary arterial (PA) wall of COPD and ILD candidates for lung transplantation (LTx). METHODS: A cohort of 73 patients, 63 pre-LTx (30 COPD, 33 ILD), and ten controls underwent simultaneous right heart catheterisation and intravascular ultrasound (IVUS). Total pulmonary resistance (TPR), capacitance (Cp), and the TPR-Cp relationship were assessed. PA stiffness and the relative area of wall thickness were estimated as pulse PA pressure/IVUS pulsatility and as [(external sectional area-intimal area)/external sectional area] × 100, respectively. RESULTS: Twenty-seven percent of patients had pulmonary arterial wedge pressure > 15 mmHg and were not analyzed. PA stiffness and the area of wall thickness were increased in comparison with controls, even in patients without PH (p < 0.05). ILD patients showed a significant higher PA stiffness, and lower Cp beyond mean PA pressure (mPAP) and lower area of wall thickness than COPD patients (p < 0.05). TPR-Cp relationship was shifted downward left for ILD patients. CONCLUSIONS: Significant increase of PA stiffness and area of wall thickness were present even in patients without PH and can make the diagnosis of pulmonary vasculopathy at a preclinical stage in PH-lung disease candidates for LTx. ILD patients showed the worst PA stiffness and Cp with respect to COPD.

Impairment of pulmonary vascular reserve and right ventricular systolic reserve in pulmonary arterial hypertension.

BACKGROUND: Exercise capacity is impaired in pulmonary arterial hypertension (PAH). We hypothesized that cardiovascular reserve abnormalities would be associated with impaired hemodynamic response to pharmacological stress and worse outcome in PAH. METHODS: Eighteen PAH patients (p) group 1 NYHA class II/III and ten controls underwent simultaneous right cardiac catheterization and intravascular ultrasound at rest and during low dose-dobutamine (10 mcg/kg/min) with trendelenburg (DST). We estimated cardiac output (CO), pulmonary vascular resistance (PVR) and capacitance (PC), and PA elastic modulus (EM). We concomitantly measured tricuspid annular plane systolic excursion (TAPSE), RV myocardial peak systolic velocity (Sm) and isovolumic myocardial acceleration (IVA) in PAH patients. Based on the rounded mean + 2 SD of the increase in mPAP in our healthy control group during DST (2.8 + 1.8 mm Hg), PAH p were divided into two groups according to mean PA pressure (mPAP) response during DST, 1: ΔmPAP > 5 mm Hg and 2: ΔmPAP ≤ 5 mm Hg. Cardiovascular reserve was estimated as the change (delta, Δ) during DST compared with rest, including ΔmPAP with respect to ΔCO (ΔmPAP/ΔCO). All patients were prospectively followed up for 2 years. RESULTS: PAH p showed significant lower heart rate and CO increase than controls during DST, with a significant mPAP and pulse PAP increase and higher ΔmPAP/ΔCO (p < 0.05). Neither hemodynamic, IVUS and echocardiographic data were different between both PAH groups at rest. In group 1, DST caused a higher ΔEM, ΔmPAP/ΔCO, ΔPVR, and ΔTAPSE than group 2, with a lower IVA increase and a negative ΔSV (p < 0.05). TAPSE correlated with mPAP and RVP (p < 0.05) and, IVA and Sm correlated with CO (p < 0.05). ΔEM correlated with ΔmPAP and ΔIVA with ΔCO (p < 0.05). There were two deaths/pulmonary transplantations in group 1 and one death in group 2 during the follow-up (p > 0.05). CONCLUSIONS: Pulmonary vascular reserve and RV systolic reserve are significantly impaired in patients with PAH. The lower recruitable cardiovascular reserve is significantly related to a worse hemodynamic response to DST and it could be associated with a poor clinical outcome.

Pulmonary vascular pressure respiratory swings in COPD and ILD candidates for lung transplantation: Large but different.

We analyzed the effect of respiratory swings on interpreting intravascular pulmonary vascular pressures (PVPs) in chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) candidates for lung transplantation (LTx) and the role of the alterations in pulmonary function tests on the dynamic respiratory variations. Twenty-eight consecutive patients were included. All patients underwent a complete hemodynamic study (right atrial, mean pulmonary arterial, and pulmonary arterial occlusion pressures [RAP, mPAP, and PAOP]-) and pulmonary function testing (force vital capacity [FVC], forced expiratory volume in the first second [FEV1], and residual volume [RV]). A subgroup of 10 patients underwent simultaneous esophageal pressure (PES). All hemodynamic parameters and PES were collected during apnea after an unforced expiration (ee) and during spontaneous breathing averaging five respiratory cycles (mrc). The respiratory swing (osc) was estimated as the difference between maximum-minimum values of pressures during the respiratory cycle. Intravascular RAPee, mPAPee, and PAOPee were higher than mrc values (p < 0.05), leading to 11% of pulmonary hypertension (PH) misdiagnosis and 37% of postcapillary PH misclassification. PAOPosc of COPD was higher than ILD patients and RAPosc (p < 0.05). Only PAOPosc correlated with FVC, FEV1, and RV (p < 0.05). ILD PESmrc was lower than COPD (p < 0.05), and it was associated with a significantly higher transmural than intravascular RAPmrc, mPAPmrc, and PAOPmrc. PESmrc was significantly correlated with FVC. Transmural mPAPmrc and PAOPmrc readings determined around 20% of reclassification of the patients compared to ee measurements. Candidates for LTx showed large respiratory swings in PVP, which were correlated with pulmonary function alterations. mrc PVP would be more closely approximated to the true transmural PVP leading to PH reclassification. Adjusting PVP for PES should be considered in COPD and ILD candidates of LTx with severe alterations in pulmonary functional tests and suspicion of a PESmrc far from 0. PES respiratory swings could be different in ILD to COPD patients.