Pulmonary Venous Hypertension in End-Stage COPD and Preserved Systolic Left Ventricular Function: Vascular Lesions in Explanted Lungs after Transplantation

Abstract

Purpose Pulmonary venous hypertension (PVH) with preserved systolic left ventricular ejection fraction is an established comorbidity in chronic obstructive pulmonary disease, COPD. PVH is characterized by mPAP ≥25mmHg and PCWP >15mmHg. Vascular morphological changes in PVH remain unclear. Methods and Materials A retrospective analysis of 33 patients with COPD/emphysema lung transplanted at Rigshospitalet, Denmark (1991-2010) was performed. PVH was diagnosed with right heart catheterization. Patients were stratified into two groups: (1) transpulmonary gradient (TPG) ≤12mmHg (passive PVH) and (2) TPG >12mmHg (“out of proportion” PVH). Arterial lesions were graded (1-6) according to a modified Heath and Edwards (HE) scale, and venous lesions as grade 0 : no venous vascular involvement, grade 1 : intimal fibrosis, medial hypertrophy and arterialization, and grade 2 : grade1 with >50% lumen reduction and/or aneurysmatic dilatation, secondary lumina, venolitis, fibrinoid necrosis or thrombosis. Results The mean age at evaluation was 55±6 years (73% women). All patients had NYHA functional class III-IV with FEV 1 22±7% and total lung capacity 116±21% of predicted. All had preserved left systolic ventricular function. Group I : n=16 (81% women), age 56±6 years, mPAP 28.4.2±2.8mmHg, PCWP 19.4±3.2mmHg. Mean TPG was 9.0±2.2 and median HE grading was 1 (range 0-2) with medial hypertrophy of muscular pulmonary arteries and muscularization of pulmonary arterioles. Median venous grade was 1 (range 0-2) with intimal fibrosis, medial hypertrophy and arterialization. Group II : n=17 (65% women), age 54±5 years, mPAP 37.1±6.2mmHg, PCWP 17.9±1.7mmHg, TPG 19.1±6.2 mmHg. Median HE grading was 0 (range 0-2). Median venous grade was 1 (range 0-2). Conclusions Although no difference in grades between patients with “out-of proportion” or passive PVH were observed, PVH appears to induce significant myofibroblast proliferation in both pulmonary arteries and veins.