Three Decades Single Center Experience of Airway Complications After Lung Transplantation.

Post lung transplantation airway complications like necrosis, stenosis, malacia and dehiscence cause significant morbidity, and are most likely caused by post-operative hypo perfusion of the anastomosis. Treatment can be challenging, and airway stent placement can be necessary in severe cases. Risk factors for development of airway complications vary between studies. In this single center retrospective cohort study, all lung transplant recipients between November 1990 and September 2020 were analyzed and clinically relevant airway complications of the anastomosis or distal airways were identified and scored according to the ISHLT grading system. We studied potential risk factors for development of airway complications and evaluated the impact on survival. The treatment modalities were described. In 651 patients with 1,191 airway anastomoses, 63 patients developed 76 clinically relevant airway complications of the airway anastomoses or distal airways leading to an incidence of 6.4% of all anastomoses, mainly consisting of airway stenosis (67%). Development of airway complications significantly affects median survival in post lung transplant patients compared to patients without airway complication (101 months versus 136 months, p = 0.044). No significant risk factors for development of airway complication could be identified. Previously described risk factors could not be confirmed. Airway stents were required in 55% of the affected patients. Median survival is impaired by airway complications after lung transplantation. In our cohort, no significant risk factors for the development of airway complications could be identified.

Extent of MRI delayed enhancement of myocardial mass is related to right ventricular dysfunction in pulmonary artery hypertension.

OBJECTIVE: The purpose of our study was to assess the presence and extent of delayed contrast enhancement of ventricular myocardium in pulmonary artery hypertension. SUBJECTS AND METHODS: Fifteen patients (age, 45.6 +/- 13 years; 13 New York Heart Association class III) with pulmonary artery hypertension (11 idiopathic, four systemic sclerosis) were studied. All patients had undergone a comprehensive diagnostic workup, and pulmonary artery hypertension (mean pulmonary artery pressure, 54 +/- 16 mm Hg) was confirmed by cardiac catheterization. Cardiac MRI was performed on a 1.5-T scanner to determine ventricular volumes and mass. Delayed contrast enhancement of a mass was seen 10-20 minutes after the i.v. injection of 0.2 mmol/kg of gadopentetate dimeglumine using an inversion recovery gradient-echo sequence. RESULTS: All patients showed delayed contrast enhancement at the insertion points of the right ventricular free wall to the interventricular septum (15 inferior, 13 anterior). The mean weight of the delayed contrast-enhanced myocardial mass was 3.1 +/- 1.9 g (size range, 0.3-3.9% of the total myocardial mass). The extent of the delayed contrast-enhancing myocardium was inversely related to the right ventricular ejection fraction (r = -0.63, p = 0.001), right ventricular stroke volume (r = -0.67, p = 0.006), and right ventricular end-systolic volume index (r = -0.51, p = 0.05) but not to any invasively measured hemodynamic index or N-terminal pro brain natriuretic peptide. CONCLUSION: Myocardial delayed contrast enhancement occurs frequently in patients with severe symptomatic pulmonary artery hypertension and is inversely related to measures of right ventricular systolic function.

A review of pulmonary arterial hypertension: Part 1. Novel insights and classification.

Pulmonary arterial hypertension (PAH) is a disease characterised by an increased pulmonary artery pressure. The precapillary pulmonary arteries show distinct pathobiological changes, i.e. medial hypertrophy, intimal fibrosis, microthrombi and plexiform lesions. Although the pathogenesis is not completely understood, pulmonary vascular proliferation and remodelling, due to a variety of mediators, is believed to play the pathogenetic key role. Genetic research reveals molecular deformities and gene mutations associated with phenotypic PAH. This article covers novel insights into pathobiology, pathogenesis and genes of PAH, which led to a novel classification system and a diagnostic work-up, emanated from the World Health Organisation Symposium on Pulmonary Hypertension in Venice in June 2003.

A review of pulmonary arterial hypertension: Part 2: Current and expected treatments.

Medical therapy for pulmonary arterial hypertension (PAH) focuses on pulmonary vascular remodelling and smooth muscle cell proliferation. This article covers the drugs which are approved or are in sight and the evidence-based treatment strategies that target the different pathobiological pathways, emanated from the World Health Organisation Symposium on Pulmonary Hypertension in Venice, June 2003. In addition we briefly look at the 'Venice consensus' on surgical treatment. In the past five and a half years more than 360 patients were seen for pulmonary hypertension in the Free University Medical Centre (VUmc). Present-day treatment, research studies and novel treatment strategies in the VUmc will be reviewed. Future treatments will be on the basis of insights into pathobiology, pathogenesis and genes in PAH and should focus on drug combinations, which theoretically target different or similar pathobiological pathways.

Stroke volume increase to exercise in chronic obstructive pulmonary disease is limited by increased pulmonary artery pressure.

AIMS: This study was designed to investigate the mechanisms by which the right ventricle is able to increase stroke volume (SV) during exercise in chronic obstructive pulmonary disease (COPD). A second aim was to determine whether resting pulmonary artery pressure (Ppa) is predictive of exercise SV. METHODS: 16 COPD patients (GOLD stages II-IV) underwent right heart catheterisation at rest and during exercise. In this group and eight age-matched controls resting and exercise right ventricular SV, end-diastolic volume (RVEDV) and end-systolic volume (RVESV) were assessed by magnetic resonance imaging (MRI). The exercise protocol during both measurements consisted of 3 minutes of cycling in supine position at 40% of maximal workload. RESULTS: In all patients mean Ppa increased significantly in response to exercise (21 (8) vs 33 (11) mm Hg, p<0.01), whereas pulmonary vascular resistance did not change. In the patient group, RVEDV (129 (42) vs 135 (42) ml, p<0.05) and SV (63 (13) vs 69 (14) ml, p<0.05) increased significantly from rest to exercise, but RVESV and RV ejection fraction remained unaltered. In contrast, in healthy controls SV is augmented (81 (22) vs 101 (28) ml, p<0.05) by both increased RVEDV (123 (33) vs 134 134) ml, p<0.05) and reduced RVESV (37 (9) vs 27 (10) ml, p<0.05). Resting mean Ppa was related to SV during exercise (r = -0.59, p<0.02). CONCLUSION: As a consequence of unaltered pulmonary vascular resistance to exercise in COPD patients, Ppa increases and SV response to exercise is limited and results from an increased preload only. Ppa at rest predicts exercise SV.

NT-proBNP reflects right ventricular structure and function in pulmonary hypertension.

The aim of the current study was to investigate whether alterations in N-terminal pro brain natriuretic peptide (NT-proBNP) reflect changes in right ventricular structure and function in pulmonary hypertension patients during treatment. The study consisted of 30 pulmonary hypertension patients; 15 newly diagnosed and 15 on long-term treatment. NT-proBNP, right heart catheterisation and cardiac magnetic resonance imaging measurements were performed, at baseline and follow-up. There were no significant differences between newly diagnosed patients and those on treatment at baseline or follow-up with respect to NT-proBNP, haemodynamics and right ventricular parameters. Relative changes in NT-proBNP during treatment were correlated to the relative changes in right ventricular end-diastolic volume index (r = 0.59), right ventricular mass index (r = 0.62) and right ventricular ejection fraction (r = -0.81). N-terminal pro brain natriuretic peptide measurements reflect changes in magnetic resonance imaging-measured right ventricular structure and function in pulmonary hypertension patients. An increase in N-terminal pro brain natriuretic peptide over time reflects right ventricular dilatation concomitant to hypertrophy and deterioration of systolic function.