A model for estimating the health economic impact of earlier diagnosis of chronic thromboembolic pulmonary hypertension

Background Diagnostic delay of chronic thromboembolic pulmonary hypertension (CTEPH) exceeds 1 year, contributing to higher mortality. Health economic consequences of late CTEPH diagnosis are unknown. We aimed to develop a model for quantifying the impact of diagnosing CTEPH earlier on survival, quality-adjusted life-years (QALYs) and healthcare costs. Material and methods A Markov model was developed to estimate lifelong outcomes, depending on the degree of delay. Data on survival and quality of life were obtained from published literature. Hospital costs were assessed from patient records (n=498) at the Amsterdam UMC - VUmc, which is a Dutch CTEPH referral center. Medication costs were based on a mix of standard medication regimens. Results For 63-year-old CTEPH patients with a 14-month diagnostic delay of CTEPH (median age and delay of patients in the European CTEPH Registry), lifelong healthcare costs were estimated at EUR 117 100 for a mix of treatment options. In a hypothetical scenario of maximal reduction of current delay, improved survival was estimated at a gain of 3.01 life-years and 2.04 QALYs. The associated cost increase was EUR 44 654, of which 87% was due to prolonged medication use. This accounts for an incremental cost-utility ratio of EUR 21 900/QALY. Conclusion Our constructed model based on the Dutch healthcare setting demonstrates a substantial health gain when CTEPH is diagnosed earlier. According to Dutch health economic standards, additional costs remain below the deemed acceptable limit of EUR 50 000/QALY for the particular disease burden. This model can be used for evaluating cost-effectiveness of diagnostic strategies aimed at reducing the diagnostic delay

Pulmonary hypertension

Pulmonary hypertension (PH) is a haemodynamic condition that leads to a progressive increase in pulmonary vascular resistance and mean pulmonary artery pressure. Irrespective of its aetiology, the main cause of death in PH patients is right ventricular (RV) failure. Noninvasive imaging techniques play an essential role in diagnosing PH and monitoring disease progression. This chapter provides an overview of the most important noninvasive imaging tools for assessing pulmonary pressures, RV function and monitoring

Right ventricular stiffness impairs right atrial function in pulmonary arterial hypertension

Background: In pulmonary arterial hypertension (PAH) patients, right ventricular (RV) stiffness is associated with disease severity and mortality. However, the interplay between RV stiffness, ventricular filling and right atrial (RA) function remains elusive.Aim: To investigate whether RV stiffness influences RA function and RV filling in PAH patients.Methods: We determined end-diastolic elastance (stiffness, Eed) in 31 controls and 97 PAH patients. RA strain and RV volumes were measured with magnetic resonance imaging.Results: Median Eed was higher in patients than controls (0.635 [0.40-0.99] vs. 0.20 [0.15-0.24] mmHg/ml; plt;0.001). Patients had reduced RA reservoir (14.3textpm5.19.1textpm4.3 plt;0.001) and conduit strain (-5.6textpm3.412.4textpm3.3 plt;0.001), while RA active strain was enhanced (-9.0textpm4.07.5textpm2.8 p=0.019). Passive RV filling was reduced (33textpm19ml vs. 48textpm19ml; plt;0.001), while active RV filling was preserved (22textpm17ml vs. 24textpm13ml; p=0.38).In patients with a stiff RV (Eed gt; median), RA conduit strain was worse than in patients with a compliant RV (figure). However, no correlation between RA active strain and Eed was observed (Spearman rho 0.06; p=0.57).Conclusions: RV stiffness in PAH patients is accompanied by decreased RA conduit strain, but did not correlate with RA active strain. Passive RV filling in patients is impaired, but active filling is preserved.FootnotesCite this article as: European Respiratory Journal 2020; 56: Suppl. 64, 4047.This abstract was presented at the 2020 ERS International Congress, in session textquotedblleftRespiratory viruses in the "pre COVID-19" eratextquotedblright.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only)

The quantitative assessment of interstitial lung disease with positron emission tomography scanning in systemic sclerosis patients

OBJECTIVES: The reversibility of interstitial lung disease (ILD) in SSc is difficult to assess by current diagnostic modalities and there is clinical need for imaging techniques that allow for treatment stratification and monitoring. 18F-Fluorodeoxyglucose (FDG) PET/CT scanning may be of interest for this purpose by detection of metabolic activity in lung tissue. This study aimed to investigate the potential role of 18F-FDG PET/CT scanning for the quantitative assessment of SSc-related active ILD. METHODS: 18F-FDG PET/CT scans and high resolution CT scans of eight SSc patients, including five with ILD, were analysed. For comparison, reference groups were included: eight SLE patients and four primary Sjögren's syndrome (pSS) patients, all without ILD. A total of 22 regions of interest were drawn in each patient at apical, medial and dorsobasal lung levels. 18F-FDG uptake was measured as mean standardized uptake value (SUVmean) in each region of interest. Subsequently, basal/apical (B/A) and medial/apical (M/A) ratios were calculated at patient level (B/A-p and M/A-p) and at tissue level (B/A-t and M/A-t). RESULTS: SUVmean values in dorsobasal ROIs and B/A-p ratios were increased in SSc with ILD compared with SSc without ILD (P = 0.04 and P = 0.07, respectively), SLE (P = 0.003 and P = 0.002, respectively) and pSS (P = 0.03 and P = 0.02, respectively). Increased uptake in the dorsobasal lungs and increased B/A-t ratios corresponded to both ground glass and reticulation on high resolution CT. CONCLUSION: Semi-quantitative assessment of 18F-FDG PET/CT is able to distinguish ILD from non-affected lung tissue in SSc, suggesting that it may be used as a new biomarker for SSc-ILD disease activity