Publications by authors named "Vasile Foris"

There is an unmet need for breath-based markers for pulmonary vascular disease (PVD). We developed a fully-automatic algorithm to analyze expiratory COflow from resting ventilation and evaluated the clinical associations of our readouts. We enrolled patients with chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD), pulmonary arterial hypertension (PAH) and healthy controls and evaluated fractionated volumes for dead space, mixed space (MSV) and alveolar space, their respective COvolumes and ventilatory equivalents for CO(EqCO) and the maximum slope of the first derivative of the cumulative expiratory COvolume over expired volume (MSV-slope) as primary readouts.

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Chronic obstructive pulmonary disease (COPD) is a severe, progressive, and heterogeneous disease with a poor outcome. Inflammation plays a central role in disease pathogenesis; however, the interplay between immune changes and disease heterogeneity has been difficult to unravel. We performed a multilevel immunoinflammatory characterization of patients with COPD using flow cytometry, cytokine profiling, single-cell, or spatial transcriptomics in combination with machine learning algorithms.

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Purpose: The pulmonary vascular involvement of COPD ranges from severe airway obstruction without pulmonary hypertension (PH) to mild airway obstruction with severe PH. Iron-dependent molecular regulators like hypoxia-inducible factor-2 (HIF-2) may contribute to these phenotypic variations. We explored the role of soluble transferrin receptor-1 (sTfR1) for diagnosis and prognosis of PH associated with COPD.

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Evaluating the predictive role of endothelial dysfunction in the development of vasculopathy-mediated complications in patients with limited cutaneous systemic sclerosis (lcSSc). 38 patients with lcSSc who were naïve for vasculopathy-mediated complications, defined as absent pre-existing digital ulcers (DU), pulmonary hypertension (PH) and symptomatic atherosclerotic cardiovascular diseases, were prospectively observed during a 3-years follow-up period. At study enrolment, functional and laboratory parameters of endothelial dysfunction were assessed.

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Pulmonary hypertension (PH) poses a significant health threat. Current biomarkers for PH lack specificity and have poor prognostic capabilities. To develop better biomarkers for PH that are useful for patient identification and management.

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Severe pulmonary hypertension (PH) in chronic obstructive pulmonary disease (COPD) is currently defined by an elevated mean pulmonary arterial pressure and strongly elevated pulmonary vascular resistance >5 wood units. Clinically, these patients show a male predominance, and usually present with very severe dyspnea, severe hypoxemia, strongly decreased exercise capacity and poor prognosis, even though the clinical picture is frequently associated with less severe airflow obstruction. Explanted lung samples of patients with COPD and severe PH show severe remodeling of small pulmonary arterioles, predominantly in the intima and media of the vessels.

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Background: The gut-lung axis could be a potential therapeutic target for improving post-acute COVID-19 symptoms, and probiotics have been proposed as possible modulators.

Aim: We conducted a pilot study to understand alterations in the gut-lung axis and to explore the effects of a probiotic in post-acute COVID-19 disease.

Methods: We included patients after severe COVID-19 disease (sCOV, n = 21) in a randomized, placebo-controlled trial to test the effect of a probiotic (Pro-Vi 5, Institute Allergosan, Graz, Austria) in a six-month intervention and used patients after mild disease (mCOV, n = 10) as controls, to compare the intestinal microbiome, metabolome, and patient-reported outcomes and biomarkers along the gut-lung axis at baseline and throughout probiotic intervention.

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Article Synopsis
  • The study investigates the significance of the tricuspid annular plane systolic excursion (TAPSE) to systolic pulmonary arterial pressure (sPAP) ratio in predicting outcomes for patients suspected of having pulmonary hypertension (PH), particularly those with normal or mildly elevated mean pulmonary arterial pressure (mPAP).
  • Researchers analyzed data from 237 patients with mPAP < 25 mm Hg over an observation period of 63 months, finding that the TAPSE to sPAP ratio was a strong independent predictor of mortality and clinical worsening events.
  • The results also indicated that this ratio correlates with exercise capacity (measured by the 6-minute walk distance) and the hemodynamics related to exercise, emphasizing its potential
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Purpose Of Review: In this review, we provide an overview of the prognostic implications of exPH in patients with various common cardiac and pulmonary diseases.

Recent Findings: Exercise pulmonary hypertension (exPH) has been recently re-introduced in the current European Society of Cardiology/European Respiratory Society pulmonary hypertension guidelines. Accordingly, exPH is defined as a mean pulmonary arterial pressure (mPAP)/cardiac output ( CO ) slope greater than 3 mmHg/l/min.

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Pulmonary fibrosis (PF) can be a fatal disease characterized by progressive lung scarring. It is still poorly understood how the pulmonary endothelium is involved in the disease pathogenesis. Differences of the pulmonary vasculature between patients and donors were analyzed using transmission electron microscopy, immunohistochemistry, and single-cell RNA sequencing.

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Changes in the extracellular matrix of pulmonary arteries (PAs) are a key aspect of vascular remodeling in pulmonary hypertension (PH). Yet, our understanding of the alterations affecting the proteoglycan (PG) family remains limited. We sought to investigate the expression and spatial distribution of major vascular PGs in PAs from healthy individuals and various PH groups (chronic obstructive pulmonary disease: PH-COPD, pulmonary fibrosis: PH-PF, idiopathic: IPAH).

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Background: In patients with end-stage chronic obstructive pulmonary disease (COPD), severe pulmonary hypertension (PH) is frequently associated with less severe airway obstruction as compared to mild or no PH. However, the histologic correlate of this finding is not clear. We aimed to quantify remodeling of pulmonary arteries, airways, and parenchyma in random samples of explanted end-stage COPD lungs.

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Lung diseases and hypoventilation syndromes are often associated with pulmonary hypertension (PH). In most cases, PH is not severe. This is defined hemodynamically by a mean pulmonary arterial pressure (PAPm) > 20 mmHg, a pulmonary arterial wedge pressure (PAWP) ≤ 15 mmHg and a pulmonary vascular resistance of ≤ 5 Wood units (WU).

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Article Synopsis
  • The new European guidelines for pulmonary hypertension provide detailed information on genetic testing and counseling specifically for pulmonary arterial hypertension patients.
  • They emphasize the need for clinical screening of healthy mutation carriers and recommend genetic testing for patients suspected of having pulmonary veno-occlusive disease.
  • The guidelines also suggest future developments in treatments, highlighting novel approaches like Sotatercept and advancements in targeting ion channels.
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Deposition of basement membrane components, such as collagen IVα5, is associated with altered endothelial cell function in pulmonary hypertension. Collagen IVα5 harbors a functionally active fragment within its C-terminal noncollageneous (NC1) domain, called pentastatin, whose role in pulmonary endothelial cell behavior remains unknown. Here, we demonstrate that pentastatin serves as a mediator of pulmonary endothelial cell dysfunction, contributing to pulmonary hypertension.

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Objectives: Pathways contributing to endothelial dysfunction in patients with limited cutaneous systemic sclerosis (lcSSc) are largely unknown. The aim of this study was to investigate potential associations of amino acids and parameters of bone metabolism with endothelial dysfunction and vasculopathy-related changes in patients with lcSSc and early-stage vasculopathy.

Methods: Amino acids, calciotropic parameters, including 25-hydroxyvitamin D and parathyroid hormone (PTH), and bone turnover parameters, including osteocalcin and N-terminal peptide of procollagen-3 (P3NP), were measured in 38 lcSSc patients and 38 controls.

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Background: Pulmonary hypertension (PH) poses a significant health threat with high morbidity and mortality, necessitating improved diagnostic tools for enhanced management. Current biomarkers for PH lack functionality and comprehensive diagnostic and prognostic capabilities. Therefore, there is a critical need to develop biomarkers that address these gaps in PH diagnostics and prognosis.

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NT-proBNP and GDF-15 are established blood-derived biomarkers for risk assessment in pulmonary hypertension (PH), despite limited sensitivity and specificity. Apelin has a crucial function in endothelial homeostasis, thus it might represent a new biomarker for PH. However, there are numerous circulating apelin isoforms, and their potential role in this setting is unknown.

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COPD is a heterogeneous disease with multiple clinical phenotypes. COPD endotypes can be determined by different expressions of hypoxia-inducible factors (HIFs), which, in combination with individual susceptibility and environmental factors, may cause predominant airway or vascular changes in the lung. The pulmonary vascular phenotype is relatively rare among COPD patients and characterised by out-of-proportion pulmonary hypertension (PH) and low diffusing capacity of the lung for carbon monoxide, but only mild-to-moderate airway obstruction.

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Background: Pulmonary hypertension (PH) is a frequent complication in COPD and it is associated with decreased exercise capacity and poor prognosis. We hypothesized that even in COPD patients without significant PH at rest, abnormal pulmonary hemodynamics during exercise affect exercise capacity.

Methods: Consecutive COPD patients with clinically indicated right heart catheterization and resting mean pulmonary arterial pressure (mPAP) < 25 mmHg and age- and sex-matched controls with the same limits of pulmonary hemodynamics but no chronic lung disease who underwent clinical work-up including invasive hemodynamic assessment during exercise, were retrospectively analyzed.

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