Patent foramen ovale in idiopathic pulmonary arterial hypertension: Long-term risk and morbidity

Moraes, Alice Gallo De; Vakil, Abhay; Moua, Teng

doi:10.1016/j.rmed.2016.07.007

Cited by 11 publications

(12 citation statements)

References 33 publications

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“…Finally, we did not examine the presence of patent foramen ovale (PFO) that occasionally induces hypoxaemia by postural change. The reported PFO prevalence among PAH patients is 27% . Although not all PFO patients show hypoxaemia by postural change, those with PFO might affect the results of the present study.…”

Section: Discussionmentioning

confidence: 54%

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Non‐invasive screening using ventilatory gas analysis to distinguish between chronic thromboembolic pulmonary hypertension and pulmonary arterial hypertension

et al. 2019

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Background and objective Clinical presentations associated with chronic thromboembolic pulmonary hypertension (CTEPH) and pulmonary arterial hypertension (PAH) at rest are highly similar. Differentiating between CTEPH and PAH using non‐invasive techniques remains challenging. Thus, we examined whether analysis of ventilatory gas in response to postural changes can be useful as a non‐invasive screening method for pulmonary hypertension (PH), and help differentiate CTEPH from PAH. Methods We prospectively enrolled 90 patients with suspected PH and performed right heart catheterization, ventilation/perfusion scan and ventilatory gas analysis. Various pulmonary function parameters were examined in the supine and sitting postures, and postural changes were calculated (Δ(supine − sitting)). Results In total, 25 patients with newly diagnosed PAH, 40 patients with newly diagnosed CTEPH and 25 non‐PH patients were included. ΔEnd‐tidal CO2 pressure (PETCO2) was significantly lower in patients with CTEPH and PAH than in non‐PH patients (both P < 0.001). ΔPETCO2 < 0 mm Hg could effectively differentiate PH from non‐PH (area under the curve (AUC) = 0.969, sensitivity = 89%, specificity = 100%). Postural change from sitting to supine significantly increased the ratio of ventilation to CO2 production (VE/VCO2) in the CTEPH group (P < 0.001). By contrast, VE/VCO2 significantly decreased in the PAH group (P = 0.001). Notably, CTEPH presented with higher ΔVE/VCO2 than PAH, although no differences were observed in haemodynamic and echocardiographic parameters between the two groups (P < 0.001). Furthermore, ΔVE/VCO2 > 0.8 could effectively differentiate CTEPH from PAH (AUC = 0.849, sensitivity = 78%, specificity = 88%). Conclusion Postural changes in ventilatory gas analysis are useful as a non‐invasive bedside evaluation to screen for the presence of PH and distinguish between CTEPH and PAH.

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Section: Discussionmentioning

confidence: 54%

“…The reported PFO prevalence among PAH patients is 27%. 40 Although not all PFO patients show hypoxaemia by postural change, those with PFO might affect the results of the present study.…”

Section: Study Limitationsmentioning

confidence: 66%

Non‐invasive screening using ventilatory gas analysis to distinguish between chronic thromboembolic pulmonary hypertension and pulmonary arterial hypertension

et al. 2019

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“…As the prevalence of patent foramen ovale is no higher in PAH patients than in the general population (25%), we assumed patients with a central catheter did not have an increased risk of stroke from paradoxical embolism. [57][58][59] We only modeled AC with a VKA, as no studies to date explored the use of any of the direct oral anticoagulant medications. For those receiving catheter therapy, we considered the risk of DVT from the central catheter to be additive to the incidence of DVT in the more general PAH population.…”

Section: Assumptionsmentioning

confidence: 99%

Anticoagulation in pulmonary arterial hypertension: a decision analysis

2019

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Systemic anticoagulation may be beneficial in pulmonary arterial hypertension, but there is no randomized clinical trial data to guide therapeutic decision making, and current guidelines do not account for patient preferences or quality of life. Decision analytic models to evaluate the potential risks and benefits of systemic anticoagulation in pulmonary arterial hypertension patients, focusing on the benefit in quality-adjusted life years, may be helpful in clarifying this uncertainty. We constructed a 31-state Markov decision analytic model to explore anticoagulation and no anticoagulation strategies. Modeled patient characteristics included gender, use of central catheter-based pulmonary arterial hypertension therapy, type of pulmonary arterial hypertension (idiopathic, idiopathic pulmonary arterial hypertension, or connective-tissue associated, connective tissue disease-pulmonary arterial hypertension), and use of oral contraceptive medication by females. Modeled events included mortality, thromboembolic complications, atrial fibrillation, stroke, and anticoagulation bleeding. Deterministic and probabilistic sensitivity analyses were performed. Anticoagulation was favored in all idiopathic pulmonary arterial hypertension cases, with a gain of 0.43–0.51 quality-adjusted life years, and detrimental in all connective tissue disease-pulmonary arterial hypertension cases, with a loss of 0.66–1.89 quality-adjusted life years. Anticoagulation would need to demonstrate a hazard ratio for pulmonary arterial hypertension mortality of 0.95 or better to be favored. In our model, idiopathic pulmonary arterial hypertension patients benefit from anticoagulation in terms of quality-adjusted life years, and connective tissue disease-pulmonary arterial hypertension patients were harmed, with a hazard ratio for pulmonary arterial hypertension mortality of 0.95 or better being required to favorably impact quality-adjusted life years. These results suggest that anticoagulation significantly improves quality adjusted life years and should be offered to all idiopathic pulmonary arterial hypertension patients. Shared decision models based on these results may help clarify therapeutic decision-making uncertainty in pulmonary arterial hypertension patients.

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“…Idiopathic pulmonary arterial hypertension (IPAH) is a pulmonary proliferative vasculopathy ( Gallo de Moraes et al, 2016 ). Pathological changes including plexiform lesions, cellular proliferation, fibrosis, in situ thrombosis of the small pulmonary arteries and arterioles, and angiogenic dysfunction, leading to increased pulmonary vascular resistance, result in IPAH ( Barnes et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Identification of Hub Genes and MicroRNAs Associated With Idiopathic Pulmonary Arterial Hypertension by Integrated Bioinformatics Analyses

et al. 2021

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ObjectiveThe aim of this study is the identification of hub genes associated with idiopathic pulmonary arterial hypertension (IPAH).Materials and MethodsGSE15197 gene expression data was downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified by screening IPAH patients and controls. The 5,000 genes with the greatest variances were analyzed using a weighted gene co-expression network analysis (WGCNA). Modules with the strongest correlation with IPAH were chosen, followed by a functional enrichment analysis. Protein–protein interaction (PPI) networks were constructed to identify hub gene candidates using calculated degrees. Real hub genes were found from the overlap of DEGs and candidate hub genes. microRNAs (miRNAs) targeting real hub genes were found by screening miRNet 2.0. The most important IPAH miRNAs were identified.ResultsThere were 4,395 DEGs identified. WGCNA indicated that green and brown modules associated most strongly with IPAH. Functional enrichment analysis showed that green and brown module genes were mainly involved in protein digestion and absorption and proteoglycans in cancer, respectively. The top ten candidate hub genes in green and brown modules were identified, respectively. After overlapping with DEGs, 11 real hub genes were identified: EP300, MMP2, CDH2, CDK2, GNG10, ALB, SMC2, DHX15, CUL3, BTBD1, and LTN1. These genes were expressed with significant differences in IPAH versus controls, indicating a high diagnostic ability. The miRNA–gene network showed that hsa-mir-1-3p could associate with IPAH.ConclusionEP300, MMP2, CDH2, CDK2, GNG10, ALB, SMC2, DHX15, CUL3, BTBD1, and LTN1 may play essential roles in IPAH. Predicted miRNA hsa-mir-1-3p could regulate gene expression in IPAH. Such hub genes may contribute to the pathology and progression in IPAH, providing potential diagnostic and therapeutic opportunities for IPAH patients.

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Patent foramen ovale in idiopathic pulmonary arterial hypertension: Long-term risk and morbidity

Abstract: Patent foramen ovale is seen in a quarter of patients with idiopathic pulmonary arterial hypertension and associated with increased prevalence of severe hypoxemia but had no effect on long term survival.

Cited by 11 publications

References 33 publications

Non‐invasive screening using ventilatory gas analysis to distinguish between chronic thromboembolic pulmonary hypertension and pulmonary arterial hypertension

Non‐invasive screening using ventilatory gas analysis to distinguish between chronic thromboembolic pulmonary hypertension and pulmonary arterial hypertension

Anticoagulation in pulmonary arterial hypertension: a decision analysis

Identification of Hub Genes and MicroRNAs Associated With Idiopathic Pulmonary Arterial Hypertension by Integrated Bioinformatics Analyses

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