Screening, Early Detection, and Diagnosis of Pulmonary Arterial Hypertension

The most important long-term complication of pulmonary thromboembolism is chronic thromboembolic pulmonary hypertension (CTEPH) that is associated with considerable morbidity and mortality. It is uncertain why some patients with acute pulmonary embolism (PE) develop CTEPH and others do not. Elevated red cell distribution width (RDW) has been associated with adverse outcomes of heart failure, PE, and idiopathic pulmonary hypertension. The aim of the present study was to investigate whether RDW might be a predictor of CTEPH in PE patients or not. This study is a retrospective cohort study. A total of 203 consecutive patients with acute PE were included. The RDW was higher in the CTEPH patients than the patients without CTEPH (17.04 + 3.46, 14.64 + 1.82, respectively, p ¼ 0.015). RDW was also higher in the CTEPH patients at the time of diagnosis of CTEPH during follow-up compared with the baseline RDW level at the time of PE diagnosis (18.63 + 3.58, 17.02 + 3.59, respectively, p ¼ 0.014). The optimal cutoff value of the RDW for predicting CTEPH was 14.65. The area under the curve of RDW for the prediction of CTEPH was 0.735 (95% confidence interval (CI): 0.600-0.869); in cases with RDW levels >14.65%, the specificity, sensitivity, and negative predictive value for CTEPH were 62% (95% CI: 0.55-0.69), 75% (95% CI: 0.47-0.92), and 96.7% (95% CI: 0.91-0.99), respectively. A multivariate regression analysis showed that RDW, hazard ratio: 1.58 (95% CI: 1.09-2.30), was a predictor of CTEPH (p ¼ 0.016). High level of RDW was an independent predictor of CTEPH in PE patients. Therefore, RDW levels may provide a prediction for CTEPH in PE patients.

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“…The diagnosis of CTEPH was excluded in the case of normal or low-probability perfusion scintigraphy that has been previously described. 13,16 …”

Section: Diagnosis Of Pe and Ctephmentioning

confidence: 99%

Red cell distribution width

et al. 2014

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“…Current guidelines recommend serological testing for connective tissue disease and testing for HIV in cases of unexplained PAH [7]. Otherwise, blood tests are not routinely used in the diagnosis or follow-up of PAH.…”

Section: Biomarkers In Pulmonary Hypertensionmentioning

confidence: 99%

Biomarkers in pulmonary hypertension

Warwick

Thomas²,

Yates³

2008

Eur Respir J

140

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There have been significant recent advances in the understanding of the pathophysiology of pulmonary hypertension, and a growing number of therapeutic agents have become available to the treating physician. Traditional methods of diagnosing and monitoring this condition have comprised echocardiography and right heart catheterisation, in addition to functional measures, such as estimation of functional class and the 6-min walk test. An increasing number of biomarkers have been described that are elevated in pulmonary hypertension and which may assist the clinician in diagnosis and in the assessment of disease severity and response to treatment.The present article details the more important biomarkers, their potential applications and the evidence supporting their use.

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“…Some individuals are genetically predisposed to develop the vascular injury that ultimately progresses to PAH through the possession of mutations in key molecules, such as the BMPR2 gene, which encodes for a transforming growth factor (TGF)-b type II receptor [1]. This may be associated with a secondary trigger, such as the presence of underlying diseases, including connective tissue disease [2], congenital heart disease [3] or HIV infection [4]. Whatever the origins of the initial vascular insult, the end result is vascular smooth muscle cell dysfunction and endothelial cell dysfunction.…”

mentioning

confidence: 99%

Endothelin: setting the scene in PAH

Dupuis¹

2007

Eur Respir Rev

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Endothelin (ET), a 21-amino acid peptide secreted by the vascular endothelial cells, is frequently reported to be one of the most potent vasoconstrictors. ET induces endothelial cell, smooth muscle cell and fibroblast dysfunction and is now well recognised as a contributor to the complex pathogenesis of pulmonary arterial hypertension, a devastating chronic disease characterised by progressive vascular remodelling and occlusion of the pulmonary arterioles.ET produces its effects through the stimulation of two receptor subtypes, ETA and ETB, both of which are expressed on smooth muscle cells of pulmonary arterioles. Only the ETB receptor is expressed on vascular endothelial cells. In pre-clinical studies, dual blockade of both receptor subtypes was shown to produce greater inhibition of ET-induced contraction compared with blockade of either of the two receptor subtypes alone. There is also evidence that both the ETA and ETB receptors contribute to pulmonary artery smooth muscle cell proliferation. Pre-clinical research in various models of pulmonary arterial hypertension suggests that simultaneous blockade of the two receptor subtypes would be an effective therapeutic approach in the management of patients with pulmonary arterial hypertension. This has been shown to be the case in a number of randomised controlled clinical trials in pulmonary arterial hypertension due to a number of aetiologies.

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Screening, Early Detection, and Diagnosis of Pulmonary Arterial Hypertension

Cited by 796 publications

References 146 publications

Red cell distribution width

Red cell distribution width

Biomarkers in pulmonary hypertension

Endothelin: setting the scene in PAH

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