Circulating biomarkers in chronic thromboembolic pulmonary hypertension

Abstract

Chronic thromboembolic pulmonary hypertension (CTEPH) is a serious condition characterized with chronic organized thrombi that obstruct the pulmonary vessels, leading to pulmonary hypertension (PH) and ultimately right heart failure. Although CTEPH is the only form of PH that can be cured with surgical intervention, not all patients with CTEPH will be deemed operable. Some CTEPH patients still have a poor prognosis. Therefore, the determination of diagnostic and prognostic biomarkers of CTEPH is of great importance for the early intervention to improve prognosis of patients with CTEPH. Several markers related to multiple mechanisms of CTEPH have been recently identified as circulating diagnostic and prognostic biomarkers in these patients. However, the existing literature review of biomarkers of CTEPH is relatively sparse. In this article, we review recent advances in circulating biomarkers of CTEPH and describe future applications of these biomarkers in the management of CTEPH.

Peripheral microangiopathy in precapillary pulmonary hypertension: a nailfold video capillaroscopy prospective study

“…Besides obstructive macrovascular disorder, CTEPH also encapsulates a "secondary arteriopathy" component of small sized pulmonary arterioles in which inflammation, oxidative stress and endothelial dysfunction play an important role [29]. In the current study, patients with CTEPH presented not only with mild capillaroscopic alterations similar to NVC changes observed in IPAH, but also with a higher degree of abnormal capillaries and capillary thrombi compared to IPAH patients.…”

“…For example, the imbalance between vasodilation and vasoconstrictor mediators, culminating in excessive vasoconstriction, endothelial and smooth muscle proliferation may account for pulmonary vascular remodeling as well as peripheral vascular changes in ΙPΑH [4]. Vascular endothelial growth factor (VEGF) and proinflammatory cytokines are likely mediators of chronic hypoxia-driven pulmonary and peripheral vascular remodeling in PAH, by mobilizing endothelial progenitor cells (EPCs) [26][27][28][29]. A severe reduction in circulating EPCs despite VEGF stimulus in late stages of SSc and its positive correlation with the reduction in capillary density may explain peripheral microvascular alterations [28], observed among entities of precapillary PH in our study.…”

Peripheral Microangiopathy in Pre-capillary Pulmonary Hypertension: A Nailfold Video Capillaroscopy Prospective Study

“…Besides an obstructive macrovascular disorder, CTEPH also encapsulates a "secondary arteriopathy" component of small sized pulmonary arterioles in which in ammation, oxidative stress and endothelial dysfunction play an important role [27]. In the current study, patients with CTEPH presented not only with mild capillaroscopic alterations similar to NVC changes observed in IPAH, but also with a higher degree of abnormal capillaries and capillary thrombi compared to IPAH patients.…”

“…For example, the imbalance between vasodilation and vasoconstrictor mediators, culminating in excessive vasoconstriction, endothelial and smooth muscle proliferation may account for pulmonary vascular remodeling as well as peripheral vascular changes in PH [4]. Vascular endothelial growth factor (VEGF) and proin ammatory cytokines are likely mediators of chronic hypoxia-driven pulmonary and peripheral vascular remodeling in pre-capillary PH, by mobilizing endothelial progenitor cells (EPCs) [24][25][26][27]. A severe reduction in circulating EPCs despite VEGF stimulus in late stages of SSc and its positive correlation with the reduction in capillary density may explain peripheral microvascular alterations [26], observed among various entities of precapillary PH in our study.…”

A Novel Clinical Perspective on New Masses after Lead Extraction (Ghosts) by Means of Intracardiac Echocardiography

“…In our view the last hypothesis (lysis and microembolism) is the most realistic as no major episode of clinically evident embolism occurred in the group of patients whose mass had disappeared at the follow-up. In our study, we did not monitor microembolism, but as reported in the literature there are several biomarkers that can be used in monitoring thrombo-microembolism [ 25 ]. Such monitoring is certainly warranted in our ghost patients and must be done in the future.…”