Dilatation of Bronchial Arteries Correlates With Extent of Central Disease in Patients With Chronic Thromboembolic Pulmonary Hypertension

Shimizu, Hidefumi; Tanabe, Nobuhiro; Terada, Jiro; Masuda, Masahisa; Sakao, Seiichiro; Kasahara, Yasunori; Takiguchi, Yuichi; Tatsumi, Koichiro; Kuriyama, Takayuki

doi:10.1253/circj.72.1136

Cited by 53 publications

(38 citation statements)

References 23 publications

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“…The peak of changes in these three morphological parameters appeared to be in the area of total pulmonary arterial occlusion through ligation, while partial and progressive occlusion through repeated emboli generated the same modifications, but to a lesser extent. This observation, at least for bronchial arterial remodelling, is in accordance with findings from a study by SHIMIZU et al [29], whose retrospective analysis of computed tomography angiography from 59 patients with CTEPH showed that the cross-sectional area of the bronchial arteries positively correlated with the central extent of the thromboembolic material compared with obstruction on the segmental level. They also compared the CTEPH group to 16 patients suffering from PAH (group 1 of the Nice classification) and found significant increase in bronchial artery total area of CTEPH patients compared with PAH.…”

Section: Findings In Porcine Histologysupporting

confidence: 92%

“…Although we will not discuss this point extensively, since these findings were sparse in our analysis, the phenomenon has been shown for humans and animals under exercise conditions [26][27][28]. The pattern of hypertrophy and enlargement of systemic bronchial arteries is well known in CTEPH [25,29]. It has been speculated that a decrease of postobstructive pulmonary artery pressure and the eventual increase of the pressure gradient between bronchial arteries and pulmonary arteries might lead to an opening of pre-existing bronchopulmonary arterial anastomoses [30,31].…”

Section: Intrapulmonary Systemic Vesselsmentioning

confidence: 89%

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Microvascular disease in chronic thromboembolic pulmonary hypertension: a role for pulmonary veins and systemic vasculature

et al. 2014

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Limited numbers of operated patients with chronic thromboembolic pulmonary hypertension (CTEPH) are refractory to pulmonary endarterectomy (PEA) and experience persistent pulmonary hypertension (PH).We retrospectively assessed lung histology available from nine patients with persistent PH (ineffective PEA (inPEA) group) and from eight patients transplanted for distal CTEPH inaccessible by PEA (noPEA group). Microscopically observed peculiarities were compared with the histology of a recently developed CTEPH model in piglets. Pre-interventional clinical/haemodynamic data and medical history of patients from the inPEA and noPEA groups were collected and analysed.Conspicuous remodelling of small pulmonary arteries/arterioles, septal veins and pre-septal venules, including focal capillary haemangiomatosis, as well as pronounced hypertrophy and enlargement of bronchial systemic vessels, were the predominant pattern in histology from both groups. Most findings were reproduced in our porcine CTEPH model. Ink injection experiments unmasked abundant venular involvement in so-called small vessel or microvascular disease, as well as post-capillary bronchopulmonary shunting in human and experimental CTEPH.Microvascular disease is partly due to post-capillary remodelling in human and experimental CTEPH and appears to be related to bronchial-to-pulmonary venous shunting. Further studies are needed to clinically assess the functional importance of this finding. @ERSpublications Pulmonary veins and systemic vasculature contribute to microvascular disease in CTEPH

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Section: Findings In Porcine Histologysupporting

confidence: 92%

Section: Intrapulmonary Systemic Vesselsmentioning

confidence: 89%

Microvascular disease in chronic thromboembolic pulmonary hypertension: a role for pulmonary veins and systemic vasculature

et al. 2014

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“…In contrast to patients with PAH, CTEPH patients may display significant bronchopulmonary collateral blood flow, accounting for up to 30% of systemic blood flow draining directly into the pulmonary veins [29,30]. The presence of bronchial collaterals has been used as a ''biomarker'' for the diagnosis of CTEPH [31]. A linear correlation exists between the magnitude of bronchosystemic shunt and dilatation of the bronchial arteries in patients with CTEPH [32].…”

Section: Pulmonary Vascular Remodellingmentioning

confidence: 99%

Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension

Delcroix

Noordegraaf

Fadel

et al. 2012

European Respiratory Journal

106

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In chronic thromboembolic pulmonary hypertension (CTEPH) increased pulmonary vascular resistance is caused by fibrotic organisation of unresolved thromboemboli. CTEPH mainly differs from pulmonary arterial hypertension (PAH) by the proximal location of pulmonary artery obliteration, although distal arteriopathy can be observed as a consequence of nonoccluded area over-perfusion. Accordingly, there is proportionally more wave reflection in CTEPH, impacting on pressure and flow wave morphology. However, the time constant, i.e. resistance6compliance, is not different in CTEPH and PAH, indicating only trivial effects of proximal wave reflection on hydraulic right ventricular load. More discriminative is the analysis of the pressure decay after pulmonary arterial occlusion, which is more rapid in the absence of significant distal arteriopathy.Structure and function of the right ventricle show a similar pattern to right ventricular hypertrophy, namely dilatation and wall thickening, as well as loss of function in CTEPH and PAH. This is probably related to similar loading conditions. Hyperventilation with hypocapnia is characteristic of both PAH and CTEPH. Ventilatory equivalents for carbon dioxide, as a function of arterial carbon dioxide tension, conform to the alveolar ventilation equation in both conditions, indicating a predominant role of increased chemosensitivity. However, a slight increase in the arterial to end-tidal carbon dioxide tension gradient in CTEPH shows a contribution of increased dead space ventilation. KEYWORDS: Chronic thromboembolic pulmonary hypertension, gas exchange, pulmonary arterial hypertension, pulmonary circulation, remodelling, right ventricular function C hronic thromboembolic pulmonary hypertension (CTEPH) is characterised by the presence of unresolved thromboemboli undergoing fibrotic organisation. This results in obstruction of proximal pulmonary arteries, increased pulmonary vascular resistance (PVR), pulmonary hypertension (PH) and progressive right ventricle remodelling and failure. Pulmonary embolism, either as single or recurrent episodes, is thought to be the initiating event followed by progressive pulmonary vascular remodelling. CTEPH mainly differs from pulmonary arterial hypertension (PAH) by the proximal location of pulmonary artery obliteration, although distal arteriopathy can be observed as a consequence of non-occluded area over-perfusion [1]. Also characteristic for CTEPH is the extensive collateral blood supply to the ischemic lung, developed from the systemic circulation.Diagnosis is based on the presence of pre-capillary PH, defined by a mean pulmonary arterial pressure (PAP) o25 mmHg and a wedge pressure f15 mmHg, in combination with a lung scan showing segmental perfusion defects after a prolonged period of anticoagulation [2]. Further

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“…In fact, chronic PE is more frequently associated with dilated bronchial arteries than acute PE as seen on CTPA [51,52]. Interestingly, systemic blood flow may increase by up to 30% with PE, in comparison to the original blood flow [53,54].…”

Section: Chronic Pulmonary Embolism Dual-energy Ctmentioning

confidence: 99%

Where do we stand? Functional imaging in acute and chronic pulmonary embolism with state-of-the-art CT

Meyer

Haubenreisser

Sudarski

et al. 2015

European Journal of Radiology

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Dilatation of Bronchial Arteries Correlates With Extent of Central Disease in Patients With Chronic Thromboembolic Pulmonary Hypertension

Cited by 53 publications

References 23 publications

Microvascular disease in chronic thromboembolic pulmonary hypertension: a role for pulmonary veins and systemic vasculature

Microvascular disease in chronic thromboembolic pulmonary hypertension: a role for pulmonary veins and systemic vasculature

Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension

Where do we stand? Functional imaging in acute and chronic pulmonary embolism with state-of-the-art CT

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