Occlusion pressure analysis role in partitioning of pulmonary vascular resistance in CTEPH

Toshner, Mark; Suntharalingam, Jay; Fesler, Pierre; Soon, Elaine; Sheares, Karen; Jenkins, David P.; White, Paul A.; Morrell, Nicholas W.; Naeije, Robert; Pepke‐Zaba, Joanna

doi:10.1183/09031936.00134111

Cited by 34 publications

(23 citation statements)

References 15 publications

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“…However, PVR partitioning is technically challenging requiring a perfect position of the Swan Ganz catheter with regular pressure decay after occlusion, and has, for a long time, not been further implemented and validated. A recent study on a large number of patients seems to confirm previous findings but also shows that discrimination on an individual basis is insufficient for clinical decision [25].…”

Section: Pulmonary Vascular Remodellingsupporting

confidence: 69%

Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension

et al. 2012

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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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Section: Pulmonary Vascular Remodellingsupporting

confidence: 69%

Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension

et al. 2012

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“…This technique would allow for preoperative assessment of small-vessel disease, but its reproducibility has recently been questioned. 85 …”

Section: Hemodynamics and Right Ventricular Functionmentioning

confidence: 99%

Update on Chronic Thromboembolic Pulmonary Hypertension

2014

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“…3 Upstream resistance is significantly higher in operable CTEPH than in nonoperable CTEPH and iPAH. 79 Patients with higher downstream and lower upstream resistance before PEA appear to be at increased risk for persistent PH and poor outcomes after PEA. 80 Data indicate that patients with upstream resistance of less than 60% are at highest risk for adverse outcomes after PEA.…”

Section: Rv Afterload In Ctephmentioning

confidence: 99%

Right Ventricle in Acute and Chronic Pulmonary Embolism (2013 Grover Conference Series)

2014

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Venous thromboembolism (VTE) encompasses deep-vein thrombosis and pulmonary embolism (PE). It is the third-most-frequent cardiovascular disease, with an overall annual incidence of 1-2 per 1,000 population. Chronic thromboembolic pulmonary hypertension (CTEPH) is regarded as a late sequela of PE, with a reported incidence varying between 0.1% and 9.1% of those surviving acute VTE. Right ventricular (RV) function is dependent on afterload. The most precise technique to describe RV function is invasive assessment of the RV-to-pulmonary vascular coupling. However, assessments of RV afterload (i.e., steady and pulsatile flow components and their product, the RC-time) may be useful hemodynamic surrogates of coupling. RV load is different in acute and chronic PE. In acute PE, more than 60% occlusion of the crosssectional area of the pulmonary artery within a short period of time leads to abrupt hemodynamic collapse. If the time of occlusion is limited to ∼15 seconds, significant decreases in fractional area change, tricuspid annulus systolic excursion, and RV free-wall deformation (strain) occur, with the latter showing significant postsystolic shortening. These changes have similarities to ischemic stunning, and they recover within minutes. In CTEPH, studies of pulmonary vascular resistance (PVR) and pulmonary arterial compliance demonstrated low RC-times that were further lowered after pulmonary endarterectomy (PEA). Immediate postoperative PVR was the only predictor of long-term survival/freedom from lung transplantation, suggesting that the effect of PEA on opening vascular territories to flow outweighs its effect on proximal stiffness. This review summarizes the current knowledge on vascular and intrinsic RV adaptation to VTE, including CTEPH, and the role of imaging.Keywords: right ventricle, hemodynamics, pulmonary heart disease, pulmonary embolism. Venous thromboembolism (VTE) encompasses deep-vein thrombosis (DVT) and pulmonary embolism (PE).It is the third-most-frequent cardiovascular disease, with an overall annual incidence of 1-2 per 1,000 population. Chronic thromboembolic pulmonary hypertension (CTEPH) is regarded as a late sequela of PE. Right ventricular (RV) function is an important determinant of long-term outcome in patients with acute PE and CTEPH. In these conditions, the right ventricle (RV) is subjected to abnormal and increased loading that varies in timing, magnitude, and duration. Consequently, RV dysfunction and pulmonary hypertension (PH) are variably present at initial presentation of acute PE. After an episode of PE, pulmonary hemodynamics and RV function normalize within a few weeks in the majority of patients. CTEPH results from persistence of thrombotic obstructions in the pulmonary vasculature in the presence of significant positive and obliterative vascular remodeling and chronic elevation in pulmonary pressures. CTEPH leads to a progressive increase in RV afterload, causing RV dysfunction and eventually RV failure and death. The condition is underdiagnosed, and the true ...

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Occlusion pressure analysis role in partitioning of pulmonary vascular resistance in CTEPH

Cited by 34 publications

References 15 publications

Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension

Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension

Update on Chronic Thromboembolic Pulmonary Hypertension

Right Ventricle in Acute and Chronic Pulmonary Embolism (2013 Grover Conference Series)

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