Early Postoperative Pulmonary Vascular Compliance Predicts Outcome After Pulmonary Endarterectomy for Chronic Thromboembolic Pulmonary Hypertension

Perrot, Marc de; McRae, Karen; Shargall, Yaron; Thenganatt, John; Moric, Jakov; Mak, Susanna; Granton, John

doi:10.1378/chest.10-1263

Cited by 36 publications

(30 citation statements)

References 27 publications

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“…Notch ratio t1/t2 SERIES: CTEPH [49]. This similar relationship in CTEPH and PAH predicts that, for a similar PVR, right ventricular load must be similar [50,51].…”

Section: Notch Ratio <1mentioning

confidence: 80%

“…Proportionality of the PAPsys and PAPdias can only be explained if the time constant, which is the product of resistance and compliance, is constant at the same value in CTEPH and idiopathic PAH [46]. Indeed, several studies have confirmed that the load of the right ventricle, described by resistance 6 compliance product, is similar for CTEPH and idiopathic PAH [47][48][49]. For example, LANKHAAR et al [46] showed that in patients with CTEPH (n510), idiopathic PAH (n59) and controls without PH (n510), the time constant was always equal to 0.72 s. The explanation for this is that compliance and resistance are equally distributed over the pulmonary vascular bed.…”

Section: Pressure and Flow Wave Morphologymentioning

confidence: 99%

“…One explanation for these observations is recent evidence that right ventricle loading conditions are not normalised in CTEPH patients although PAP nearly normalised [48,49]. After successful PEA with persistent exertional dyspnoea, patients display an abnormal pulmonary haemodynamic response to exercise, characterised by increased PVR and decreased compliance, which is an independent predictor of limited exercise capacity [48].…”

Section: Right Ventricular Remodellingmentioning

confidence: 99%

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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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“…Notch ratio t1/t2 SERIES: CTEPH [49]. This similar relationship in CTEPH and PAH predicts that, for a similar PVR, right ventricular load must be similar [50,51].…”

Section: Notch Ratio <1mentioning

confidence: 80%

Section: Pressure and Flow Wave Morphologymentioning

confidence: 99%

Section: Right Ventricular Remodellingmentioning

confidence: 99%

See 1 more Smart Citation

Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension

Delcroix

Noordegraaf

Fadel

et al. 2012

European Respiratory Journal

106

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“…It has been proposed that a unique feature of the pulmonary circulation is that PVR and total arterial compliance are tightly coupled through an inverse hyperbolic relationship, resulting in a constant RC-time product that prevails in both health and disease [8][9][10][11][12][13][14][15][16][17][18][19][20][21]. A constant RC-time product has important implications for the assessment of RV afterload, namely that PVR and total arterial compliance are redundant measurements and knowledge of one enables the derivation of the other.…”

Section: Introductionmentioning

confidence: 99%

Pulmonary vascular resistance and compliance relationship in pulmonary hypertension

et al. 2015

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Right ventricular adaptation to the increased pulmonary arterial load is a key determinant of outcomes in pulmonary hypertension (PH). Pulmonary vascular resistance (PVR) and total arterial compliance (C) quantify resistive and elastic properties of pulmonary arteries that modulate the steady and pulsatile components of pulmonary arterial load, respectively. PVR is commonly calculated as transpulmonary pressure gradient over pulmonary flow and total arterial compliance as stroke volume over pulmonary arterial pulse pressure (SV/PApp). Assuming that there is an inverse, hyperbolic relationship between PVR and C, recent studies have popularised the concept that their product (RC-time of the pulmonary circulation, in seconds) is "constant" in health and diseases. However, emerging evidence suggests that this concept should be challenged, with shortened RC-times documented in post-capillary PH and normotensive subjects. Furthermore, reported RC-times in the literature have consistently demonstrated significant scatter around the mean. In precapillary PH, the true PVR can be overestimated if one uses the standard PVR equation because the zero-flow pressure may be significantly higher than pulmonary arterial wedge pressure. Furthermore, SV/PApp may also overestimate true C. Further studies are needed to clarify some of the inconsistencies of pulmonary RC-time, as this has major implications for our understanding of the arterial load in diseases of the pulmonary circulation. @ERSpublications Empiric estimates of pulmonary arterial load are prone to errors and may result in overestimation of RC-time

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“…In healthy individuals and in patients with PAH, it has been demonstrated that PVR and PAC are inversely related in such way that their product forms a constant 13 . This even holds true during treatment for pulmonary arterial hypertension 14–16 . This implies that early in the course of PAH, small increases in PVR are accompanied by large decreases in PAC, likely accounting for the superior prognostic ability of the latter.…”

mentioning

confidence: 98%

Prognostic Role of Pulmonary Arterial Capacitance in Advanced Heart Failure

Dupont

Mullens

Skouri

et al. 2012

Circ: Heart Failure

132

116

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Background RV dysfunction frequently occurs and independently prognosticates in left-sided HF. It is not clear which right ventricular (RV) afterload measure has the greatest impact on RV function and prognosis. We examined the determinants, prognostic role and response to treatment of pulmonary arterial capacitance (PAC, ratio of stroke volume over pulmonary pulse pressure), in relation to pulmonary vascular resistance (PVR) in heart failure (HF). Methods and Results We reviewed 724 consecutive patients with HF who underwent right heart catheterization between 2000 and 2005. Changes in PAC were explored in an independent cohort of 75 subjects treated for acute decompensated HF. PAC showed a strong inverse relation with PVR (r=−0.64) and wedge pressure (r=−0.73), and provides stronger prediction of significant RV failure than PVR (AUC ROC 0.74 vs 0.67 respectively, p = 0.003). During a mean follow-up of 3.2 ± 2.2 years, both lower PAC (p<0.0001) and higher PVR (p<0.0001) portend more adverse clinical events (all-cause mortality and cardiac transplantation). In multivariate analysis, PAC (but not PVR) remains an independent predictor (Hazard ratio =0.92 [95% confidence interval: 0.84–1.0, p=0.037]). Treatment of HF resulted in a decrease in PVR (270±165 to 211±88 dynes·sec·cm−5, p=0.002), a larger increase in PAC (1.65±0.64 to 2.61±1.42 ml/mmHg, p<0.0001), leading to an increase in pulmonary arterial time constant (PVR × PAC) (0.29±0.12 to 0.37±0.15 sec, p<0.0001). Conclusions PAC bundles the effects of PVR and left sided filling pressures on RV afterload, explaining its strong relation with RV dysfunction, poor long-term prognosis, and response to therapy.

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Early Postoperative Pulmonary Vascular Compliance Predicts Outcome After Pulmonary Endarterectomy for Chronic Thromboembolic Pulmonary Hypertension

Cited by 36 publications

References 27 publications

Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension

Vascular and right ventricular remodelling in chronic thromboembolic pulmonary hypertension

Pulmonary vascular resistance and compliance relationship in pulmonary hypertension

Prognostic Role of Pulmonary Arterial Capacitance in Advanced Heart Failure

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