Treatment of right heart failure on pulmonary arterial hypertension: is going left a step in the right direction?

Naeije, Robert

doi:10.1183/09059180.00008509

Cited by 14 publications

(11 citation statements)

References 28 publications

(42 reference statements)

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“…Although the pulmonary vasculature is highly abnormal in the setting of PAH, there is usually little derangement in mechanical lung function. Patients with PAH may occasionally display mild restriction in lung volumes but values are usually within normal limits . Diffusing capacity for carbon monoxide (DL CO ) is mildly to moderately reduced; patients with SScPAH generally have lower DL CO values compared with idiopathic PAH .…”

Section: Pulmonary Factorsmentioning

confidence: 99%

“…Patients with PAH may occasionally display mild restriction in lung volumes but values are usually within normal limits. 60 Diffusing capacity for carbon monoxide (DL CO ) is mildly to moderately reduced; patients with SScPAH generally have lower DL CO values compared with idiopathic PAH. 61 An increase in small airway resistance has been shown, but the precise mechanism accounting for this remains unclear.…”

Section: Pulmonary Factorsmentioning

confidence: 99%

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Pathophysiology of exercise intolerance in pulmonary arterial hypertension

et al. 2017

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Pulmonary arterial hypertension (PAH) is a chronic disease with poor prognosis and important exercise limitation despite the proliferation of treatment options in the last decade. Chronically increased right ventricular (RV) afterload results in right heart failure and without treatment, rapid clinical deterioration is common. Exercise intolerance is the cardinal feature of the disease impacting upon quality of life and clinical outcome. The pathophysiological mechanisms that lead to reduced exercise capacity in this population are complex with ventriculoarterial uncoupling likely to be the predominant feature. The relative contributions of additional factors that contribute to exercise limitation beyond ventriculoarterial uncoupling have not been characterized. This review addresses these factors with a focus on recent developments and uncertainties. RV maladaptation and the intricate interplay between the heart, abnormal pulmonary vascular bed and peripheral factors such as dysfunction of the respiratory and peripheral muscles are discussed in detail.

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Section: Pulmonary Factorsmentioning

confidence: 99%

Section: Pulmonary Factorsmentioning

confidence: 99%

Pathophysiology of exercise intolerance in pulmonary arterial hypertension

et al. 2017

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“…Even though patients with PAH may present with mild-to-moderate ventilation/perfusion mismatch abnormalities, the main determinant of exercise capacity is right ventricular function (and cardiac output) [31]. In PAH, exercise capacity is dependent on the ability of the RV to respond to the increase in cardiac output required for the metabolic requirements of exercise [32].…”

Section: Figurementioning

confidence: 99%

Dobutamine stress for evaluation of right ventricular reserve in pulmonary arterial hypertension

et al. 2014

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Right ventricular contractile response to pharmacological stress in pulmonary arterial hypertension (PAH) has not been characterised. We evaluated right ventricular contractile reserve in adults with PAH using dobutamine stress echocardiography.16 PAH patients and 18 age-matched controls underwent low-dose dobutamine stress echocardiography. Contractile reserve was assessed by the change (Δ; peak stress minus rest value) in tricuspid annular plane systolic excursion (TAPSE) and tricuspid annular systolic velocity (S′). A subgroup of 13 PAH patients underwent treadmill cardiopulmonary exercise testing for peak oxygen uptake (V′O 2 peak).At rest, TAPSE and S′ were reduced in the PAH group compared with controls (1.7±0.4 versus 2.4±0.2 cm and 9.7±2.6 versus 12.5±1.2 cm·s −1 , respectively; p<0.05). Contractile reserve was markedly attenuated in PAH compared to controls (ΔTAPSE 0.1±0.2 versus 0.6±0.3 cm and ΔS′ 4.6±2.8 versus 11.2±3.6 cm·s −1 ; p<0.0001). In the sub-group of PAH patients with preserved right ventricular systolic function at rest, contractile reserve remained depressed compared to controls. V′O 2 peak was significantly correlated with ΔS′ (r=0.87, p=0.0003) and change in stroke volume (r=0.59, p=0.03).Dobutamine stress can reveal sub-clinical reduction in right ventricular contractile reserve in patients with PAH. A correlation with exercise capacity suggests potential clinical value beyond resting measurements. @ERSpublications Dobutamine-induced right ventricular contractile reserve is impaired in PAH and correlates with exercise capacity

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“…The clinical significance of patients with EI‐PAH not only is highlighted by the fact that symptoms might not be evident by subjective assessments of exercise capacity but also noninvasive estimates of PASP may not accurately reflect actual hemodynamics . EI‐PAH has been described by decreased exercise capacity and explained by an excessive increase in PASP that is mainly limited by a compromised cardiac output and likely manifested by a decrease in RV function . Unfortunately, it remains unclear if EI‐PAH identifies patients that will develop resting PAH .…”

mentioning

confidence: 99%