The Role of Exercise Testing in Pulmonary Vascular Disease

Systrom, David; Warren, Arabella; Naeije, Robert

doi:10.1016/j.ccm.2020.11.003

Cited by 9 publications

(8 citation statements)

References 76 publications

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“…Studies with more comprehensive CPET may be needed allow for a better understanding of long COVID. Combining CPET with right heart catheterization or cardiac imaging may uncover exercise pulmonary hypertension, uncoupling of the right heart from the pulmonary circulation or altered matching of convective and diffusive O 2 transport mechanisms [ 29 ]. Such analyses were recently reported in patients with chronic thromboembolic pulmonary hypertension [ 30 ] or heart failure [ 31 ].…”

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confidence: 99%

Phenotyping long COVID

Naeije¹,

Caravita

2021

Eur Respir J

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mentioning

confidence: 99%

Phenotyping long COVID

Naeije¹,

Caravita

2021

Eur Respir J

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“…Some of the discrepancy between 6MWD and CPET measures may be attributed to the experience of investigators and patients, time lag between tests and other logistics; others may simply reflect that these two tests do not measure the same physiobiological process. However, due to the correlation between these two measurements, the 6MWD may still be used as a simple surrogate to V ′ O 2 max [ 35 ], even if its prediction has been shown to be inaccurate.…”

Section: Discussionmentioning

confidence: 99%

Prediction of maximal oxygen uptake from 6-min walk test in pulmonary hypertension

et al. 2022

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Maximal oxygen consumption (VO2max) assessed by cardiopulmonary exercise training (CPET), is an important parameter for risk assessment in patients with pulmonary hypertension (PH). However, CPET may not be available for all PH-patients. Thus, we aimed to test previously published predictive models of VO2max from the 6-min walk distance (6 MWD) for their accuracy and to create a new model.We tested four models (Ross (2010), Miyamoto (2000) and Zapico et al. (2019)). To derive a new model, data was split into a training and testing dataset (70:30) and step-wise linear regression was performed. To compare the different models standard error of estimate (SEE) was calculated and the models have been graphically compared by Bland-Altman plots. Sensitivity and specificity for correct prediction into low risk classification (VO2max>15 mL min kg−1) was calculated for all models.276 observations were included in the analysis (194/82 training/ testing dataset). 6 MWD and VO2max significantly correlated (r=0.65, p<0.001). Linear regression showed significant correlation of 6 MWD, weight and heart rate response (HRR) with VO2max and the best fitting prediction equation was: VO2max=1.83+0.031×6 MWD(m)–0.023×weight(kg)–0.015×HRR(bpm). SEE for the different models were 3.03, 3.22, 4.36 and 3.08 mL min kg−1 for Ross, Miyamoto, Zapico et al. and the new model respectively. Predicted mean VO2max was 16.5 mL min kg−1 (versus observed 16.1 mL min kg−1).6 MWD and VO2max reveal good correlation in all models. However, the accuracy of all models is inadequate for clinical use. Thus, CPET and 6 MWD measures both remain valuable risk assessment tools in the management of PH.

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“…Decreased respiratory muscle strength has also been reported (13). However, these alterations in lung mechanics and respiratory muscle function do not appear to limit aerobic exercise capacity (14,15). Arterial blood gas analysis in PAH is characterized by normal or decreased arterial partial pressures of oxygen and carbon dioxide (PaO2 and PaCO2) (8,9,16).…”

Section: Lung Mechanics Ventilation and Gas Exchangementioning

confidence: 99%

“…A measure of VO2max can be considered as an indirect RV stress test as the main determinant of aerobic capacity in PAH is maximum cardiac output as determined by RV-PA coupling (134). However, VO2max in PAH like in heart failure is also influenced by extracardiac factors including meuro-humoral changes and matching of muscle convectional and diffusional O2 transport mechanisms (15). Clinical relevance.…”

Section: Stressing the Right Ventriclementioning

confidence: 99%

The physiological basis of pulmonary arterial hypertension

Naeije¹,

Richter

Rubin

2021

Eur Respir J

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Pulmonary arterial hypertension (PAH) is a rare dyspnea-fatigue syndrome caused by a progressive increase in pulmonary vascular resistance (PVR) and eventual right ventricular (RV) failure. In spite of extensive pulmonary vascular remodeling, lung function in PAH is generally well preserved, with hyperventilation and increased physiologic dead space, but minimal changes in lung mechanics and only mild to moderate hypoxemia and hypocapnia. Hypoxemia is mainly caused by a low mixed venous PO2 from a decreased cardiac output. Hypocapnia is mainly caused by an increased chemosensitivity. Exercise limitation in PAH is cardiovascular rather than ventilatory or muscular. The extent of pulmonary vascular disease in PAH is defined by multipoint pulmonary vascular pressure-flow relationships with a correction for hematocrit. Pulsatile pulmonary vascular pressure-flow relationships in PAH allow for the assessment of RV hydraulic load. This analysis is possible either in the frequency-domain or in the time-domain. The RV in PAH adapts to increased afterload by an increased contractility to preserve its coupling to the pulmonary circulation. When this homeometric mechanism is exhausted, the RV dilates to preserve flow output by an additional heterometric mechanism. Right heart failure is then diagnosed by imaging of increased right heart dimensions and clinical systemic congestion signs and symptoms. The coupling of the RV to the pulmonary circulation is assessed by the ratio of end-systolic to arterial elastances, but these measurements are difficult. Simplified estimates of RV-PA coupling can be obtained by magnetic resonance or echocardiographic imaging of ejection fraction.

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The Role of Exercise Testing in Pulmonary Vascular Disease

Cited by 9 publications

References 76 publications

Phenotyping long COVID

Phenotyping long COVID

Prediction of maximal oxygen uptake from 6-min walk test in pulmonary hypertension

The physiological basis of pulmonary arterial hypertension

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