Criteria for diagnosis of exercise pulmonary hypertension (original) (raw)
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Resting pulmonary artery pressure of 21-24 mmHg predicts abnormal exercise haemodynamics
The European respiratory journal, 2016
A resting mean pulmonary artery pressure (mPAP) of 21-24 mmHg is above the upper limit of normal but does not reach criteria for the diagnosis of pulmonary hypertension (PH). We sought to determine whether an mPAP of 21-24 mmHg is associated with an increased risk of developing an abnormal pulmonary vascular response during exercise.Consecutive patients (n=290) with resting mPAP <25 mmHg who underwent invasive exercise haemodynamics were analysed. Risk factors for pulmonary vascular disease or left heart disease were present in 63.4% and 43.8% of subjects. An abnormal pulmonary vascular response (or exercise PH) was defined by mPAP >30 mmHg and total pulmonary vascular resistance >3 WU at maximal exercise.Exercise PH occurred in 74 (86.0%) out of 86 versus 96 (47.1%) out of 204 in the mPAP of 21-24 mmHg and mPAP <21 mmHg groups, respectively (OR 6.9, 95% CI: 3.6-13.6; p<0.0001). Patients with mPAP of 21-24 mmHg had lower 6-min walk distance (p=0.002) and higher New Yo...
European Journal of Heart Failure, 2014
Between 2004 and 2012, 200 symptomatic patients with exertional dyspnoea, preserved left ventricular systolic function and suspected pulmonary hypertension, underwent right heart catheterization. Included in the study were 63 patients with resting pulmonary arterial wedge pressure (PAWP) ≤15 mmHg. Patients were divided to three tertiles based on their peak exercise PAWP. Mean age was 60 ± 20 years and 29% were males. Mean pulmonary arterial pressure was 31 ± 14 mmHg at rest and 42 ± 18 mmHg upon exercise. Mean change in PAWP between rest and exercise was 0.0 ± 4.3, 4.6 ± 2.4, and 16.6 ± 7.1 mmHg in the lower, middle, and upper tertiles, respectively (P < 0.001). Higher exercise PAWP tertiles were associated with reduced pulmonary vascular resistance (8.3 ± 6.7, 2.9 ± 2.7, and 5.8 ± 4.6 Woods units, respectively; P = 0.004). A multivariate linear regression model demonstrated that each 5 kg/m 2 increase in body mass index was associated with 2.5 ± 1.0 mmHg increase in exercise PAWP (P = 0.017). A multivariate binary logistic model showed that subjects with borderline PAWP at rest (12-15 mmHg) were 4.5 times more likely to be in the upper tertile of exercise PAWP (P = 0.011).
Haemodynamics, exercise capacity and clinical events in pulmonary arterial hypertension
European Respiratory Journal, 2012
The purpose of this study was to clarify whether changes in cardiopulmonary haemodynamics induced by pharmacological therapy correlate with exercise capacity and clinical events in patients with pulmonary arterial hypertension. 16 randomised trials including 2353 patients, followed up for 16.4¡10.6 weeks, measuring cardiopulmonary haemodynamics by right heart catheterisation and reporting clinical events were included. Meta-analysis and meta-regression analysis were performed to assess the effects of treatments on clinical events and the relationship between haemodynamic changes (pulmonary artery pressure, pulmonary vascular resistance, cardiac index and right atrial pressure) and clinical events. Treatments significantly reduced all-cause death (OR 0.5, 95% CI 0.3-0.7; p,0.01), hospitalisation for pulmonary arterial hypertension (OR 0.4, 95% CI 0.2-0.7; p,0.01), initiation of rescue therapy (OR 0.3, 95% CI 0.2-0.6; p,0.01) and the composite outcome (OR 0.3, 95% CI 0.3-0.5; p,0.01). No relationship was found between changes of haemodynamic parameters and clinical events, whereas changes of cardiac index and pulmonary vascular resistance significantly correlated with changes in the 6-min walking distance (r50.64, p50.03; r5-0.55, p50.04, respectively). In patients with pulmonary arterial hypertension, improvements of cardiopulmonary haemodynamics observed in randomised clinical trials correlate with exercise capacity changes but do not predict clinical events in a short-term follow-up. @ERSpublications In PAH, cardiopulmonary haemodynamic improvements correlate with exercise capacity changes but not with clinical events http://ow.ly/lzTdC This article has supplementary material available from www.erj.ersjournals.com
Cardiopulmonary Exercise Testing in Pulmonary Hypertension
International Journal of Cardiovascular Sciences, 2016
The cardiopulmonary exercise test (CPET) is a complementary test that provides important data about the patient's actual functional capacity, metabolic and ventilatory responses, and gas exchange. Thus, it enables a classification of the cardiorespiratory fitness of an individual and identification of disorders that limit exercise continuity by analyzing several variables drawn from this diagnostic and prognostic propaedeutic method. In this regard, situations that are relatively common in clinical practice but are not often identified, such as pulmonary hypertension (PH), can be better addressed, assessed, and measured. Thus, the analysis of exhaled gases using CPET may provide better PH management by enabling a classification of the aerobic capacity, ventilatory response and gas exchange in patients with this pulmonary vascular disorder.
Exercise pulmonary haemodynamics: a test in search of purpose
European Respiratory Journal, 2016
Ever since the entity of "exercise induced pulmonary hypertension" was banned from the pulmonary hypertension (PH) dictionary in 2008, during the World Symposium on Pulmonary Hypertension at Dana Point (CA, USA) [1], there has been a concern that by just measuring pulmonary haemodynamics at rest, many patients with subclinical pulmonary vascular disease go unrecognised. This could be harmful, if subjects with an abnormal pulmonary haemodynamic response to exercise are at particular risk of developing PH and that early recognition of PH in these patients would improve their outcome. It may even be that the presence of an abnormal pulmonary haemodynamic response to exercise represents a treatable condition. To date, there is no proof to validate any of these assumptions. The plea in favour of invasive exercise testing so far has failed to overcome several important obstacles. First, there has been a lack of standardisation of invasive cardiopulmonary exercise testing, while the mode of testing and intensity of exercise may certainly affect outcomes. For example, particularly elderly patients may fulfil criteria of an abnormal haemodynamic response at submaximal exercise levels, but no longer at maximal exercise [2]. Second, there remains uncertainty about the physiological limits of a normal response to exercise of pulmonary artery pressure, cardiac output and pulmonary vascular resistance. Third, there is no evidence that treatment of subjects with an abnormal pulmonary haemodynamic response but without PH would improve their outcome. An additional question, to the usefulness of invasive exercise testing, is whether the population of subjects with an abnormal pulmonary haemodynamic response to exercise overlaps with another population that physicians are struggling with, i.e. those with resting mean pulmonary artery pressures (Ppa) below the definition of PH, but clearly higher than the normal physiological limits. Just like patients with abnormal exercise pulmonary haemodynamics, these subjects suffer from increased mortality and hospitalisation [3]. In this issue of the European Respiratory Journal LAU et al. [4] report on exercise pulmonary haemodynamics in 290 consecutive patients at risk for PH with a resting mean Ppa of ⩽25 mmHg. They found that an "abnormal" response was common in those with borderline elevation of resting pressures (86%) and further that the likelihood of an "abnormal" response increased progressively as resting mean pressure increased from 13 mmHg upwards. There was no systematic follow-up, thus we have no direct insight into the prognostic significance of these observations. However, patients with exercise PH were more symptomatic and had reduced exercise tolerance. We must, therefore, consider whether the proposed definition of an "abnormal" exercise response is valid, whether the population investigated includes biases that would increase the
Prognostic value of exercise pulmonary haemodynamics in pulmonary arterial hypertension
European Respiratory Journal, 2014
The aim of the study was to investigate the prognostic value of right heart catheterisation variables measured during exercise. 55 incident patients with idiopathic, familial or anorexigen-associated pulmonary arterial hypertension (PAH) underwent right heart catheterisation at rest and during exercise and 6-min walk testing before PAH treatment initiation. Patients were treated according to recommendations within the next 2 weeks. Right heart catheterisation was repeated 3-5 months into the PAH treatment in 20 patients. Exercise cardiac index decreased gradually as New York Heart Association (NYHA) functional class increased whereas cardiac index at rest was not significantly different across NYHA groups. Baseline 6-min walk distance correlated significantly with exercise and change in cardiac index from rest to exercise (r50.414 and r50.481, respectively; p,0.01). Change in 6-min walk distance from baseline to 3-5 months under PAH treatment was highly correlated with change in exercise cardiac index (r50.746, p,0.001). The most significant baseline covariates associated with survival were change in systolic pulmonary artery pressure from rest to exercise and exercise cardiac index (hazard ratio 0.56 (95% CI 0.37-0.86) and 0.14 (95% CI 0.05-0.43), respectively). Change in pulmonary haemodynamics during exercise is an important tool for assessing disease severity and may help devise optimal treat-to-target strategies.
Pulmonary vascular responses to exercise: a haemodynamic observation
European Respiratory Journal, 2012
xercise testing provides additional information over resting variables and is a standard of care in the assessment of coronary artery disease with less subsequent cardiovascular events. In pulmonary hypertension (PH), right ventricular function is clearly an important determinant of survival. However, right ventricular impairment is currently assessed only during resting conditions. Exercise (stress) testing may provide further insight into the complex paradigm of right ventricular dysfunction, right ventricular-left ventricular interdependence and right ventricular-pulmonary artery coupling. Whether pulmonary artery pressure (Ppa)-flow relationships during exercise provides a window into earlier diagnosis of functionally significant PH or adds incrementally to our armamentarium of diagnostic tests and prognostic indicators in PH, is a topic of ongoing investigation. In this issue of the European Respiratory Journal (ERJ), the studies by KOVACS et al. [1] and WHYTE et al. [2] discuss the potential clinical utility of identifying ''normal'' and ''abnormal'' pulmonary vascular response patterns to exercise in patients aged f50 yrs.
The association between resting and mild-to-moderate exercise pulmonary artery pressure
European …, 2011
The mean pulmonary artery pressure (Ppa) achieved on mild-to-moderate exercise is age related and its haemodynamic correlates remain to be documented in patients free of pulmonary hypertension (PH). Our retrospective study involved patients free of PH investigated in our centre for possible pulmonary vascular disease between January 1, 2007 and October 31, 2009 who underwent right heart catheterisation at rest and during supine exercise up to 60 W. The 38 out of 99 patients aged ,50 yrs were included and a Ppa of 30 mmHg was considered the upper limit of normal on exercise. The 24 subjects who developed Ppa.30 mmHg on exercise had higher resting Ppa (19¡3 versus 15¡4 mmHg) and indexed pulmonary vascular resistance (PVRi; 3.4¡1.5 versus 2.2¡1.1 WU?m 2 ; p,0.05) than the remaining 14 subjects. Resting Ppa .15 mmHg predicted exercise Ppa .30 mmHg with 88% sensitivity and 57% specificity. The eight patients with resting Ppa 22-24 mmHg all had exercise Ppa .30 mmHg. In subjects aged ,50 yrs investigated for possible pulmonary vascular disease and free of PH, patients with mild-to-moderate exercise Ppa .30 mmHg had higher resting PVRi and higher resting Ppa, although there was no resting Ppa threshold value that could predict normal response on mild-to-moderate exercise. The clinical relevance of such findings deserves further long-term follow-up studies.
Exercise-induced Pulmonary Hypertension
American Journal of Respiratory and Critical Care Medicine, 2013
Exercise stresses the pulmonary circulation through increases in cardiac output (_ Q) and left atrial pressure. Invasive as well as noninvasive studies in healthy volunteers show that the slope of mean pulmonary artery pressure (mPAP)-flow relationships ranges from 0.5 to 3 mm Hg$min$L 21. The upper limit of normal mPAP at exercise thus approximates 30 mm Hg at a _ Q of less than 10 L$min 21 or a total pulmonary vascular resistance at exercise of less than 3 Wood units. Left atrial pressure increases at exercise with an average upstream transmission to PAP in a close to one-for-one mm Hg fashion. Multipoint PAP-flow relationships are usually described by a linear approximation, but present with a slight curvilinearity, which is explained by resistive vessel distensibility. When mPAP is expressed as a function of oxygen uptake or workload, plateau patterns may be observed in patients with systolic heart failure who cannot further increase _ Q at the highest levels of exercise. Exercise has to be dynamic to avoid the increase in systemic vascular resistance and abrupt changes in intrathoracic pressure that occur with resistive exercise and can lead to unpredictable effects on the pulmonary circulation. Postexercise measurements are unreliable because of the rapid return of pulmonary vascular pressures and flows to the baseline resting state. Recent studies suggest that exercise-induced increase in PAP to a mean higher than 30 mm Hg may be associated with dyspnea-fatigue symptomatology.