Exercise-induced Pulmonary Hypertension Research Articles

Exercise capacity in COPD patients with exercise-induced pulmonary hypertension

BackgroundPulmonary hypertension (PH) in patients with COPD is associated with reduced exercise capacity. A subgroup of COPD patients has normal mean pulmonary artery pressure (mPAP) at rest, but develops high mPAP relative to cardiac output (CO) during exercise, a condition we refer to as exercise-induced pulmonary hypertension (EIPH). We hypothesized that COPD patients with EIPH could be identified by cardiopulmonary exercise test (CPET) and that these patients have lower exercise capacity and more abnormal CPET parameters compared to COPD patients with normal hemodynamic exercise response.MethodsNinety-three stable outpatients with COPD underwent right heart catheterization with the measurement of mPAP, CO, and capillary wedge pressure at rest and during supine exercise. Resting mPAP <25 mmHg with ΔmPAP/ΔCO slope above or below 3 mmHg/L/min were defined as COPD-EIPH and COPD-normal, respectively. Pulmonary function tests and CPET with arterial blood gases were performed. Linear mixed models were fitted to estimate differences between the groups with adjustment for gender, age, and airflow obstruction.ResultsEIPH was observed in 45% of the study population. Maximal workload was lower in COPD-EIPH compared to COPD-normal, whereas other CPET measurements at peak exercise in % predicted values were similar between the two groups. After adjustment for gender, age, and airflow obstruction, patients with COPD-EIPH showed significantly greater increase in oxygen uptake, ventilation, respiratory frequency, heart rate, and lactate with increasing work load, as well as more reduction in pH compared to those with normal hemodynamic responses.ConclusionCOPD-EIPH could not be discriminated from COPD-normal by CPET. However, COPD-EIPH experienced a higher cost of exercise in terms of higher oxygen uptake, ventilation, respiratory frequency, heart rate, and lactate for a given increase in workload compared to COPD-normal.

Effect of Cardiac Resynchronization Therapy on Exercise-Induced Pulmonary Hypertension and Right Ventricular-Arterial Coupling.

Background Acute and chronic effects of cardiac resynchronization therapy (CRT) on pulmonary pressures, right ventricular function, and ventricular-vascular coupling during exercise are insufficiently understood. Yet, these factors are strongly associated with functional status and outcome. Methods and Results Heart failure patients with reduced ejection fraction indicated for CRT were prospectively included to undergo exercise echocardiography simultaneously with cardiopulmonary exercise testing before (pre_CRT), 1 day after (post_CRT), and 6 months (post6_CRT) after CRT implant. Right ventricular-arterial coupling was assessed by the tricuspid annular plane systolic excursion (TAPSE)/systolic pulmonary artery pressure (SPAP) ratio. A total of 31 heart failure patients with reduced ejection fraction (age=66±13 years) were prospectively included. CRT resulted in an immediate reduction in rest SPAP (pre_CRT=32±16 versus post_CRT=23±16 mm Hg; P=0.006) and rest effective regurgitant orifice (pre_CRT=0.32±0.1 versus post_CRT=0.18±0.2; P=0.001) without changes in exercise mitral regurgitation or exercise SPAP indexed for cardiac output. Six months after CRT, in parallel with left ventricular reverse remodeling and a reduction in exercise mitral regurgitation and exercise E/e' ratio, the exercise SPAP/cardiac output significantly improved (post_CRT=5.6±3.1 versus post6_CRT=4.3±2.9 mm Hg·L-1·min-1; P=0.039), which was also illustrated by a reduced slope of ΔSPAP/Δcardiac output (post_CRT=5.2±3.7 versus post6_CRT=2.9±2.7 mm Hg·L-1·min-1; P=0.002). CRT did not result in an acute or chronic effect on TAPSE or TAPSE/SPAP ratio at rest. However, exercise revealed the presence of right ventricular-arterial uncoupling which was not affected by an acute CRT effect ( P=0.396) but only improved by a chronic CRT effect ( P<0.001; TAPSE/SPAP ratio: pre_CRT= 0.39±0.6 mm/mm Hg; post_CRT=0.42±0.5 mm/mm Hg; post6_CRT =0.84±0.12 mm/mm Hg). Of all exercise echocardiography variables, the TAPSE/SPAP ratio demonstrated the strongest correlation with Vo2 peak ( r=0.475), VE/Vco2 ( r=-0.585), and workload ( r=0.476) during cardiopulmonary exercise testing ( P<0.05 all). Multivariate predictors affecting exercise ventricular-arterial coupling after CRT included metrics of residual exercise mitral regurgitation and systolic and diastolic left ventricular function. Conclusions Chronic CRT beneficially influences pulmonary pressures and right ventricular-arterial coupling during exercise, which strongly relates to functional status. These findings are mechanistically linked to reverse remodeling with improved interventricular dependence and reduction in exercise mitral regurgitation.

P4406Significance of exercise-induced pulmonary hypertension in patients with hypertrophic cardiomyopathy

P4406Significance of exercise-induced pulmonary hypertension in patients with hypertrophic cardiomyopathy

Coital Hemoptysis Due to Cardiac AL Amyloidosis

A 48-year-old woman presented with recurrent hemoptysis during intercourse. The computed tomography (CT) pulmonary angiogram demonstrated bilateral patchy ground glass opacities and no pulmonary embolism and a small pulmonary cyst (Figure A, arrow). She was treated with azithromycin, and follow-up chest CT 12 days later demonstrated complete resolution (Figure D). Stress echocardiogram suggested multivessel coronary artery disease (CAD), but coronary angiogram demonstrated only mild CAD. An exercise right-heart catheterization showed exercise-induced pulmonary arterial hypertension and elevated filling pressures. Cardiac magnetic resonance imaging showed delayed subendocardial enhancement, left ventricular hypertrophy, and biatrial enlargement (Supplemental Figure: 3-chamber and 4-chamber views, available online at http://www.mayoclinicproceedings.org). Subsequent right ventricular biopsy at 200× magnification showed a pericellular pattern of amyloid deposition (Figure B, arrow) on Congo red stain with characteristic apple-green birefringence (Figure C, arrow) under polarized light diagnostic of AL (lambda) cardiac amyloidosis. Coital hemoptysis is infrequently described and typically due to cardiac etiology such as heart failure, mitral valve disease, or CAD.1Fuks L. Shitrit D. Amital A. Fox B.D. Kramer M.R. Postcoital hemoptysis: our experience and review of the literature.Respir Med. 2009; 103: 1828-1831Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar Amyloidosis is an uncommon cause of hemoptysis, but more often due to pulmonary parenchymal disease and pulmonary vascular fragility rather than cardiac disease.2Road J.D. Jacques J. Sparling J.R. Diffuse alveolar septal amyloidosis presenting with recurrent hemoptysis and medial dissection of pulmonary arteries.Am Rev Respir Dis. 1985; 132: 1368-1370PubMed Google Scholar We hypothesize that when imposed on a noncompliant, amyloid-infiltrated heart, increased cardiac workload and systemic arterial pressures during intercourse caused a dramatic elevation in left ventricular filling pressures leading to flash pulmonary edema. The cystic pulmonary lesion may indicate pulmonary involvement, with possible increased pulmonary microvascular involvement and a predisposition to hemoptysis. If present, pulmonary microvascular involvement may have predisposed to hemoptysis in the setting of rapidly increased cardiac filling pressures. After a positive serum protein electrophoresis, a bone marrow biopsy revealed multiple myeloma for which the patient underwent autologous stem cell transplant and is doing well. We thank Omar F. AbouEzzeddine, MDCM, MS, and Mandeep Singh, MD, MPH, for their mentorship and assistance in manuscript preparation. Supplemental material can be found online at http://www.mayoclinicproceedings.org. Supplemental material attached to journal articles has not been edited, and the authors take responsibility for the accuracy of all data.

Hemodynamic Mechanisms of Exercise-Induced Pulmonary Hypertension in Patients with Lymphangioleiomyomatosis: The Role of Exercise Stress Echocardiography

The pathogenesis of pulmonary hypertension (PH) in lymphangioleiomyomatosis (LAM) has not yet been completely clarified. The aim of this study was to conduct a noninvasive evaluation of the main hemodynamic mechanisms of exercise-induced PH in patients with LAM, assessed using exercise stress echocardiography. Fifteen patients with LAM (mean age, 47±13years; all women) without resting PH were enrolled in a prospective single-center study and compared with 15 healthy female control subjects (mean age, 45.2±8years; P=.65). A complete echocardiographic study with Doppler tissue imaging was performed at baseline and during semisupine symptom-limited exercise testing to evaluate (1) left ventricular systolic and diastolic function, (2) right ventricular contractile function, (3) estimated pulmonary capillary wedge pressure, (4) estimated systolic and mean pulmonary artery pressure, and (5) estimated pulmonary vascular resistance. Compared with healthy control subjects, patients with LAM during exercise showed echocardiographic signs of right ventricular overload and right ventricular systolic dysfunction and significant increases in mean pulmonary artery pressure (14.4±6.5 vs 4.2±3.1mm Hg, P<.0001), pulmonary vascular resistance(+68.3±42.1 vs -0.1±18.3 dyne-sec/cm5, P<.0001), and, unexpectedly, pulmonary capillary wedge pressure (+8.3±5.3 vs -0.5±1.3mm Hg, P<.0001). Exercise-induced PH in patients with LAM could be related not only to hypoxic pulmonary vascular vasoconstriction during exercise (precapillary PH) but also to a significant exercise-induced increase in estimated pulmonary capillary wedge pressure, probably secondary to diastolic dysfunction (postcapillary PH).

GAS EXCHANGE SCORE WITH REST ETCO2 AND VE/VCO2 PREDICTS PULMONARY VASCULAR DISEASE AT REST AND EXERCISE IN PATIENTS WITH DYSPNEA OF UNCLEAR ETIOLOGY

Detection of exercise-induced pulmonary hypertension (PH) and behavior of resting PH with exercise can provide insight into the physiological basis of unexplained dyspnea. We sought to predict this exercise behavior with gas exchange parameters. We reviewed clinical, echocardiographic, hemodynamics

Exercise-Induced Pulmonary Hypertension: Translating Pathophysiological Concepts Into Clinical Practice

Exercise stress testing of the pulmonary circulation for the diagnosis of latent or early-stage pulmonary hypertension (PH) is gaining acceptance. There is emerging consensus to define exercise-induced PH by a mean pulmonary artery pressure > 30mmHg at a cardiac output< 10 L/min and a total pulmonary vascular resistance> 3 Wood units at maximum exercise, in the absence of PH at rest. Exercise-induced PH has been reported in association with a bone morphogenetic receptor-2 gene mutation, in systemic sclerosis, in left heart conditions, in chronic lung diseases, and in chronic pulmonary thromboembolism. Exercise-induced PH is a cause of decreased exercise capacity, may precede the development of manifest PH in a proportion of patients, and is associated with a decreased life expectancy. Exercise stress testing of the pulmonary circulation has to be dynamic and rely on measurements of the components of the pulmonary vascular equation during, not after exercise. Noninvasive imaging measurements may be sufficiently accurate in experienced hands, but suffer from lack of precision, so that invasive measurements are required for individual decision-making. Exercise-induced PH is caused either by pulmonary vasoconstriction, pulmonary vascular remodeling, or by increased upstream transmission of pulmonary venous pressure. This differential diagnosis is clinical. Left heart disease as a cause of exercise-induced PH can be further ascertained by a pulmonary artery wedge pressure above or below 20mmHg at a cardiac output< 10 L/min or a pulmonary artery wedge pressure-flow relationship above or below 2mmHg/L/min during exercise.

Variable Hemodynamic Responses during Diastolic Stress Echocardiography in Patients Who Have Relaxation Abnormality with Possible Elevated Filling Pressure.

Background and ObjectivesThe clinical characteristics of patients with diastolic dysfunction characterized by a relaxation abnormality with possible elevated filling pressure is remain to be determined. We sought to test whether diastolic stress echocardiography (DSE) is useful for characterization of these patients.MethodsA total of 120 patients (58 men, mean age of 64±7 years) with E/A ratio <1.0 (mean±SD, 0.7±0.1) and 10≤ E/e' <15 at rest echocardiography was enrolled prospectively for supine bicycle exercise up to 50 W.ResultsDuring exercise, 47 patients (39%) showed high left ventricular filling pressure (E/e' >15, hLVFP) and 40 (30%) developed exercise-induced pulmonary hypertension (systolic pulomary arterial pressure >50 mmHg, EiPH) without hLVFP. The remaining 33 patients did not show hLVFP or EiPH. The incidence of EiPH with hLVFP was 21% (25/120). By multivariate analysis, age (odds ratio [OR], 1.07; 95% confidence interval [CI], 1.00–1.13; p=0.039) and systolic pulmonary artery pressure at rest (OR, 1.14; 95% CI, 1.02–1.27; p=0.02) were associated with EiPH, whereas late diastolic transmitral velocity (OR, 1.04; 95% CI, 1.00–1.08; p=0.03) and diastolic blood pressure (OR, 0.94; 95% CI, 0.90–0.99; p=0.02) were associated with hLVFP during exercise.ConclusionsPatients with relaxation abnormality and possibly hLVFP showed markedly heterogeneous hemodynamic changes during low-level exercise and DSE was useful to characterize these patients.

Design of the exercise MRI evaluation of HIV-pulmonary arterial hypertension longitudinal determinants (EXALTED) trial.

Pulmonary arterial hypertension (PAH) is a potentially serious cause of dyspnea and exercise limitation in patients with HIV infection. In this trial, we propose using exercise MRI in conjunction with cardiopulmonary testing to delineate PAH from other causes of cardiovascular dysfunction, identify individuals with exercise-induced PAH who are at high risk of developing resting PAH, and provide longitudinal estimates of progression of PAH and right ventricular function. In this prospective observational study, HIV patients with dyspnea and exercise limitation in the absence of identifiable causes and those who meet the inclusion criteria will be enrolled based on resting pulmonary artery pressure (≤ or >40 mmHg) on a screening echocardiogram and exercise limitation on the Modified Medical Research Council dyspnea scale. Patients without evidence of resting PAH will be enrolled into both rest and exercise MRI and cardiopulmonary testing protocol, whereas patients with evidence of PAH on resting echocardiograms will undergo only resting cardiac MRI studies to evaluate right ventricular function and fibrosis. Both patient subgroups will be followed for 24 months to obtain longitudinal progression of the disease. In a sub-study, we will further analyze inflammatory variables that may predict these changes, thus allowing early identification of these patients. This trial will be the first study to provide an understanding of the mechanisms underpinning the functional deterioration of the right ventricle in patients with HIV and will impart insight into the immune mediators of PAH progression and right ventricular functional deterioration in patients with HIV-PAH.

Estado del arte en hipertensión pulmonar y cateterismo cardiaco derecho

The universally accepted definition of pulmonary hypertension corresponds to all those patients with a mean pulmonary arterial pressure of equal to or greater than 25mm Hg at rest, measured using right-heart catheterisation. It should not be forgotten that the mean normal pulmonary arterial pressure is a maximum of 20mm Hg, which means that patients with a mean pulmonary arterial pressure between 20 and 24mm Hg need to be followed-up. It should also be remembered to be clear on differentiating between pulmonary hypertension and pulmonary arterial hypertension. Pulmonary hypertension includes five groups, among which pulmonary arterial hypertension is Group 1. The concept of exercise-induced pulmonary arterial hypertension can be defined as all those patients with a pulmonary arterial hypertension above 30mm Hg at a cardiac output less than 10 L, or a total pulmonary resistance of more than 3 Wood units. Exercise-induced pulmonary hypertension is a research field that has been little investigated up until now. The classification still has five groups, and is dynamic in accordance with the progress in understanding the pathophysiology of each disease.

Symptoms Are More Useful Than Echocardiography in Patient Selection for Pulmonary Endarterectomy

Chronic thromboembolic pulmonary hypertension (CTEPH) is still largely underdiagnosed in the general population. Although transthoracic echocardiogram (TTE) is recommended to screen for CTEPH, it may not detect patients with chronic thromboembolic disease (CTED) and mild or exercise-induced pulmonary hypertension (PH) who could also benefit from pulmonary endarterectomy (PEA). All patients referred to our CTEPH program with persistent mismatched perfusion defects on ventilation-perfusion (VQ) scan between January 2005 and June 2015 were divided into three groups according to TTE and right heart catheterization (RHC) as follows: (1)typical CTEPH group (PH on RHC and TTE), (2) TTE-negative (neg) CTEPH group (PH on RHC, but not TTE), or (3) CTED group (no PH on RHC and TTE). Of 225 patients with abnormal VQ scans, 188 (84%) had typical CTEPH, 15 had TTE-neg CTEPH, and 22 had CTED. PEA was performed in 179 patients (80%). Reasons for exclusion in CTEPH patients included primarily distal disease (n= 11) and comorbidities (n= 10). In contrast, the absence of functional limitation was the main cause of exclusion in CTED patients (75% versus 3% in CTEPH patients, p < 0.0001). The 90-day mortality rate after PEA was 4% in the typical CTEPH group and 0% in the TTE-neg CTEPH and CTED groups. Pulmonary arterial pressures and functional class significantly improved after PEA in all three groups. Patients with mild CTEPH can benefit from PEA, but may not be detected by TTE. Symptomatic patients with functional limitation and persistent mismatched perfusion defects on VQ scan should undergo further investigations with pulmonary angiogram and RHC.

Cardiovascular outcome in systemic sclerosis.

Cardiovascular involvement is recognized as a poor prognostic factor in systemic sclerosis (SSc). The aim of this study was to evaluate the usefulness of nailfold video-capillaroscopy (NVC), brain natriuretic peptide (BNP) blood level and exercise echocardiography to predict the occurrence of cardiovascular events in SSc. We prospectively enrolled 65 patients with SSc (age 54±14 years, 30% female) followed in CHU Sart-Tilman, Liège, Belgium. All patients underwent graded semi-supine exercise echocardiography. Both baseline resting pulmonary hypertension (PH) and PH during follow-up (FUPH) were defined as systolic pulmonary arterial pressure (sPAP)>35 mmHg, and exercise-induced PH (EIPH) as sPAP>50 mmHg during exercise. EIPH was present in 21 patients. During FU (27±18 months), 13 patients developed FUPH and 9 presented cardiovascular complications. Patients with cardiovascular events were significantly older (63±14 vs 52±13 years; P=0.03), presented more frequently NVC grade>2 (89 vs 43%; P=0.009), had higher resting and exercise sPAP (30±6 vs 24±6; P=0.007 and 57±13 vs 44±13 vs mmHg; P=0.01, respectively), and higher BNP blood level (112±106 vs 26±19 pg/ml; P=0.0001). After adjustment for age and gender, NVC grade>2 (ß=2.4±1.1; P=0.03), EIPH (ß=2.30±1.13; P=0.04), FUPH (ß=0.24±0.09; P=0.01 and ß=3.52±1.16; P=0.002, respectively;) and BNP (ß=0.08±0.04; P=0.02) were independent predictors of CV events. Beyond age, an incremental value of EIPH, BNP and NVC grade>2 was predictive of cardiovascular events (P<0.001). Cardiovascular complications are not rare in SSc (18%). NVC, BNP blood level assessment and exercise echocardiography could be useful tools to identify patients at risk of SSc.

Abstract 476: Exercise Induced Pulmonary Hypertension in Patient Presenting With Acute Cardiac Symptoms

Introduction: Patients presenting with symptoms of angina, dyspnea, and fatigue with negative cardiac and pulmonary test findings are often investigated with exercise right heart catheterization. Patients displaying pulmonary hypertension or exercise-induced pulmonary hypertension (EIPH) were isolated and studied further to elaborate upon similarities and differences with patients with normal pressures. Hypothesis: EIPH may be an under-recognized cause of cardiac complaints. Methods: Clinical data was obtained from 172 randomly and retrospectively selected patients including data on hemodynamics, cardiopulmonary exercise testing (CPET), and echocardiogram findings. Patients with EIPH had a resting mean pulmonary arterial pressure below 25 mmHg and on exercise above 25 mmHg. Patients with resting pulmonary hypertension were stratified into WHO group 1 (pulmonary arterial) and WHO group 2 (due to left heart). Prior response to treatment with long-acting nitrates was also reviewed. Results: 27 patients had EIPH, 24 had WHO group 1 pulmonary hypertension, 37 had WHO group 2 pulmonary hypertension, 54 did not have pulmonary hypertension, and 30 did not have any exercise data. No significant differences were found across any groups in resting or exercise CPET performance. The mean age of those with pulmonary hypertension was 71.67 years and 58.89 for those without (p&lt;0.01). Both had a mean left ventricular ejection fraction between 53-57%. The mean VO2 max for those with resting pulmonary hypertension or EIPH was below 20 ml/kg/min. For every 1-year increase in age the odds of developing EIPH increased by 1.08. The use of long-acting nitrate was associated with improvement of symptoms in symptomatic patients. Most of the EIPH patients were noted to have exercise-induced diastolic dysfunction and many also had concomitant chronotropic incompetance. Conclusions: EIPH represents those who have negative left-heart stress cardiac findings yet have underlying abnormalities significant enough to require symptomatic treatment during exercise. This includes diastolic dysfunction and chronotropic incompetency. Cardiovascular performance was found to be equally poor in patients with EIPH as compared to those with resting pulmonary hypertension.

Predictors of Exercise-Induced Pulmonary Hypertension in Patients with Asymptomatic Degenerative Mitral Regurgitation: Mechanistic Insights from 2D Speckle-Tracking Echocardiography

Presence of exercise-induced pulmonary hypertension (EIPH) in asymptomatic degenerative mitral regurgitation (DMR) determines prognosis. This study aimed to elucidate the mechanism and predictors of EIPH in asymptomatic DMR. Ninety-one consecutive asymptomatic patients with DMR who underwent exercise stress echocardiography were prospectively included. We obtained various conventional echocardiographic parameters at rest and during peak exercise, as well as left atrial (LA) function at rest using 2-dimensional speckle-tracking analysis. The 25 patients (33.3%) with EIPH were significantly older and had a greater ratio of mitral peak velocity of early filling to early diastolic mitral annular velocity during peak exercise than those without EIPH. LA strain (LAS)-s and LAS-e, indices of LA reservoir and conduit function, respectively, were significantly lower in those with EIPH than in those without EIPH. Multivariate analysis indicated that LAS-s was the only resting echocardiographic parameter that independently predicted EIPH, with a cut-off value of 26.9%. Furthermore, Kaplan-Meier curve analysis showed that symptom-free survival was markedly lower among those with reduced LAS-s. In conclusion, decreased LA reservoir function contributes to EIPH, and LAS-s at rest is a useful indicator for predicting EIPH in asymptomatic patients with DMR.

Use of thermodilution cardiac output overestimates diagnoses of exercise-induced pulmonary hypertension.

Two new definitions of exercise-induced pulmonary hypertension (EIPH) have emerged. Both rely on measuring cardiac output (CO), yet this remains unstandardized. In our cohort of patients undergoing invasive cardiopulmonary exercise testing, we found that using thermodilution CO rather than direct Fick CO led to a significant excess of EIPH diagnoses.

A Case of Exercise-Induced Chest Pain Due to Anomalous Right Coronary Artery

A 58-year-old male presented with 6-month history of exertional chest pain on a background of family history of family history of sudden death in brother at the age of 50. He underwent coronary angiogram and subsequent CTCA after positive exercise stress test. There was anomalous anterior origin of right coronary artery arising from left coronary cusp, coursing between the pulmonary artery and aorta without significant coronary stenosis. (Fig. 1). Heart team meeting consensus was that chest pain was due to exercise-induced pulmonary hypertension and patient was offered single coronary artery bypass grafting. Patient is doing well without recurrence of pain at 3 months of follow-up. The clinical outcome for ARCA is most often benign. Exercise induced cyclical compression and distorted slit-like ostium are thought to be mechanism of ischaemia. Patients who have symptoms of ischaemia or arrhythmia warrant more urgent surgical intervention, both for management of symptoms and reduction in risk of sudden cardiac death [[1]Ghosh P.K. Agarwal S.K. Kumar R. Chandra N. Puri V.K. Anomalous origin of right coronary artery from left aortic sinus.J Cardiovasc Surg (Torino). 1994; 35: 65-70PubMed Google Scholar]. This case illustrates the importance of considering ARCA as a differential diagnosis in patients presenting with exercise induced ischaemic chest pain, without any alternative explanations.

When exploring patients during exercise makes sense?

This editorial refers to ‘Clinical characteristics and determinants of exercise-induced pulmonary hypertension in patients with preserved left ventricular ejection fraction’, by A. Young Lim et al. doi: 10.1093/ehjci/jew199. Dealing with exertional dyspnoea or unexplained shortness of breath is a common problem in clinical practice. However, the exploration of such symptoms is difficult and does not always lead to definite positive diagnosis and thus appropriate treatment. Moreover, the perception of dyspnoea is subjective and relies on determinants that are often unclear. In these patients, exploring pulmonary pressures and diastolic function during exercise appears to be an interesting way to assess the potential causes triggering their symptoms. In this issue of European Heart Journal - Cardiovascular Imaging , Lim et al. 1 present a remarkable study exploring the value of exercise-induced pulmonary hypertension (EIPH) in patients with preserved left ventricular ejection fraction and complaining about unexplained dyspnoea. This exhaustive work included a large number of patients (1383 were analysed) and enabled a comprehensive description of the clinical aspects and features of EIPH in this population. To date, this population has not been well characterized, so the data published in this issue allow interesting insights in this not-so-well-known clinical entity. EIPH has been explored and demonstrated as clinically interesting in the field of heart valve diseases and in the prognostic assessment of patients diagnosed for a heart failure with preserved ejection fraction.2–4 Notably, larger studies confirming those first results are mandatory to justify a more generalized use of exercise stress echocardiography in our routine clinical practice. The first surprising fact in the study by Lim et al . appears to be the population with …

Left ventricular deformation at rest predicts exercise-induced elevation in pulmonary artery wedge pressure in patients with unexplained dyspnoea.

Impaired left ventricular (LV) deformation despite preserved LV ejection fraction (LVEF) is common and predicts outcomes in heart failure with preserved LVEF. We hypothesized that impaired LV deformation at rest is a marker of impaired cardiac systolic and diastolic reserve, and aimed to determine whether resting longitudinal (LS) and circumferential strain (CS) are associated with invasively measured haemodynamic response to exercise in patients with dyspnoea and a normal LVEF. We studied 85 patients with LVEF ≥50% and free of significant valvular disease who were referred for evaluation of dyspnoea. All patients underwent rest echocardiography followed by right heart catheterization and cardiopulmonary exercise testing with concomitant invasive haemodynamic monitoring. The LS, CS and CS/LS ratio were measured by two-dimensional speckle-tracking echocardiography at rest. Lower absolute LS at rest was associated with greater increase in pulmonary arterial wedge pressure (PAWP) from rest to peak exercise (r = 0.23, P = 0.034). In contrast, higher absolute CS at rest predicted a greater increase in PAWP (r = - 0.27, P = 0.032) and greater stroke volume augmentation with exercise (r = - 0.26, P = 0.021). Higher CS/LS ratio was most predictive of elevation in PAWP with exercise (r = 0.30, P = 0.015). Of the measures of LV systolic and diastolic function assessed, the CS/LS ratio resulted in the highest area under the curve and specificity for the presence of rest- or exercise-induced pulmonary venous hypertension. Left ventricular deformation at rest predicts exercise-induced rise in PAWP among patients with dyspnoea and a preserved LVEF. A pattern of rest deformation characterized by worse LS and exaggerated CS is most strongly associated with exercise-induced rise in PAWP.

Exercise-induced pulmonary hypertension by stress echocardiography: Prevalence and correlation with right heart hemodynamics

ObjectivesThe aim of this study was to determine the prevalence of exercise-induced pulmonary hypertension (EIPH) in consecutive subjects referred for stress echocardiography for chest pain or shortness of breath and correlate echocardiographic diagnosis of EIPH with hemodynamics at right heart catheterization (RHC). BackgroundElevated pulmonary pressure can lead to significant morbidity and mortality. EIPH by ehocardiography has been described in patients with connective tissue disease. It's prevalence in the setting of routine clinically indicated stress echocardiography unknown. MethodsIn a retrospective analysis of 4068 consecutive stress subjects undergoing stress echocardiography, 479 subjects with EIPH were identified. All 479 subjects with EIPH were compared to 479 age and sex matched subjects with normal pulmonary artery pressures post exercise. EIPH was defined as PASP>50mmHg or peak tricuspid regurgitation velocity>3.2m/s. Of 100 patients with EIPH who underwent RHC we identified variables which predicted abnormal hemodynamic findings on RHC. ResultsThe prevalence of EIPH in subjects referred for stress echocardiography was 11.7%. A greater proportion of subjects with EIPH were obese or had lung disease or connective tissue disease. Of 100 subjects who underwent RHC, 65 had abnormal results. Age>55years (OR 5.1, p<0.01]) or dilated left atrium (OR 4.4, p=0.02]) were independently associated with abnormal right heart hemodynamics. ConclusionsThe results demonstrate that 11.7% of patients undergoing clinically indicated stress echocardiography have EIPH. Of those who underwent RHC abnormal hemodynamics were significantly associated with a dilated left atrium or age older than 55years.

Ventricular-Arterial Coupling and Exercise-Induced Pulmonary Hypertension During Low-Level Exercise in Heart Failure With Preserved or Reduced Ejection Fraction

BackgroundExercise-induced pulmonary hypertension (EIPH) may develop even at low workloads in heart failure (HF) patients. Ventricular-arterial stiffening plays an important role in the pathophysiology of HF with preserved ejection fraction (HFpEF). This study aimed to compare the response of ventricular-arterial coupling and PH during low-level exercise between HFpEF and HF with reduced EF (HFrEF). Methods and ResultsEchocardiography was performed at rest and during 10 W of bicycle exercise in HFpEF (n = 37) and HFrEF (n = 43). Load-independent contractility (end-systolic elastance [Ees], preload recruitable stroke work [PRSW], and peak power index [PWRI]), arterial afterload (arterial elastance [Ea]), and ventricular-arterial interaction (Ea/Ees) were measured with the use of a noninvasive single-beat technique. EIPH was defined as an estimated pulmonary arterial systolic pressure (PASP) of ≥50 mm Hg at 10 W of exercise. PASP was significantly increased during 10 W of exercise in both HF types, and ~50% of HFpEF patients developed EIPH. Arterial afterload was increased significantly during exercise in both groups. HFrEF and HFpEF patients showed a significant increase in LV contractility assessed by Ees, PRSW, and PWRI during exercise. Although Ea/Ees ratio decreased significantly in HFrEF, reduction in Ea/Ees was attenuated because of blunted Ees increases in patients with HFpEF compared with HFrEF. ConclusionsEven at low-level exercise, ~50% of HFpEF patients developed EIPH. Reduction in Ea/Ees was attenuated owing to less Ees increase in HFpEF compared with HFrEF. Further studies are needed to elucidate the association between ventricular-arterial coupling and EIPH in HFpEF.