TY - JOUR
AU - Kasprzak, Jarosław, Damian
AB - Abstract Aims Echocardiography can estimate pulmonary arterial pressure (PAP) from tricuspid regurgitation velocity (TRV) or acceleration time (ACT) of pulmonary flow. We assessed the feasibility of TRV and ACT measurements during exercise stress echocardiography (ESE) and their correlation in all stages of ESE. Methods and results We performed ESE in 102 subjects [mean age 49 ± 17 years, 50 females, 39 healthy, 30 with cardiovascular risk factors, and 33 with pulmonary hypertension (PH)] referred for the assessment of exercise tolerance and ischaemia exclusion. ESE was performed on cycloergometer with the load increasing by 25 W for each 2 min. Assessment of TRV with continuous wave and ACT with pulsed Doppler were attempted in 306 time points: at rest, peak exercise, and recovery. In 20 PH patients we evaluated the correlations of TRV and ACT with invasively measured PAP. The success rate was 183/306 for TRV and 304/306 for ACT (feasibility: 60 vs. 99%, P < 0.0001). There was a close correlation between TRV and ACT: r = 0.787, P < 0.001 and ACT at peak ≤67 ms showed 94% specificity for elevated systolic PAP detection. Moreover, TRV and ACT at peak exercise reflected better that resting data the invasive systolic PAP and mean PAP with r = 0.76, P = 0.0004 and r = −0.67, P = 0.0018, respectively. Conclusion ACT is closely correlated with and substantially more feasible than TRV during ESE and inclusion of both parameters (TRACT approach) expands the possibility of PAP assessment, especially at exercise when TRV feasibility is the lowest but correlation with invasive PAP seems to increase. systolic pulmonary artery pressure, mean pulmonary artery pressure, tricuspid regurgitation velocity, pulmonary flow acceleration time, exercise stress echocardiography Introduction The pulmonary haemodynamics are of utmost prognostic importance in many clinical conditions and right heart catheterization remains still the diagnostic gold standard despite invasiveness, risks, costs, and radiation.1,2 Transthoracic echocardiography (TTE) being widely available, safe and cost-effective can estimate systolic pulmonary arterial pressure (SPAP) from tricuspid regurgitation velocity (TRV).3,4 However, TRV requires the presence of a more than trivial tricuspid regurgitation (TR), which is found in only 50% of subjects referred to TTE. The feasibility further decreases during exercise, because of the degradation of image quality and the enhancement of contractility which may diminish TR. Despite feasibility being higher up to 61% in pulmonary hypertension (PH)5,6 the TRV loses the strength of correlation with invasive measurements in presence of massive TR and may substantially underestimate SPAP in such settings.3,7 An alternative and potentially complementary approach relay on the measurement of acceleration time (ACT) of systolic pulmonary flow velocity which is present in all subjects, and does not require a pathologic regurgitant flow as TRV8 or methods based on pulmonary regurgitation.9 ACT is closely and linearly correlated with invasively assessed pulmonary pressures10,11 and with TRV.12 It may be attractive for exercise stress echocardiography (ESE) applications, due to its high success rate also during stress, but limited evidence to date supports the use of ACT during ESE together with, or in lieu of, TRV.13 The aim of this study was to assess the feasibility of TRV and ACT, and their correlation, in consecutive patients referred for ESE in a tertiary centre for PH. For wider range of conditions, we included healthy controls (H) and patients with cardiovascular (CV) risk factors. Additionally, in 20 patients with PH, the correlation of TRV and ACT at rest and peak exercise with gold-standard invasive SPAP and mean pulmonary artery pressure (MPAP) were analysed. Methods The study, approved by the local Ethical Committee, number RNN 33/18/KE, was performed in Cardiology Department of Lodz University, Poland, from March 2016 to March 2018. All patients gave their informed consent to enter the study. Study group We included 102 subjects; 50 women, mean age 49 ± 17 years, without the contraindications to exercise referred to ESE for the assessment of exercise tolerance [PH and healthy group (H)] as well as for coronary artery disease diagnosis/exclusion. We included patients with diagnosed PH with right heart catheterization on basis of MPAP ≥25 mmHg and pharmacologically treated in our department [PH, 33 subjects, 30 patients with risk factors of coronary artery disease (CV), and 39 healthy controls]. Into healthy group, we included patients free from CV risk factors especially hypertension, diabetes, smoking, and known dyslipidaemia (defined as LDL cholesterol ≥3 mmol/L in blood tests from last year and the lack of current use of hypolipaemic treatment). As far as angina is concerned all healthy patients were asymptomatic, whereas in CV group six patients reported chest pain history. Echocardiographic assessment TTE at rest and ESE was performed with E9 (GE, Vingmed, Norway) or VIVID 7 (GE Vingmed Ultrasound AS, Horten, Norway) systems using M4S/M5S probes. During the echocardiography, an electrocardiogram (ECG) tracing was displayed on the monitor. The echocardiographic measurements (including measures of left ventricular and right ventricular function and atrial volumes) were taken following the recommendations.3,4,14 Assessment of TRV and ACT TRV was derived with continuous wave Doppler from the apical four-chamber or the parasternal right ventricular inflow view. The right ventricular systolic pressure was assumed to equal SPAP and was calculated with the Bernoulli equation (TRV in m/s): SPAP= 4 TRV2 + right atrial pressure (RAP). RAP was estimated from the inferior vena cava (IVC) diameter and collapsing during the inspiration. We added RAP of 3 mmHg (IVC diameter <2.1 cm, collapsing >50% with a sniff), or 15 mmHg (diameter >2.1 cm, collapsing ≤50% with a sniff), or 8 mmHg in mixed scenarios.3 The value calculated at rest was applied also at stress and recovery.15 ACT was measured in right ventricular outflow tract as the time in milliseconds from the beginning of the pulmonary ejection until the maximum of the systolic velocity by pulsed wave Doppler with the sample volume positioned at the annulus of the pulmonary artery, in the parasternal short axis or in the subcostal view. The normal value is >110 ms, the abnormal <105, and indeterminate between 105 and 110.5 When the heart rate exceeds 100 or drops below 70, the measurement can be indexed by heart rate dividing ACT by RR interval8,10 or square root of RR interval.16,17 From the raw data of ACT, SPAP was derived on the basis of the linear correlation linking ACT to TRV as follows: log10 SPAP= −0.004 (ACT) + 2.1.12 Exercise stress echocardiography All patients underwent semi-supine bicycle ESE as described by recent recommendations.4 The study protocol is displayed in Figure 1. ESE was performed at an initial workload of 25 W lasting for 2 min, then the workload increased stepwise by 25 W at 2-min intervals. ECG and blood pressure were monitored and all studies were performed by cardiologist experienced in different kind of stress echo examinations and analysis (K.W.D.) assisted by the nurse or the doctor. A 12-lead ECG was recorded before starting and after termination of test. Criteria for interrupting the test were chest pain, induced wall motion abnormalities, significant rhythm disturbances, excessive fatigue, blood pressure increase (systolic ≥240 mmHg, diastolic ≥120 mmHg), limiting dyspnoea, legs pain, or predicted heart rate. Echocardiographic imaging was performed from different views, using conventional two-dimensional echocardiography. Video loops of heart cycles were acquired and digitally stored for further analysis. All doctors and nurses involved were trained in Basic and Advanced Cardiac Life Support. Figure 1 Open in new tabDownload slide The study protocol with assessment of TRV and ACT for SPAP estimation. ACT, acceleration time of pulmonary flow; CW, continuous wave; ECG, electrocardiogram; PW, pulsed wave; SE, stress echocardiography; TRV, tricuspid regurgitant velocity. Figure 1 Open in new tabDownload slide The study protocol with assessment of TRV and ACT for SPAP estimation. ACT, acceleration time of pulmonary flow; CW, continuous wave; ECG, electrocardiogram; PW, pulsed wave; SE, stress echocardiography; TRV, tricuspid regurgitant velocity. Subgroup analysis of right heart catheterization data In the subgroup of 20 subjects with PH we had the resting right heart catheterization data obtained in Cardiology Department in Lodz with median difference between ESE and catheterization of 120 days, in seven patients <10 days of difference, which we used for the retrospective assessment of the correlation of ACT and TRV with invasively derived MPAP as well as with the SPAP. The remaining 13 patients had last right heart catheterization done before 48 month period and were not included to analysis. Reproducibility of Doppler measurements All echocardiographers had passed additional quality control of reading examinations as required by Stress Echo 2020 study with interobserver reproducibility ≥90%.18 All studies were performed by a single observer who also did all measurements included in database (K.W.D.). For the intraobserver variability assessment 14 patients were randomly selected and analysed after 8 weeks since the last patient enrolment and for interobserver variability assessment were done by the second observer (J.D.K.). The intraobserver and interobserver variability of ACT and TRV were expressed as intraclass correlation coefficient as well as was Bland–Altman graphs (see Supplementary data online, Figure S1 for graphs). ACT was feasible in all patients, whereas TRV in 12 patients at rest and in 9 at stress. Statistical analysis Data are expressed as mean ± standard deviation for continuous or frequency for categorical data. The distribution was assessed with the D'Agostino–Pearson test and adequate parametric or non-parametric tests were used. For correlation Pearson’s or Spearman coefficients were calculated. One-sample comparisons were performed with paired t-test, Wilcoxon test, or χ2 test for categorical data. Multiple-samples comparison was performed with analysis of variance and Newmann–Keuls test. Cut-off values were established by receiver operating curve analysis. Statistical significance was set at P < 0.05. Analyses were conducted with MedCalc V. 12.1.4. (Frank Schoonjans, Belgium). Results The repeatability was acceptable for both parameters at all ESE stages with the slightly lower variation of TRV when this parameter was feasible (see Table 1). Bland–Altman analysis confirmed the good intraobserver and interobserver agreement for both parameters (see Supplementary data online, Figure S1A and B). Table 1 The intraobserver and interobserver variability expressed as intraclass correlation coefficient (ICC) calculated in randomly chosen 14 patients Parameters/number of feasible measurements in group of 14 patients ICC intraobserver value ICC intraobserver 95% CI ICC interobserver value ICC interobserver 95% CI ACT rest (n = 14) 0.96 0.88–0.99 0.94 0.8–0.98 ACT stress (n = 14) 0.89 0.66–0.97 0.92 0.74–0.97 TRV rest (n = 12) 0.99 0.98–1.0 0.99 0.97–1.0 TRV stress (n = 9) 0.96 0.81–0.99 0.93 0.69–0.98 Parameters/number of feasible measurements in group of 14 patients ICC intraobserver value ICC intraobserver 95% CI ICC interobserver value ICC interobserver 95% CI ACT rest (n = 14) 0.96 0.88–0.99 0.94 0.8–0.98 ACT stress (n = 14) 0.89 0.66–0.97 0.92 0.74–0.97 TRV rest (n = 12) 0.99 0.98–1.0 0.99 0.97–1.0 TRV stress (n = 9) 0.96 0.81–0.99 0.93 0.69–0.98 In this group, ACT assessment was feasible in all patients, whereas TRV at rest in 12 patients and at stress in 9 patients. ACT, acceleration time of pulmonary flow; CI, confidence interval; ICC, intraclass correlation coefficient; TRV, tricuspid regurgitant velocity. Open in new tab Table 1 The intraobserver and interobserver variability expressed as intraclass correlation coefficient (ICC) calculated in randomly chosen 14 patients Parameters/number of feasible measurements in group of 14 patients ICC intraobserver value ICC intraobserver 95% CI ICC interobserver value ICC interobserver 95% CI ACT rest (n = 14) 0.96 0.88–0.99 0.94 0.8–0.98 ACT stress (n = 14) 0.89 0.66–0.97 0.92 0.74–0.97 TRV rest (n = 12) 0.99 0.98–1.0 0.99 0.97–1.0 TRV stress (n = 9) 0.96 0.81–0.99 0.93 0.69–0.98 Parameters/number of feasible measurements in group of 14 patients ICC intraobserver value ICC intraobserver 95% CI ICC interobserver value ICC interobserver 95% CI ACT rest (n = 14) 0.96 0.88–0.99 0.94 0.8–0.98 ACT stress (n = 14) 0.89 0.66–0.97 0.92 0.74–0.97 TRV rest (n = 12) 0.99 0.98–1.0 0.99 0.97–1.0 TRV stress (n = 9) 0.96 0.81–0.99 0.93 0.69–0.98 In this group, ACT assessment was feasible in all patients, whereas TRV at rest in 12 patients and at stress in 9 patients. ACT, acceleration time of pulmonary flow; CI, confidence interval; ICC, intraclass correlation coefficient; TRV, tricuspid regurgitant velocity. Open in new tab The clinical characteristics of the patients are listed in Table 2. The haemodynamic data related to ESE are presented in Table 3 and echocardiographic measurements are displayed in Table 4. Table 2 Clinical characteristics of the patients Parameters Mean value ± SD and range or n/% Age (years) 49 ± 17 (18–88) Sex (male/female) 52/51% BSA (m2) 1.89 ± 0.22 (1.4–2.4) Body mass index (kg/m2) 26 ± 4 (18–39) Pulmonary hypertension 33/32%  Idiopathic PAH 11/11%  Congenital heart disease related PH 8/8%  Connective tissue disease related PH 7/7%  Chronic thromboembolic PH 6/6%  Mitral valve disease related PH 1/1% Patients with CAD risk factors 30/29% Healthy subjects 39/38% WHO class for patients/% in PH subgroup  I 2/6%  II 22/67%  III 9/27% CAD risk factors in whole group  Hypertension 31/30%  Diabetes 5/5%  Smoking 8/8%  Hypercholesterolaemia 23/23% Treatment  ACE-I 27/27%  Ca antagonists 8/8%  Diuretics 30/30%  Digitalis 3/3%  Anticoagulants 17/17%  Antiplatelets 4/4% Parameters Mean value ± SD and range or n/% Age (years) 49 ± 17 (18–88) Sex (male/female) 52/51% BSA (m2) 1.89 ± 0.22 (1.4–2.4) Body mass index (kg/m2) 26 ± 4 (18–39) Pulmonary hypertension 33/32%  Idiopathic PAH 11/11%  Congenital heart disease related PH 8/8%  Connective tissue disease related PH 7/7%  Chronic thromboembolic PH 6/6%  Mitral valve disease related PH 1/1% Patients with CAD risk factors 30/29% Healthy subjects 39/38% WHO class for patients/% in PH subgroup  I 2/6%  II 22/67%  III 9/27% CAD risk factors in whole group  Hypertension 31/30%  Diabetes 5/5%  Smoking 8/8%  Hypercholesterolaemia 23/23% Treatment  ACE-I 27/27%  Ca antagonists 8/8%  Diuretics 30/30%  Digitalis 3/3%  Anticoagulants 17/17%  Antiplatelets 4/4% ACE-I, angiotensin-converting enzyme inhibitors; BSA, body surface area; CAD, coronary artery disease; PAH, pulmonary arterial hypertension; PH, pulmonary hypertension; SD, standard deviation; WHO, World Health Organization. Open in new tab Table 2 Clinical characteristics of the patients Parameters Mean value ± SD and range or n/% Age (years) 49 ± 17 (18–88) Sex (male/female) 52/51% BSA (m2) 1.89 ± 0.22 (1.4–2.4) Body mass index (kg/m2) 26 ± 4 (18–39) Pulmonary hypertension 33/32%  Idiopathic PAH 11/11%  Congenital heart disease related PH 8/8%  Connective tissue disease related PH 7/7%  Chronic thromboembolic PH 6/6%  Mitral valve disease related PH 1/1% Patients with CAD risk factors 30/29% Healthy subjects 39/38% WHO class for patients/% in PH subgroup  I 2/6%  II 22/67%  III 9/27% CAD risk factors in whole group  Hypertension 31/30%  Diabetes 5/5%  Smoking 8/8%  Hypercholesterolaemia 23/23% Treatment  ACE-I 27/27%  Ca antagonists 8/8%  Diuretics 30/30%  Digitalis 3/3%  Anticoagulants 17/17%  Antiplatelets 4/4% Parameters Mean value ± SD and range or n/% Age (years) 49 ± 17 (18–88) Sex (male/female) 52/51% BSA (m2) 1.89 ± 0.22 (1.4–2.4) Body mass index (kg/m2) 26 ± 4 (18–39) Pulmonary hypertension 33/32%  Idiopathic PAH 11/11%  Congenital heart disease related PH 8/8%  Connective tissue disease related PH 7/7%  Chronic thromboembolic PH 6/6%  Mitral valve disease related PH 1/1% Patients with CAD risk factors 30/29% Healthy subjects 39/38% WHO class for patients/% in PH subgroup  I 2/6%  II 22/67%  III 9/27% CAD risk factors in whole group  Hypertension 31/30%  Diabetes 5/5%  Smoking 8/8%  Hypercholesterolaemia 23/23% Treatment  ACE-I 27/27%  Ca antagonists 8/8%  Diuretics 30/30%  Digitalis 3/3%  Anticoagulants 17/17%  Antiplatelets 4/4% ACE-I, angiotensin-converting enzyme inhibitors; BSA, body surface area; CAD, coronary artery disease; PAH, pulmonary arterial hypertension; PH, pulmonary hypertension; SD, standard deviation; WHO, World Health Organization. Open in new tab Table 3 Haemodynamic findings at rest and during stress Parameters Rest Peak stress Recovery Heart rate 71 ± 12 (48–110) 131 ± 22 (78–173)* 83 ± 12 (57–110)* Systolic BP 131 ± 18 (96–174) 172 ± 31 (99–240)* 130 ± 18 (98–173) Diastolic BP 80 ± 12 (51–115) 93 ± 18 (43–181)* 79 ± 11 (59–110) O2 saturation 95 ± 6 (70–100) 92 ± 10 (55–100)* 95 ± 5 (72–100) Workload achieved (W) NA 119 ± 51 (50–225) NA Time of exercise (min) NA 9.5 ± 4 NA Tiredness in Borg scale (from 1 to 10) NA 7.7 ± 1 (4–10) NA Parameters Rest Peak stress Recovery Heart rate 71 ± 12 (48–110) 131 ± 22 (78–173)* 83 ± 12 (57–110)* Systolic BP 131 ± 18 (96–174) 172 ± 31 (99–240)* 130 ± 18 (98–173) Diastolic BP 80 ± 12 (51–115) 93 ± 18 (43–181)* 79 ± 11 (59–110) O2 saturation 95 ± 6 (70–100) 92 ± 10 (55–100)* 95 ± 5 (72–100) Workload achieved (W) NA 119 ± 51 (50–225) NA Time of exercise (min) NA 9.5 ± 4 NA Tiredness in Borg scale (from 1 to 10) NA 7.7 ± 1 (4–10) NA * P < 0.0001 (paired t-test) in comparison to rest values. BP, blood pressure; NA, not applicable. Open in new tab Table 3 Haemodynamic findings at rest and during stress Parameters Rest Peak stress Recovery Heart rate 71 ± 12 (48–110) 131 ± 22 (78–173)* 83 ± 12 (57–110)* Systolic BP 131 ± 18 (96–174) 172 ± 31 (99–240)* 130 ± 18 (98–173) Diastolic BP 80 ± 12 (51–115) 93 ± 18 (43–181)* 79 ± 11 (59–110) O2 saturation 95 ± 6 (70–100) 92 ± 10 (55–100)* 95 ± 5 (72–100) Workload achieved (W) NA 119 ± 51 (50–225) NA Time of exercise (min) NA 9.5 ± 4 NA Tiredness in Borg scale (from 1 to 10) NA 7.7 ± 1 (4–10) NA Parameters Rest Peak stress Recovery Heart rate 71 ± 12 (48–110) 131 ± 22 (78–173)* 83 ± 12 (57–110)* Systolic BP 131 ± 18 (96–174) 172 ± 31 (99–240)* 130 ± 18 (98–173) Diastolic BP 80 ± 12 (51–115) 93 ± 18 (43–181)* 79 ± 11 (59–110) O2 saturation 95 ± 6 (70–100) 92 ± 10 (55–100)* 95 ± 5 (72–100) Workload achieved (W) NA 119 ± 51 (50–225) NA Time of exercise (min) NA 9.5 ± 4 NA Tiredness in Borg scale (from 1 to 10) NA 7.7 ± 1 (4–10) NA * P < 0.0001 (paired t-test) in comparison to rest values. BP, blood pressure; NA, not applicable. Open in new tab Table 4 Echocardiographic findings Parameters Rest Peak stress Recovery TRV (cm/s) 290 ± 112 (133–567) 363 ± 143 (146–620)* 273 ± 118 (115–540)** ACT (ms) 101 ± 32 (42–175) 83 ± 26 (28–152)* 97 ± 29 (30–163) Ejection notch 24/24% 24/24% 22/22% SPAP (TRV based) (mmHg) 44 ± 33 (12–143) 71 ± 47 (14–169)* 45 ± 34 (10–132) PVR (Wood Units) 2.6 ± 1.74 (0.94–9.03) 3.12 ± 2.16 (0.76–9.0) 2.49 ± 1.86 (0.7–10.29) LV EDV (mL) 77 ± 25 (10–147) 70 ± 30 (8–145)*** NA LV ESV (mL) 31 ± 13 (6–76) 26 ± 13 (4–64)* NA LV EF (%) 60 ± 9 (29–90) 63 ± 9 (31–79) NA LA volume (mL) 52 + 24 (18–176) NA NA RA volume (mL) 55 ± 32 (18–162) NA NA RV FAC (%) 38 ± 11 (12–59) 41 ± 13***** NA TAPSE (mm) 22 ± 4 (11–31) 28 ± 8 (11–49)* 23 ± 5 (13–41)***** Parameters Rest Peak stress Recovery TRV (cm/s) 290 ± 112 (133–567) 363 ± 143 (146–620)* 273 ± 118 (115–540)** ACT (ms) 101 ± 32 (42–175) 83 ± 26 (28–152)* 97 ± 29 (30–163) Ejection notch 24/24% 24/24% 22/22% SPAP (TRV based) (mmHg) 44 ± 33 (12–143) 71 ± 47 (14–169)* 45 ± 34 (10–132) PVR (Wood Units) 2.6 ± 1.74 (0.94–9.03) 3.12 ± 2.16 (0.76–9.0) 2.49 ± 1.86 (0.7–10.29) LV EDV (mL) 77 ± 25 (10–147) 70 ± 30 (8–145)*** NA LV ESV (mL) 31 ± 13 (6–76) 26 ± 13 (4–64)* NA LV EF (%) 60 ± 9 (29–90) 63 ± 9 (31–79) NA LA volume (mL) 52 + 24 (18–176) NA NA RA volume (mL) 55 ± 32 (18–162) NA NA RV FAC (%) 38 ± 11 (12–59) 41 ± 13***** NA TAPSE (mm) 22 ± 4 (11–31) 28 ± 8 (11–49)* 23 ± 5 (13–41)***** Continuous values are expressed as mean ± standard deviation. * P < 0.0001 vs. rest, **P = 0.0001, ***P = 0.0008, ****P = 0.0042, *****P = 0.0101. PVR calculated according to Abbas formula: PVR (Wood Units) = TRV (m/s)/VTI RVOT (cm) * 10 + 0.16. ACT, acceleration time of pulmonary flow; EDV, end-diastolic volume; EF, ejection fraction; ESV, end-systolic volume; FAC, fractional area change; LA, left atrium; LV, left ventricle; PVR, pulmonary vascular resistance; RA, right atrium; RV, right ventricle; SPAP, systolic pulmonary artery pressure; TAPSE, tricuspid annulus systolic plane excursion; TRV, tricuspid regurgitant velocity. Open in new tab Table 4 Echocardiographic findings Parameters Rest Peak stress Recovery TRV (cm/s) 290 ± 112 (133–567) 363 ± 143 (146–620)* 273 ± 118 (115–540)** ACT (ms) 101 ± 32 (42–175) 83 ± 26 (28–152)* 97 ± 29 (30–163) Ejection notch 24/24% 24/24% 22/22% SPAP (TRV based) (mmHg) 44 ± 33 (12–143) 71 ± 47 (14–169)* 45 ± 34 (10–132) PVR (Wood Units) 2.6 ± 1.74 (0.94–9.03) 3.12 ± 2.16 (0.76–9.0) 2.49 ± 1.86 (0.7–10.29) LV EDV (mL) 77 ± 25 (10–147) 70 ± 30 (8–145)*** NA LV ESV (mL) 31 ± 13 (6–76) 26 ± 13 (4–64)* NA LV EF (%) 60 ± 9 (29–90) 63 ± 9 (31–79) NA LA volume (mL) 52 + 24 (18–176) NA NA RA volume (mL) 55 ± 32 (18–162) NA NA RV FAC (%) 38 ± 11 (12–59) 41 ± 13***** NA TAPSE (mm) 22 ± 4 (11–31) 28 ± 8 (11–49)* 23 ± 5 (13–41)***** Parameters Rest Peak stress Recovery TRV (cm/s) 290 ± 112 (133–567) 363 ± 143 (146–620)* 273 ± 118 (115–540)** ACT (ms) 101 ± 32 (42–175) 83 ± 26 (28–152)* 97 ± 29 (30–163) Ejection notch 24/24% 24/24% 22/22% SPAP (TRV based) (mmHg) 44 ± 33 (12–143) 71 ± 47 (14–169)* 45 ± 34 (10–132) PVR (Wood Units) 2.6 ± 1.74 (0.94–9.03) 3.12 ± 2.16 (0.76–9.0) 2.49 ± 1.86 (0.7–10.29) LV EDV (mL) 77 ± 25 (10–147) 70 ± 30 (8–145)*** NA LV ESV (mL) 31 ± 13 (6–76) 26 ± 13 (4–64)* NA LV EF (%) 60 ± 9 (29–90) 63 ± 9 (31–79) NA LA volume (mL) 52 + 24 (18–176) NA NA RA volume (mL) 55 ± 32 (18–162) NA NA RV FAC (%) 38 ± 11 (12–59) 41 ± 13***** NA TAPSE (mm) 22 ± 4 (11–31) 28 ± 8 (11–49)* 23 ± 5 (13–41)***** Continuous values are expressed as mean ± standard deviation. * P < 0.0001 vs. rest, **P = 0.0001, ***P = 0.0008, ****P = 0.0042, *****P = 0.0101. PVR calculated according to Abbas formula: PVR (Wood Units) = TRV (m/s)/VTI RVOT (cm) * 10 + 0.16. ACT, acceleration time of pulmonary flow; EDV, end-diastolic volume; EF, ejection fraction; ESV, end-systolic volume; FAC, fractional area change; LA, left atrium; LV, left ventricle; PVR, pulmonary vascular resistance; RA, right atrium; RV, right ventricle; SPAP, systolic pulmonary artery pressure; TAPSE, tricuspid annulus systolic plane excursion; TRV, tricuspid regurgitant velocity. Open in new tab No patient had induced left ventricular dysfunction but in 12 patients with PH we observed the decrease of TAPSE (delta TAPSE <0) and in 16 the decrease of right ventricular fractional area change during ESE indicating stress induced right ventricular dysfunction. Nevertheless, neither the increase of TRV nor the decrease of ACT during ESE differed between so categorized subgroups with or without right ventricular dysfunction. Furthermore, we compared feasibility and values of TRV, ACT, and their changes during ESE among studied subgroups of PH, CV, and H subjects (see Table 5). Table 5 Feasibility and results comparison of TRV, ACT, and their changes among groups Parameters PH group A = 33 CV risk factors group B = 30 Healthy group C = 39 P-value (A vs. B) P-value (A vs. C) P-value (B vs. C) Age (years), mean ± SD 57 ± 18 55 ± 17 38 ± 9 NS <0.001 <0.001 TRV at rest, n (%) 31 (94) 19 (63) 22 (56) =0.0066 =0.0008 NS ACT at rest, n (%) 33 (100) 30 (100) 39 (100) NS NS NS TRV at peak, n (%) 26 (79) 13 (43) 10 (26) =0.0074 <0.0001 NS ACT at peak, n (%) 33 (100) 29 (97) 39 (100) NS NS NS TRV at recovery, n (%) 30 (91) 15 (50) 17 (44) =0.0009 =0.0001 NS ACT at recovery, n (%) 33 (100) 29 (97) 39 (100) NS NS NS ΔTRV stress–rest, n (%) 26 (79) 11 (37) 8 (21) =0.0018 <0.0001 NS ΔTRV stress–recovery, n (%) 26 (79) 11 (37) 6 (15) =0.0018 <0.0001 NS ΔACT stress–rest, n (%) 33 (100) 29 (97) 39 (100) NS NS NS ΔACT stress–recovery, n (%) 33 (100) 28 (93) 39 (100) NS NS NS TRV at rest (cm/s), mean ± SD 386 ± 104 231 ± 57 204 ± 31 <0.0001 <0.0001 NS TRV at peak (cm/s), mean ± SD 476 ± 86 261 ± 70 204 ± 53 <0.0001 <0.0001 =0.045 TRV at recovery (cm/s), mean ± SD 362 ± 104 214 ± 50 167 ± 31 <0.0001 <0.0001 =0.0035 ACT at rest (ms), mean ± SD 68 ± 19 102 ± 19 128 ± 20 <0.0001 <0.0001 <0.0001 ACT at peak (ms), mean ± SD 60 ± 17 94 ± 22 94 ± 22 <0.0001 <0.0001 NS ACT at recovery (ms), mean ± SD 67 ± 17 106 ± 23 117 ± 17 <0.0001 <0.0001 =0.028 ΔTRV (stress–rest) (cm/s), mean ± SD 82 ± 83 49 ± 50 18 ± 50 NS 0.047 NS ΔTRV (stress–recovery) (cm/s), mean ± SD 111 ± 84 50 ± 43 33 ± 37 =0.031 =0.035 NS ΔACT (stress–rest) (ms), mean ± SD −9 ± 17 −8 ± 24 −34 ± 30 NS =0.0001 =0.0002 ΔACT (stress–recovery) (ms), mean ± SD −7 ± 15 −11 ± 23 −23 ± 26 NS =0.0034 NS Parameters PH group A = 33 CV risk factors group B = 30 Healthy group C = 39 P-value (A vs. B) P-value (A vs. C) P-value (B vs. C) Age (years), mean ± SD 57 ± 18 55 ± 17 38 ± 9 NS <0.001 <0.001 TRV at rest, n (%) 31 (94) 19 (63) 22 (56) =0.0066 =0.0008 NS ACT at rest, n (%) 33 (100) 30 (100) 39 (100) NS NS NS TRV at peak, n (%) 26 (79) 13 (43) 10 (26) =0.0074 <0.0001 NS ACT at peak, n (%) 33 (100) 29 (97) 39 (100) NS NS NS TRV at recovery, n (%) 30 (91) 15 (50) 17 (44) =0.0009 =0.0001 NS ACT at recovery, n (%) 33 (100) 29 (97) 39 (100) NS NS NS ΔTRV stress–rest, n (%) 26 (79) 11 (37) 8 (21) =0.0018 <0.0001 NS ΔTRV stress–recovery, n (%) 26 (79) 11 (37) 6 (15) =0.0018 <0.0001 NS ΔACT stress–rest, n (%) 33 (100) 29 (97) 39 (100) NS NS NS ΔACT stress–recovery, n (%) 33 (100) 28 (93) 39 (100) NS NS NS TRV at rest (cm/s), mean ± SD 386 ± 104 231 ± 57 204 ± 31 <0.0001 <0.0001 NS TRV at peak (cm/s), mean ± SD 476 ± 86 261 ± 70 204 ± 53 <0.0001 <0.0001 =0.045 TRV at recovery (cm/s), mean ± SD 362 ± 104 214 ± 50 167 ± 31 <0.0001 <0.0001 =0.0035 ACT at rest (ms), mean ± SD 68 ± 19 102 ± 19 128 ± 20 <0.0001 <0.0001 <0.0001 ACT at peak (ms), mean ± SD 60 ± 17 94 ± 22 94 ± 22 <0.0001 <0.0001 NS ACT at recovery (ms), mean ± SD 67 ± 17 106 ± 23 117 ± 17 <0.0001 <0.0001 =0.028 ΔTRV (stress–rest) (cm/s), mean ± SD 82 ± 83 49 ± 50 18 ± 50 NS 0.047 NS ΔTRV (stress–recovery) (cm/s), mean ± SD 111 ± 84 50 ± 43 33 ± 37 =0.031 =0.035 NS ΔACT (stress–rest) (ms), mean ± SD −9 ± 17 −8 ± 24 −34 ± 30 NS =0.0001 =0.0002 ΔACT (stress–recovery) (ms), mean ± SD −7 ± 15 −11 ± 23 −23 ± 26 NS =0.0034 NS ACT, acceleration time of pulmonary flow; CV, cardiovascular; NS, not significant; PH, pulmonary hypertension; TRV, tricuspid regurgitant velocity; Δ, delta; =, difference. Open in new tab Table 5 Feasibility and results comparison of TRV, ACT, and their changes among groups Parameters PH group A = 33 CV risk factors group B = 30 Healthy group C = 39 P-value (A vs. B) P-value (A vs. C) P-value (B vs. C) Age (years), mean ± SD 57 ± 18 55 ± 17 38 ± 9 NS <0.001 <0.001 TRV at rest, n (%) 31 (94) 19 (63) 22 (56) =0.0066 =0.0008 NS ACT at rest, n (%) 33 (100) 30 (100) 39 (100) NS NS NS TRV at peak, n (%) 26 (79) 13 (43) 10 (26) =0.0074 <0.0001 NS ACT at peak, n (%) 33 (100) 29 (97) 39 (100) NS NS NS TRV at recovery, n (%) 30 (91) 15 (50) 17 (44) =0.0009 =0.0001 NS ACT at recovery, n (%) 33 (100) 29 (97) 39 (100) NS NS NS ΔTRV stress–rest, n (%) 26 (79) 11 (37) 8 (21) =0.0018 <0.0001 NS ΔTRV stress–recovery, n (%) 26 (79) 11 (37) 6 (15) =0.0018 <0.0001 NS ΔACT stress–rest, n (%) 33 (100) 29 (97) 39 (100) NS NS NS ΔACT stress–recovery, n (%) 33 (100) 28 (93) 39 (100) NS NS NS TRV at rest (cm/s), mean ± SD 386 ± 104 231 ± 57 204 ± 31 <0.0001 <0.0001 NS TRV at peak (cm/s), mean ± SD 476 ± 86 261 ± 70 204 ± 53 <0.0001 <0.0001 =0.045 TRV at recovery (cm/s), mean ± SD 362 ± 104 214 ± 50 167 ± 31 <0.0001 <0.0001 =0.0035 ACT at rest (ms), mean ± SD 68 ± 19 102 ± 19 128 ± 20 <0.0001 <0.0001 <0.0001 ACT at peak (ms), mean ± SD 60 ± 17 94 ± 22 94 ± 22 <0.0001 <0.0001 NS ACT at recovery (ms), mean ± SD 67 ± 17 106 ± 23 117 ± 17 <0.0001 <0.0001 =0.028 ΔTRV (stress–rest) (cm/s), mean ± SD 82 ± 83 49 ± 50 18 ± 50 NS 0.047 NS ΔTRV (stress–recovery) (cm/s), mean ± SD 111 ± 84 50 ± 43 33 ± 37 =0.031 =0.035 NS ΔACT (stress–rest) (ms), mean ± SD −9 ± 17 −8 ± 24 −34 ± 30 NS =0.0001 =0.0002 ΔACT (stress–recovery) (ms), mean ± SD −7 ± 15 −11 ± 23 −23 ± 26 NS =0.0034 NS Parameters PH group A = 33 CV risk factors group B = 30 Healthy group C = 39 P-value (A vs. B) P-value (A vs. C) P-value (B vs. C) Age (years), mean ± SD 57 ± 18 55 ± 17 38 ± 9 NS <0.001 <0.001 TRV at rest, n (%) 31 (94) 19 (63) 22 (56) =0.0066 =0.0008 NS ACT at rest, n (%) 33 (100) 30 (100) 39 (100) NS NS NS TRV at peak, n (%) 26 (79) 13 (43) 10 (26) =0.0074 <0.0001 NS ACT at peak, n (%) 33 (100) 29 (97) 39 (100) NS NS NS TRV at recovery, n (%) 30 (91) 15 (50) 17 (44) =0.0009 =0.0001 NS ACT at recovery, n (%) 33 (100) 29 (97) 39 (100) NS NS NS ΔTRV stress–rest, n (%) 26 (79) 11 (37) 8 (21) =0.0018 <0.0001 NS ΔTRV stress–recovery, n (%) 26 (79) 11 (37) 6 (15) =0.0018 <0.0001 NS ΔACT stress–rest, n (%) 33 (100) 29 (97) 39 (100) NS NS NS ΔACT stress–recovery, n (%) 33 (100) 28 (93) 39 (100) NS NS NS TRV at rest (cm/s), mean ± SD 386 ± 104 231 ± 57 204 ± 31 <0.0001 <0.0001 NS TRV at peak (cm/s), mean ± SD 476 ± 86 261 ± 70 204 ± 53 <0.0001 <0.0001 =0.045 TRV at recovery (cm/s), mean ± SD 362 ± 104 214 ± 50 167 ± 31 <0.0001 <0.0001 =0.0035 ACT at rest (ms), mean ± SD 68 ± 19 102 ± 19 128 ± 20 <0.0001 <0.0001 <0.0001 ACT at peak (ms), mean ± SD 60 ± 17 94 ± 22 94 ± 22 <0.0001 <0.0001 NS ACT at recovery (ms), mean ± SD 67 ± 17 106 ± 23 117 ± 17 <0.0001 <0.0001 =0.028 ΔTRV (stress–rest) (cm/s), mean ± SD 82 ± 83 49 ± 50 18 ± 50 NS 0.047 NS ΔTRV (stress–recovery) (cm/s), mean ± SD 111 ± 84 50 ± 43 33 ± 37 =0.031 =0.035 NS ΔACT (stress–rest) (ms), mean ± SD −9 ± 17 −8 ± 24 −34 ± 30 NS =0.0001 =0.0002 ΔACT (stress–recovery) (ms), mean ± SD −7 ± 15 −11 ± 23 −23 ± 26 NS =0.0034 NS ACT, acceleration time of pulmonary flow; CV, cardiovascular; NS, not significant; PH, pulmonary hypertension; TRV, tricuspid regurgitant velocity; Δ, delta; =, difference. Open in new tab TRV measurements The technical success rate was 71% at baseline, decreased significantly at peak stress to 48% and again rose to 61% at recovery (see Figure 2). Moreover, when comparing the TRV feasibility between the subgroups the values for peak exercise was 79% in PH, only 26% in controls and 43% in patients with CV risk factors (see Table 5). In the whole group, TRV increased during stress from 290 ± 112 cm/s at rest to 363 ± 143 cm/s at peak stress, P < 0.0001 and again decreased in the recovery phase to 273 ± 118 cm/s, P = 0.0001 vs. stress, P = not significant (NS) for recovery vs. rest value. Figure 2 Open in new tabDownload slide The feasibility rate of TRV and ACT in the three study conditions: rest; peak stress; and recovery. ACT, acceleration time of pulmonary flow; TRV, tricuspid regurgitant velocity. Figure 2 Open in new tabDownload slide The feasibility rate of TRV and ACT in the three study conditions: rest; peak stress; and recovery. ACT, acceleration time of pulmonary flow; TRV, tricuspid regurgitant velocity. On the basis of the proposed cut-off of hypertensive response defined as exercise SPAP ≥43 mmHg PH was confirmed with TRV-based SPAP in 32 patients from 49 feasible for the TRV assessment. TRV in all stages was significantly higher in PH patients when compared with healthy (H) and CV risk subjects. Moreover, TRV at peak and recovery was higher in patients with CV risk factors than in healthy group. As far as the changes during stress echocardiography (SE) are concerned, TRV increased the most in patients with PH and the least in healthy (see Table 5). ACT measurements The technical success rate was 100% at baseline, and did not decrease significantly at peak stress or in the recovery achieving in both these stages 99% (Figure 2). ACT decreased during stress (rest = 101 ± 32 ms vs. stress = 83 ± 26 ms, P < 0.0001) and re-increased in the recovery phase (97 ± 29 ms, P < 0.0001 vs. stress, P = NS vs. rest). On the basis of SPAP value ≥43 mmHg we observed abnormal response in 43 patients according to ACT-based SPAP. When limiting the comparison to the group with both available stress data (n = 49) we observed elevated ACT-based SPAP in 32 patients. Receiver operating curves analysis provided cut-off value for ACT at peak ESE ≤67 ms, which was 67% sensitive and 94% specific for detection of elevated exercise SPAP, with area under curve (AUC) 0.841 and P < 0.0001. In turn, ACT at rest ≤106 ms revealed 94% sensitivity and 69% specificity for prediction of exercise SPAP based on TRV ≥43 mmHg with AUC 0.883, P < 0.0001. Contrary to absolute value of ACT, neither the delta ACT nor the percentage of ACT change related to ACT at rest [(ACT rest-ACT stress)/ACT at rest] indicated significant increase of SPAP because shortening of ACT during ESE was also present in subjects without PH. ACT duration in all stages was significantly shorter in PH when compared with H and CV groups. In all compared groups ACT at peak shortened when compared with rest and recovery values. The value of this shortening was however the highest in H who started with the longest ACT at rest (ΔACT stress–rest −34 ± 30 ms in H vs. −9 ± 17 in PH group and −8 ± 24 ms in CV patients, P = 0.0001 and P = 0.0002, respectively for both comparisons) (see Table 5). Integrated TRACT approach: feasibility and TRV/ACT correlation We tested the feasibility of TRACT approach combining both parameters during all stages of ESE, which afforded 100% feasibility of non-invasive SPAP estimation for each ESE stage based on at least one parameter from TRV (treated as first choice when feasible) and ACT. There was a good linear correlation between TRV and ACT (Figure 3A), which was not improved after heart rate correction neither with ACT/RR interval (R2 = 0.35, r = 0.592, P < 0.001) nor ACT/square root of RR interval (R2 = 0.53, r = 0.728, P < 0.001) but was slightly improved (R2 = 0.62, r = 0.787, P < 0.001) with a quadratic equation implemented (Figure 3B). Figure 3 Open in new tabDownload slide The correlation between TRV and ACT for all data points (rest, peak stress, and recovery measurements) of all patients with both data available. (A) Linear correlation. (B) Quadratic correlation. ACT, acceleration time of pulmonary flow; R2, coefficient of determination; TRV, tricuspid regurgitant velocity. Figure 3 Open in new tabDownload slide The correlation between TRV and ACT for all data points (rest, peak stress, and recovery measurements) of all patients with both data available. (A) Linear correlation. (B) Quadratic correlation. ACT, acceleration time of pulmonary flow; R2, coefficient of determination; TRV, tricuspid regurgitant velocity. For separate ESE stages the correlation coefficient between ACT and TRV was the highest at recovery r = −0.78 (red circles), lower at rest −0.73 (green), and at stress −0.64 (white). However, in all stages the correlation was highly significant with P < 0.001 and the differences between stages did not reach significance, P = NS. On the basis of the pre-determined SPAP values at rest (>35 mmHg) and during stress (>43 mmHg), the concordance between TRV and ACT in identifying abnormal SPAP was 92% at rest, and 76% during stress. The correlation between TRV and ACT in patients with PH did not differ as the function of PH aetiology being similar in 11 patients with idiopathic PH (r = −0.71 at rest, −0.51 at stress, and −0.77 at recovery) and in 22 patients with secondary PH (r = −0.63 at rest, −0.49 at stress, and −0.67 at recovery) for all stages, P = NS. SPAP estimated with both methods (from TRV and ACT) correlated significantly in all ESE stages with r = 0.75 at rest, P < 0.0001, r = 0.68 at peak stress, P < 0.0001 and r = 0.83 at recovery, P < 0.001. Correlation between TRV/ACT and invasive data In the subgroup of 20 PH patients, we analysed the invasive measurements of pulmonary arterial pressure (PAP) done by the resting catheterization (see Table 6). Table 6 Demographic and invasive parameters in 20 patients with PH with available right heart catheterization data Parameters Mean and standard deviation Range Age (years) 60 ± 13 33–78 SPAP (mmHg) 70 ± 26 34–122 MPAP (mmHg) 47 ± 17 21–85 RAP (mmHg) 7 ± 6 0–19 PCWP (mmHg) 10 ± 5 3–18 Parameters Mean and standard deviation Range Age (years) 60 ± 13 33–78 SPAP (mmHg) 70 ± 26 34–122 MPAP (mmHg) 47 ± 17 21–85 RAP (mmHg) 7 ± 6 0–19 PCWP (mmHg) 10 ± 5 3–18 MPAP, mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; RAP, right atrial pressure; SPAP, systolic pulmonary artery pressure. Open in new tab Table 6 Demographic and invasive parameters in 20 patients with PH with available right heart catheterization data Parameters Mean and standard deviation Range Age (years) 60 ± 13 33–78 SPAP (mmHg) 70 ± 26 34–122 MPAP (mmHg) 47 ± 17 21–85 RAP (mmHg) 7 ± 6 0–19 PCWP (mmHg) 10 ± 5 3–18 Parameters Mean and standard deviation Range Age (years) 60 ± 13 33–78 SPAP (mmHg) 70 ± 26 34–122 MPAP (mmHg) 47 ± 17 21–85 RAP (mmHg) 7 ± 6 0–19 PCWP (mmHg) 10 ± 5 3–18 MPAP, mean pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; RAP, right atrial pressure; SPAP, systolic pulmonary artery pressure. Open in new tab TRV showed significant positive correlation with invasive SPAP and MPAP, the strongest for TRV at stress with invasive SPAP, r = 0.76, P = 0.0004. For ACT significant inverse correlation was observed for exercise and recovery with the best correlation for ACT measured at stress and invasive MPAP, rho = −0.67, P = 0.0018, data in Table 7. Table 7 Correlation assessment between echocardiographic ACT and TRV vs. MPAP and SPAP measured invasively ESE stage ACT vs. MPAP TRV vs. MPAP r P-value R P-value Rest −0.35 NS 0.59 0.0095 Stress −0.67 0.0018 0.53 0.0286 Recovery −0.59 0.0073 0.47 0.0499 ACT vs. SPAP TRV vs. SPAP r P-value r P-value Rest −0.34 NS 0.54 0.0221 Stress −0.54 0.0267 0.76 0.0004 Recovery −0.52 0.0305 0.58 0.0113 ESE stage ACT vs. MPAP TRV vs. MPAP r P-value R P-value Rest −0.35 NS 0.59 0.0095 Stress −0.67 0.0018 0.53 0.0286 Recovery −0.59 0.0073 0.47 0.0499 ACT vs. SPAP TRV vs. SPAP r P-value r P-value Rest −0.34 NS 0.54 0.0221 Stress −0.54 0.0267 0.76 0.0004 Recovery −0.52 0.0305 0.58 0.0113 ACT, acceleration time of pulmonary flow; ESE, exercise stress echocardiography; MPAP, mean pulmonary artery pressure; NS, not significant; r, correlation coefficient; calculated by Pearson for TRV, Spearman for ACT; SPAP, systolic pulmonary artery pressure; TRV, tricuspid regurgitant velocity. Open in new tab Table 7 Correlation assessment between echocardiographic ACT and TRV vs. MPAP and SPAP measured invasively ESE stage ACT vs. MPAP TRV vs. MPAP r P-value R P-value Rest −0.35 NS 0.59 0.0095 Stress −0.67 0.0018 0.53 0.0286 Recovery −0.59 0.0073 0.47 0.0499 ACT vs. SPAP TRV vs. SPAP r P-value r P-value Rest −0.34 NS 0.54 0.0221 Stress −0.54 0.0267 0.76 0.0004 Recovery −0.52 0.0305 0.58 0.0113 ESE stage ACT vs. MPAP TRV vs. MPAP r P-value R P-value Rest −0.35 NS 0.59 0.0095 Stress −0.67 0.0018 0.53 0.0286 Recovery −0.59 0.0073 0.47 0.0499 ACT vs. SPAP TRV vs. SPAP r P-value r P-value Rest −0.34 NS 0.54 0.0221 Stress −0.54 0.0267 0.76 0.0004 Recovery −0.52 0.0305 0.58 0.0113 ACT, acceleration time of pulmonary flow; ESE, exercise stress echocardiography; MPAP, mean pulmonary artery pressure; NS, not significant; r, correlation coefficient; calculated by Pearson for TRV, Spearman for ACT; SPAP, systolic pulmonary artery pressure; TRV, tricuspid regurgitant velocity. Open in new tab Discussion Key findings We documented low feasibility of TRV measurements during ESE, despite utilizing different views, which especially limited the assessment of exercise-related TRV changes in subjects without PH. On the contrary, ACT feasibility was excellent also in healthy controls since it is based on a physiologic flow normally present in all subjects and detectable with a multiview approach, with high utility of subcostal view. When both TRV and ACT were available, they showed a good correlation between them and with invasively assessed gold standard PAP. Stress TRV and ACT correlated better than their resting values with resting invasive PAP. TRV is better correlated with SPAP, and ACT with MPAP. The characteristic pattern observed during ESE includes TRV increases during exercise and slightly decrease below resting level at recovery, whereas ACT shortens to its minimal values at peak stage. The increase of TRV was more pronounced in PH patients, whereas ACT shortening expressed as delta value was the largest in healthy group although in absolute values ACT reached its nadir of 60 ± 17 ms (correlating with high pulmonary MPAP) in PH group (see Table 5). Comparison with previous studies Our findings are consistent with recently published meta-analysis of eight studies with comparison of TRV, ACT, and right heart catheterization data, which showed a feasibility of TRV at rest averaging 50% and ranging from 24% to 86%, in sharp contrast with the ACT feasibility >90%.11 Moreover, Schneider et al.6 documented significant variability of resting TRV value when measured from different echocardiographic views. This elaborated multiview approach with five different measurements of TRV, done in 65 patients from whom 83% had PH, resulted in accepting higher peak TRV in 32% of patients in comparison to estimated from right ventricular focused apical view, which challenges one-view and one-parameter based strategy. Our results are not only concordant with cited studies but adds data to very limited so far evidence concerning peak and recovery stage of ESE indicating that the combination of TRV and ACT allows the evaluation of SPAP in practically all patients at rest and during ESE. Our data are also consistent with previous studies showing a good-to-excellent correlation between ACT and TRV at rest12 and an excellent concordance between TRV and ACT in identifying abnormal responses during exercise SE in limited series of patients with overt (n = 22) or preclinical (n = 8) PH.13 However, no data are available with the direct head-to-head comparison of the two indices at rest and during ESE in the garden variety of patients ranging from healthy and fit (with normal SPAP at rest and stress) to severely diseased. Clinical implications Recent expert consensus recommends TRV as the key index with ACT as a complimentary one.1 One of the reasons of its ancillary role is the lack of data at the moment of writing, but the situation is rapidly changing.11 The integrated TRACT approach allows to obtain information on SPAP with ACT in almost all patients, even when TRV is not feasible. It also provides insight on MPAP, which is better correlated to ACT than TRV. However, estimated SPAP values are flow-dependent and this is especially important during ESE, when transpulmonary flow can increase by 2-to-10 times with unpredictable inter-individual variability.1,19 The estimation of pulmonary pressures with close to 100% feasibility is the necessary conceptual and methodological prerequisite to gain insight into pulmonary vascular resistances, which are the key variable for a more comprehensive assessment of pulmonary haemodynamics derived from the Ohm’s law: pressure = flow × resistances.1 Once pressures are estimated, flow can be incorporated during ESE from measurement of cardiac output from Doppler measures or even with the proxy of minutes of exercise.20 In this way, a measurement of pulmonary vascular resistances can be derived, which is far less dependent than SPAP from flow and is therefore potentially more informative.1,4 Limitations The lack of the simultaneously taken invasive data of PAP in wider range of analysed subjects, forms the main limitation of our study, which however was focused on the feasibility of the ACT and TRV assessment in consecutive stages of ESE. The echocardiographers were not blinded to the study condition since the increased heart rate is associated with peak exercise. Also the acquisition of both parameters was not simultaneous but data were recorded in sequential manner, although with starving for the closest time-proximity. For SPAP estimation based on TRV for all ESE stages we added the value of RAP estimated according to IVC dimension and collapsibility measured at rest, which was related to impediments of the accurate assessment of IVC respiratory changes during exercise-induced tachypnoe. Finally, we did not use saline microbubble injection as an attempt to enhance TRV spectrum since this manoeuvre requires intravenous injections and further complication of an already technically demanding ESE study. Conclusion ACT is closely correlated with and substantially more feasible than TRV during ESE. The approach integrating both parameters in ‘TRACT’ protocol provides an insight into pulmonary pressures in almost all patients and should be included and tested in further studies. Funding The work was partially supported in the framework of ERASMUS PLUS training grant for Staff received by K.W.D. for travel and stay in CNR in Pisa. The study was supported by a travel grant of Erasmus plus staff training mobility from Poland to Pisa for K.W.D. (agreement number 33). Conflict of interest: none declared. References 1 Rudski LG , Gargani L , Armstrong W , Lancellotti P , Lester S , Grunig E et al. Stressing the cardiopulmonary vascular system: the role of echocardiography . J Am Soc Echocardiogr 2018 ; 31 : 527 – 50 . 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Google Scholar Crossref Search ADS PubMed WorldCat Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)
TI - The feasibility and clinical implication of tricuspid regurgitant velocity and pulmonary flow acceleration time evaluation for pulmonary pressure assessment during exercise stress echocardiography
JF - European Heart Journal - Cardiovascular Imaging
DO - 10.1093/ehjci/jez029
DA - 2019-09-01
UR - https://www.deepdyve.com/lp/oxford-university-press/the-feasibility-and-clinical-implication-of-tricuspid-regurgitant-Cr1Vergb4z
SP - 1027
VL - 20
IS - 9
DP - DeepDyve
ER -