Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa1430
O. Nishiyama, Kazuya Yoshikawa, S. Saeki, Ryo Yamazaki, H. Sano, T. Iwanaga, Y. Tohda
{"title":"Body mass index predicts survival in patients with pulmonary hypertension in chronic lung disease","authors":"O. Nishiyama, Kazuya Yoshikawa, S. Saeki, Ryo Yamazaki, H. Sano, T. Iwanaga, Y. Tohda","doi":"10.1183/13993003.congress-2019.pa1430","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa1430","url":null,"abstract":"","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87646626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa1418
E. Schiavi, S. Cantoni, G. Volpi, M. Cont, F. Pastore, S. Cavalli, F. Dardi, G. Villetti, F. Facchinetti
{"title":"Macitentan modulates pulmonary mRNA levels of gremlin 1 in a rat model of pulmonary arterial hypertension","authors":"E. Schiavi, S. Cantoni, G. Volpi, M. Cont, F. Pastore, S. Cavalli, F. Dardi, G. Villetti, F. Facchinetti","doi":"10.1183/13993003.congress-2019.pa1418","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa1418","url":null,"abstract":"","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87211075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa1426
A. Kapasi, K. Halloran, A. Hirji, D. Lien, J. Mooney, R. Raj, A. Sweatt, J. Weinkauf, R. Zamanian
Pulmonary hypertension (PH) is a common finding in chronic obstructive pulmonary disease (COPD) and is associated with poor outcomes. Our objective was to evaluate the survival implications of PH in end-stage COPD. Methods: We performed a retrospective review of adult COPD patients in the Scientific Registry of Transplant Recipients between Jan 2005 and Dec 2014. Patients were classified as: PH absent (mean pulmonary artery pressure (mPAP) Borderline PH, preserved pulmonary vascular resistance (PVR) (mPAP 21-24 mmHg, PVR Borderline PH, high PVR (PVR ≥3 WU) PH, non-elevated PVR (mPAP 25-34 mmHg, PVR PH, high PVR (PVR ≥3 WU) Severe PH (mPAP ≥35 mmHg) Groups were evaluated by log rank test and Cox regression modeling. Patients were censored at transplant. Results: Of 4339 patients, 2287 (53%) had PH, 438 (10%) had severe PH, and 1229 died. Median survival was 4.5y (95% CI 4.1-5y) in group 1, and 2.8y (95% CI 2.5-3.6y) in group 6 (p Conclusions: COPD patients with borderline PH and PH had similarly increased risks of death (regardless of PVR), and those with severe PH had a further increase in risk. These findings are distinct from other lung diseases such as IPF, and suggest the need for a separate ontology for COPD-PH.
{"title":"Survival implications of pulmonary hypertension in end-stage COPD","authors":"A. Kapasi, K. Halloran, A. Hirji, D. Lien, J. Mooney, R. Raj, A. Sweatt, J. Weinkauf, R. Zamanian","doi":"10.1183/13993003.congress-2019.pa1426","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa1426","url":null,"abstract":"Pulmonary hypertension (PH) is a common finding in chronic obstructive pulmonary disease (COPD) and is associated with poor outcomes. Our objective was to evaluate the survival implications of PH in end-stage COPD. Methods: We performed a retrospective review of adult COPD patients in the Scientific Registry of Transplant Recipients between Jan 2005 and Dec 2014. Patients were classified as:\u0000 PH absent (mean pulmonary artery pressure (mPAP) Borderline PH, preserved pulmonary vascular resistance (PVR) (mPAP 21-24 mmHg, PVR Borderline PH, high PVR (PVR ≥3 WU) PH, non-elevated PVR (mPAP 25-34 mmHg, PVR PH, high PVR (PVR ≥3 WU) Severe PH (mPAP ≥35 mmHg) Groups were evaluated by log rank test and Cox regression modeling. Patients were censored at transplant. Results: Of 4339 patients, 2287 (53%) had PH, 438 (10%) had severe PH, and 1229 died. Median survival was 4.5y (95% CI 4.1-5y) in group 1, and 2.8y (95% CI 2.5-3.6y) in group 6 (p Conclusions: COPD patients with borderline PH and PH had similarly increased risks of death (regardless of PVR), and those with severe PH had a further increase in risk. These findings are distinct from other lung diseases such as IPF, and suggest the need for a separate ontology for COPD-PH.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90497884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5469
Lucy Robertson, K. Oates, A. Fletcher, K. Sylvester
Background: Peak VO2 is the gold standard for assessing exercise capacity but 6 minute walk distance (6MWD) is mostly used surrogate measure. However, body mass may influence the predictive ability of 6MWD. Hence, 6 minute walk work (6MWW=6MWD X bodyweight) is an alternative measure but has not been fully investigated in all pulmonary vascular disease (PVD) groups. Aims: In PVD patients; 1) To determine whether 6MWW and/or other clinical parameters correlate with peak VO2. 2) Investigate the ability to predict peak VO2 from other measures, such as 6MWW. Method: Clinical data was retrospectively analysed from 38 chronic thromboembolic pulmonary hypertension (CTEPH),41 chronic thromboembolic disease (CTED), and 13 pulmonary hypertension (PH) patients. 6MWD, 6MWW, lung function, echocardiogram and right heart catheter (RHC) data were correlated with peak VO2. Results: A number of 6 minute walk measures, lung function, RHC and echocardiogram parameters correlated to peak VO2. Amongst the PVD groups 6MWW and TLCO were the highest correlated to peak VO2 (Table 1). Following linear regression analysis a predictive equation was produced in CTEPH and CTED groups. CTEPH=VO2 (ml/min) = - 252 + 0.049*6MWW (R2 = 0.79) CTED=VO2 (ml/min) = - 266 + 0.028*6MWW + 147.6*TLCO (adjusted R2 = 0.78). Conclusion: 6MWW is highly correlated to peak VO2 in PVD suggesting body mass does influence the predictive power of 6MWD. Further work is needed to validate the generated predicted equations.
{"title":"6 minute walk work and other clinical correlates of peak VO2 in pulmonary vascular disease","authors":"Lucy Robertson, K. Oates, A. Fletcher, K. Sylvester","doi":"10.1183/13993003.congress-2019.pa5469","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5469","url":null,"abstract":"Background: Peak VO2 is the gold standard for assessing exercise capacity but 6 minute walk distance (6MWD) is mostly used surrogate measure. However, body mass may influence the predictive ability of 6MWD. Hence, 6 minute walk work (6MWW=6MWD X bodyweight) is an alternative measure but has not been fully investigated in all pulmonary vascular disease (PVD) groups. Aims: In PVD patients; 1) To determine whether 6MWW and/or other clinical parameters correlate with peak VO2. 2) Investigate the ability to predict peak VO2 from other measures, such as 6MWW. Method: Clinical data was retrospectively analysed from 38 chronic thromboembolic pulmonary hypertension (CTEPH),41 chronic thromboembolic disease (CTED), and 13 pulmonary hypertension (PH) patients. 6MWD, 6MWW, lung function, echocardiogram and right heart catheter (RHC) data were correlated with peak VO2. Results: A number of 6 minute walk measures, lung function, RHC and echocardiogram parameters correlated to peak VO2. Amongst the PVD groups 6MWW and TLCO were the highest correlated to peak VO2 (Table 1). Following linear regression analysis a predictive equation was produced in CTEPH and CTED groups. CTEPH=VO2 (ml/min) = - 252 + 0.049*6MWW (R2 = 0.79) CTED=VO2 (ml/min) = - 266 + 0.028*6MWW + 147.6*TLCO (adjusted R2 = 0.78). Conclusion: 6MWW is highly correlated to peak VO2 in PVD suggesting body mass does influence the predictive power of 6MWD. Further work is needed to validate the generated predicted equations.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82290932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa5045
Martin Connolly, S. Wort, B. Garfield, A. Crosby, N. Morrell, P. Kemp
MicroRNAs (miRNAs) are small, non-coding RNAs, implicated in the control of myocardial homeostasis. miR-1 has been shown to be down-regulated in hypertrophying rodent hearts and its restoration an ameliorating factor. We used monocrotaline treatment to induce pulmonary hypertension in a cohort of rats and thereafter-showed miR-1 expression was reduced in the hypertrophying right ventricle (RV) (Fig. 1A). Bioinformatic analysis identified TGF-βR1 (ALK5) as a predicted target for miR-1, the expression of which was increased in the RV (Fig. 1B, C). Cell transfection with a miR-1-mimic reduced GFP expression from a reporter vector containing the ALK5 3’-UTR and also knocked down endogenous ALK5. Lastly, miR-1 reduced TGF-β activation of a SMAD2/3-dependent reporter. Taken together, these data confirm miR-1 targets TGF-βR1 thereby reducing TGF-β signalling, which may regulate cardiac hypertrophy.
{"title":"MiR-1-5p targets TGF-ßR1 and is suppressed in the hypertrophying hearts of rats with pulmonary arterial hypertension","authors":"Martin Connolly, S. Wort, B. Garfield, A. Crosby, N. Morrell, P. Kemp","doi":"10.1183/13993003.congress-2019.pa5045","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa5045","url":null,"abstract":"MicroRNAs (miRNAs) are small, non-coding RNAs, implicated in the control of myocardial homeostasis. miR-1 has been shown to be down-regulated in hypertrophying rodent hearts and its restoration an ameliorating factor. We used monocrotaline treatment to induce pulmonary hypertension in a cohort of rats and thereafter-showed miR-1 expression was reduced in the hypertrophying right ventricle (RV) (Fig. 1A). Bioinformatic analysis identified TGF-βR1 (ALK5) as a predicted target for miR-1, the expression of which was increased in the RV (Fig. 1B, C). Cell transfection with a miR-1-mimic reduced GFP expression from a reporter vector containing the ALK5 3’-UTR and also knocked down endogenous ALK5. Lastly, miR-1 reduced TGF-β activation of a SMAD2/3-dependent reporter. Taken together, these data confirm miR-1 targets TGF-βR1 thereby reducing TGF-β signalling, which may regulate cardiac hypertrophy.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84194981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa1417
A. Petrović, D. Kosanovic, O. Pak, Jan Niklas Schneider, A. Sydykov, N. Weissmann, W. Seeger, R. Schermuly
{"title":"Pharmacological inhibition of carbonic anhydrases 9 and 12 attenuates monocrotaline-induced pulmonary hypertension in rats","authors":"A. Petrović, D. Kosanovic, O. Pak, Jan Niklas Schneider, A. Sydykov, N. Weissmann, W. Seeger, R. Schermuly","doi":"10.1183/13993003.congress-2019.pa1417","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa1417","url":null,"abstract":"","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91545345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa1443
I. Campean, R. Sadushi-Koliçi, H. Beckmann, I. Shafran, Nika Skoro Sajer, I. Lang
{"title":"Iron Deficiency in Chronic Thromboembolic Pulmonary Hypertension","authors":"I. Campean, R. Sadushi-Koliçi, H. Beckmann, I. Shafran, Nika Skoro Sajer, I. Lang","doi":"10.1183/13993003.congress-2019.pa1443","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa1443","url":null,"abstract":"","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75745736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.oa5161
Ina Jeong, T. Fernandes, M. Alotaibi, N. Kim
Background: Patients with chronic thromboembolic pulmonary hypertension (CTEPH) should be on lifelong, effective anticoagulant therapy. The safety and efficacy of direct oral anticoagulant (DOAC) in CTEPH is unknown. Aim: To evaluate the trend of DOAC usage and correlation with subacute thrombus detection at time of pulmonary thromboendarterectomy. Methods: We performed a retrospective analysis of 405 consecutive pulmonary thromboendarterectomy (PTE) cases at the University of California, San Diego from July 2015 through July 2017. The PTE specimen were reviewed for the presence of acute or subacute thrombotic material removed at the time of PTE. Results: Of 405 consecutive PTE cases, 239 (59.0%) presented on either oral vitamin-K antagonist or chronic injectable therapy; 166 patients (41%) were anticoagulated with DOACs. There were no significant differences in baseline characteristics between DOAC and non-DOAC groups. Evidence of acute or subacute thrombi was observed in 16 (6.7%) within the non-DOAC group versus 22 (13.3%) in the DOAC group. The odds ratio (OR) of DOACs usage and evidence of recent thrombosis was 2.34 (95% CI, 1.09-5.01, p=0.028) after adjusting for age, gender, race, BMI, and history of antiphospholipid antibody syndrome. Conclusions: CTEPH patients referred for PTE while on DOAC therapy were twice as likely to have associated acute or subacute thrombi removed at the time of surgery compared with those on conventional anticoagulant therapies. This raises questions of safety and efficacy of DOACs in the chronic treatment of CTEPH. A formal study of DOACs in the management of CTEPH is indicated.
{"title":"Direct oral anticoagulant use and thrombus detection in patients with chronic thromboembolic pulmonary hypertension referred for pulmonary thromboendarterectomy","authors":"Ina Jeong, T. Fernandes, M. Alotaibi, N. Kim","doi":"10.1183/13993003.congress-2019.oa5161","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.oa5161","url":null,"abstract":"Background: Patients with chronic thromboembolic pulmonary hypertension (CTEPH) should be on lifelong, effective anticoagulant therapy. The safety and efficacy of direct oral anticoagulant (DOAC) in CTEPH is unknown. Aim: To evaluate the trend of DOAC usage and correlation with subacute thrombus detection at time of pulmonary thromboendarterectomy. Methods: We performed a retrospective analysis of 405 consecutive pulmonary thromboendarterectomy (PTE) cases at the University of California, San Diego from July 2015 through July 2017. The PTE specimen were reviewed for the presence of acute or subacute thrombotic material removed at the time of PTE. Results: Of 405 consecutive PTE cases, 239 (59.0%) presented on either oral vitamin-K antagonist or chronic injectable therapy; 166 patients (41%) were anticoagulated with DOACs. There were no significant differences in baseline characteristics between DOAC and non-DOAC groups. Evidence of acute or subacute thrombi was observed in 16 (6.7%) within the non-DOAC group versus 22 (13.3%) in the DOAC group. The odds ratio (OR) of DOACs usage and evidence of recent thrombosis was 2.34 (95% CI, 1.09-5.01, p=0.028) after adjusting for age, gender, race, BMI, and history of antiphospholipid antibody syndrome. Conclusions: CTEPH patients referred for PTE while on DOAC therapy were twice as likely to have associated acute or subacute thrombi removed at the time of surgery compared with those on conventional anticoagulant therapies. This raises questions of safety and efficacy of DOACs in the chronic treatment of CTEPH. A formal study of DOACs in the management of CTEPH is indicated.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74215450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.oa495
James J. Anderson, E. Lau, M. Lavender, R. Benza, D. Celermajer, N. Collins, C. Corrigan, N. Dwyer, J. Feenstra, M. Horrigan, D. Keating, E. Kotlyar, T. McWilliams, Bronwen Rhodes, P. Steele, V. Thakkar, T. Williams, H. Whitford, K. Whyte, R. Weintraub, J. Wrobel, A. Keogh, G. Strange
{"title":"Late Breaking Abstract - Validation of the REVEAL 2.0 Risk Score with the Australian and New Zealand Pulmonary Hypertension Registry Cohort","authors":"James J. Anderson, E. Lau, M. Lavender, R. Benza, D. Celermajer, N. Collins, C. Corrigan, N. Dwyer, J. Feenstra, M. Horrigan, D. Keating, E. Kotlyar, T. McWilliams, Bronwen Rhodes, P. Steele, V. Thakkar, T. Williams, H. Whitford, K. Whyte, R. Weintraub, J. Wrobel, A. Keogh, G. Strange","doi":"10.1183/13993003.congress-2019.oa495","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.oa495","url":null,"abstract":"","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85395932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-28DOI: 10.1183/13993003.congress-2019.pa4753
Clara Martin Ontiyuelo, Anna Rodó Pin, I. Blanco, Anna Herranz Blasco, L. M. Ferragut, L. Piccari, J. Barberà, D. R. Chiaradía
Introduction: In stable patients with Pulmonary Arterial Hypertension (PAH), exercise training (ET) in addition to appropriate pharmacological treatment is effective, safe and cost-effective. However, the long-term impact of this intervention remains unclear. For this, we evaluated exercise capacity, right ventricular response during exercise and daily physical activity (DPA) 6 months after the end of an ET program in these patients. Methods: A prospective analysis of 10 consecutive patients with PAH (idiopathic=3; VIH=3, connective tissue disease=3 and atrial septal defect=1) that successfully finished an ET program (8 weeks) was evaluated after 6 months. Incremental cardiopulmonary exercise testing (ICPET) with synchronic echocardiography and accelerometer validated for the assessment of daily DPA were used to evaluate the outcomes. Results: All patients showed training-induced increase on endurance time (mean change 287 seconds). Compared to values immediately after the completion of ET, 6 monthspeak VO2 and peak watts did not change significantly (51% vs 50% predicted, and 75% vs 67% predicted; respectively). In addition, pulmonary tricuspid valve regurgitation (TVR) and tricuspid annular plane systolic excursion (TAPSE) did not show significant differences during the follow-up at rest (4.16 vs 4.13 m/sec and 22.4 vs 22.7 cm;respectively) and at the end of exercise (3.9 vs 4.0 m/sec and 24 vs 22 cm). DPA was similar in two time points (after ET=6889 steps per day and 6 months=6753 steps per/day). Conclusions: In patients with PAH, exercise training maintains exercise capacity, right ventricular function and daily physical activity up to 6 months after the end of the program.
在稳定期肺动脉高压(PAH)患者中，运动训练(ET)加上适当的药物治疗是有效、安全且具有成本效益的。然而，这种干预的长期影响尚不清楚。为此，我们评估了这些患者在ET项目结束后6个月的运动能力、运动时的右心室反应和每日身体活动(DPA)。方法:前瞻性分析连续10例PAH患者(特发性=3;成功完成ET计划(8周)6个月后评估VIH=3，结缔组织疾病=3，房间隔缺损=1。采用同步超声心动图的增量心肺运动试验(ICPET)和经验证可评估每日DPA的加速度计来评估结果。结果:所有患者均表现出训练引起的耐力时间增加(平均变化287秒)。与ET完成后的值相比，6个月的VO2和峰值瓦没有显著变化(51% vs 50%预测，75% vs 67%预测;分别)。此外，肺动脉三尖瓣返流(TVR)和三尖瓣环面收缩漂移(TAPSE)在静息(分别为4.16 vs 4.13 m/秒和22.4 vs 22.7 cm)和运动结束(3.9 vs 4.0 m/秒和24 vs 22 cm)随访期间无显著差异。两个时间点的DPA相似(ET后=6889步/天，6个月=6753步/天)。结论:在PAH患者中，运动训练可维持运动能力、右心室功能和日常体力活动至项目结束后6个月。
{"title":"Evolution of patients with Pulmonary Arterial Hypertension (PAH) six months after an exercise training program","authors":"Clara Martin Ontiyuelo, Anna Rodó Pin, I. Blanco, Anna Herranz Blasco, L. M. Ferragut, L. Piccari, J. Barberà, D. R. Chiaradía","doi":"10.1183/13993003.congress-2019.pa4753","DOIUrl":"https://doi.org/10.1183/13993003.congress-2019.pa4753","url":null,"abstract":"Introduction: In stable patients with Pulmonary Arterial Hypertension (PAH), exercise training (ET) in addition to appropriate pharmacological treatment is effective, safe and cost-effective. However, the long-term impact of this intervention remains unclear. For this, we evaluated exercise capacity, right ventricular response during exercise and daily physical activity (DPA) 6 months after the end of an ET program in these patients. Methods: A prospective analysis of 10 consecutive patients with PAH (idiopathic=3; VIH=3, connective tissue disease=3 and atrial septal defect=1) that successfully finished an ET program (8 weeks) was evaluated after 6 months. Incremental cardiopulmonary exercise testing (ICPET) with synchronic echocardiography and accelerometer validated for the assessment of daily DPA were used to evaluate the outcomes. Results: All patients showed training-induced increase on endurance time (mean change 287 seconds). Compared to values immediately after the completion of ET, 6 monthspeak VO2 and peak watts did not change significantly (51% vs 50% predicted, and 75% vs 67% predicted; respectively). In addition, pulmonary tricuspid valve regurgitation (TVR) and tricuspid annular plane systolic excursion (TAPSE) did not show significant differences during the follow-up at rest (4.16 vs 4.13 m/sec and 22.4 vs 22.7 cm;respectively) and at the end of exercise (3.9 vs 4.0 m/sec and 24 vs 22 cm). DPA was similar in two time points (after ET=6889 steps per day and 6 months=6753 steps per/day). Conclusions: In patients with PAH, exercise training maintains exercise capacity, right ventricular function and daily physical activity up to 6 months after the end of the program.","PeriodicalId":20724,"journal":{"name":"Pulmonary hypertension","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84553250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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