Pulmonary Arterial Hypertension (PAH)PAH-SDBNCT07852403
PAH-SDB: Sleep-Disordered Breathing and Outcomes in Pulmonary Arterial Hypertension
An observational study of Pulmonary Arterial Hypertension (PAH) and Sleep-disordered Breathing (SDB), run by Chinese Pulmonary Vascular Disease Research Group at 1 site in China.
Trial summary
Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease characterized by increased pulmonary vascular resistance, right ventricular dysfunction, and clinically important morbidity and mortality. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Pulmonary Arterial Hypertension (PAH), Sleep-disordered Breathing (SDB)
- What is being tested?
- Standardized Overnight Sleep and Cardiorespiratory Monitoring
- How many people
- 1,500 participants
- Where
- 1 siteChina
- Study dates
- 1 Oct 2026to 31 Dec 2032
- How long will I take part?
- 5 Years
- Phase
- Observational
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Consecutive adult patients with RHC-confirmed WHO Group 1 PAH receiving care at participating pulmonary vascular and cardiovascular centers in China. The registry will include newly diagnosed and prevalent PAH, with enrollment strata defined by disease duration and treatment status. Participating centers will include Fuwai Hospital and additional Chinese centers with expertise in PAH and the ability to perform standardized clinical and nocturnal physiological assessments.
Who may be able to join
- Age ≥18 years at enrollment.
- Diagnosis of WHO Group 1 pulmonary arterial hypertension established by right heart catheterization using contemporary hemodynamic criteria: mean pulmonary artery pressure >20 mmHg at rest, pulmonary arterial wedge pressure ≤15 mmHg, and pulmonary vascular resistance >2 Wood units, with clinical classification consistent with Group 1 PAH.
- PAH etiology may include idiopathic, heritable, drug/toxin-associated, connective-tissue-disease-associated, congenital-heart-disease-associated PAH after appropriate clinical classification, portal-hypertension-associated PAH, HIV-associated PAH, or other recognized Group 1 PAH subtypes.
- Clinically stable enough to undergo overnight sleep/cardiorespiratory monitoring, as judged by the treating team.
- Able and willing to provide written informed consent and participate in longitudinal follow-up.
- Enrollment at a participating center with availability of the required baseline PAH dataset and a technically interpretable protocol-standardized sleep recording.
Who cannot join
- Pulmonary hypertension predominantly attributable to left heart disease (Group 2), lung disease and/or hypoxia (Group 3), chronic thromboembolic pulmonary hypertension or other pulmonary artery obstruction (Group 4), or unclear/multifactorial mechanisms (Group 5).
- Pulmonary veno-occlusive disease / pulmonary capillary hemangiomatosis when the clinical phenotype is considered separately from conventional PAH for the planned analysis, unless the protocol intentionally includes this subgroup and prespecifies it as a distinct stratum.
- Acute decompensated right heart failure, cardiogenic shock, severe active infection, or another acute condition that would make the baseline sleep recording unrepresentative or unsafe; these patients may be reconsidered after stabilization.
- Current hospitalization primarily for an acute non-PAH illness likely to substantially distort nocturnal respiratory physiology.
- Inability to obtain an adequate baseline sleep/cardiorespiratory recording after protocol-defined repeat attempt, unless the participant is retained in a registry-only stratum for non-sleep analyses.
- Inability to provide informed consent or anticipated inability to complete meaningful follow-up.
- Any other condition that, in the investigator's judgment, would prevent reliable study participation or data interpretation.
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
Zhihua Huang, MD, PhD contact
China1 site, 1 recruiting
- Recruiting
Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College
Beijing, 100037
Zhihong Liu, MD, PhD, 86-010-88398196, zhihongliufuwai@163.com
About this study
Official title: PAH-SDB: A Prospective Multicenter Cohort Study of Sleep-Disordered Breathing, Nocturnal Physiological Phenotypes, and Longitudinal Outcomes in Pulmonary Arterial Hypertension
Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease characterized by increased pulmonary vascular resistance, right ventricular dysfunction, and clinically important morbidity and mortality. Sleep-disordered breathing (SDB) and sleep-related hypoxemia are common in patients with PAH, but their prevalence, physiological determinants, longitudinal trajectories, prognostic significance, and potential role in individualized management remain incompletely defined.
PAH-SDB is a prospective, multicenter, observational patient registry enrolling adults with right-heart-catheterization-confirmed World Health Organization Group 1 PAH at pulmonary vascular centers across China. Participants will undergo standardized nocturnal sleep and cardiorespiratory monitoring together with comprehensive PAH assessment, including clinical characteristics, functional status, biomarkers, echocardiography, hemodynamics, treatment, and outcomes. Selected participants may undergo additional polysomnography, cardiac magnetic resonance imaging, wearable monitoring, repeated sleep assessments, or biospecimen collection when available and ethically approved.
The registry will characterize the prevalence and phenotypes of sleep-disordered breathing and nocturnal physiological abnormalities; examine their relationships with PAH severity and right ventricular-pulmonary vascular function; determine their value for predicting clinical worsening, hospitalization, transplantation, and mortality; evaluate longitudinal changes in sleep physiology in relation to PAH treatment and disease trajectory; and develop and validate multimodal statistical and artificial-intelligence models for phenotyping, risk prediction, and treatment-response stratification. Clinical management will remain at the discretion of treating physicians, and the registry will not assign PAH or sleep-related therapies.
Read the detailed description
PAH-SDB is designed as a disease-based prospective multicenter patient registry and longitudinal cohort. The registry addresses the interaction between sleep-disordered breathing (SDB) or nocturnal respiratory physiology and pulmonary vascular disease across the contemporary treatment era of pulmonary arterial hypertension (PAH). The study is intentionally broader than an apnea-hypopnea-index-centered cohort and will capture obstructive and central respiratory events, sustained and intermittent hypoxemia, desaturation morphology and burden, heart-rate and autonomic responses, respiratory instability, sleep fragmentation when available, and other digital physiological features derived from validated sleep or wearable devices.
Eligible participants will have WHO Group 1 PAH confirmed by right heart catheterization using contemporary hemodynamic criteria. Baseline assessment will include PAH etiology and duration, comorbidities, symptoms and WHO functional class, six-minute walk distance, natriuretic peptides and routine laboratory tests, electrocardiography, echocardiography, right-heart-catheterization variables, PAH-specific therapies, oxygen and positive-airway-pressure use, patient-reported outcomes where feasible, and a standardized overnight sleep study. The core sleep protocol will include airflow, respiratory effort, pulse oximetry, heart rate or electrocardiographic information, body position, and snoring when supported by the device. Full polysomnography will be performed in a nested subgroup according to clinical indication, center capability, or dedicated substudy protocols.
Participants will be followed longitudinally for clinical worsening, PAH-related hospitalization, therapy escalation, lung or heart-lung transplantation, and mortality. Repeated PAH assessments will be obtained according to routine clinical care, with harmonized registry time points. Repeat sleep monitoring is planned in a longitudinal subset, particularly after major changes in PAH treatment, clinically meaningful change in disease status, or initiation of sleep-related therapy. The registry will therefore support both baseline phenotype-outcome analyses and analyses of dynamic change.
Major scientific objectives are: (1) to determine the prevalence and distribution of sleep-disordered breathing and nocturnal hypoxemia in contemporary Chinese PAH; (2) to identify demographic, clinical, hemodynamic, imaging, and treatment correlates of nocturnal physiological phenotypes; (3) to quantify associations between sleep metrics and PAH severity, right ventricular structure and function, and validated risk strata; (4) to determine the incremental prognostic value of nocturnal physiological markers beyond established PAH risk tools; (5) to evaluate whether changes in sleep physiology track or precede changes in PAH status and treatment response; (6) to explore heterogeneity of associations across PAH subtypes, sex, age, body mass index, comorbidity burden, and treatment patterns; and (7) to develop and externally validate multimodal machine-learning and artificial-intelligence models for physiological endotyping, risk prediction, and individualized clinical decision support.
Registry quality procedures will include a standardized electronic case-report form, a data dictionary, investigator training, site initiation procedures, automated range and consistency checks, centralized data queries, periodic completeness reports, prespecified sleep-signal quality criteria, central or centrally supervised sleep scoring for key analyses, and adjudication of major clinical worsening events. A statistical analysis plan will be finalized before primary analyses. Conventional regression and time-to-event methods will be complemented by longitudinal mixed-effects models, internal-external validation across sites, causal-inference approaches for treatment-response analyses when appropriate, and multimodal machine-learning methods. Missing data mechanisms will be documented and addressed using prespecified statistical methods.
The registry is non-interventional. PAH therapy, oxygen therapy, positive airway pressure, and other clinical management will be prescribed by treating clinicians according to clinical judgment and prevailing guidelines. Any future substudy that prospectively assigns an intervention will be governed by a separate protocol and registered separately when required.
- Being tested
- Standardized Overnight Sleep and Cardiorespiratory Monitoring
- Keywords
- Pulmonary arterial hypertension, sleep apnea, obstructive sleep apnea, central sleep apnea, nocturnal hypoxemia, hypoxic burden, oxygen desaturation, right ventricular function, right heart catheterization, risk stratification, clinical worsening, real-world evidence, digital biomarkers, wearable devices, artificial intelligence, machine learning, precision medicine
- Medical subject headings
- Pulmonary Arterial Hypertension, Sleep Apnea Syndromes, Sleep Apnea, Obstructive, Sleep Apnea, Central
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Standardized Overnight Sleep and Cardiorespiratory MonitoringDiagnostic test
Participants undergo protocol-standardized nocturnal monitoring without study-assigned therapy. The core recording includes airflow, respiratory effort, oxygen saturation, pulse/heart rate, body position, and snoring when available. Full polysomnography, extended wearable monitoring, repeated sleep studies, and other physiological signals may be obtained in nested subcohorts. All sleep-related treatment decisions remain under routine clinical care.
| Study group | Role | What they receive |
|---|---|---|
| PAH-SDB Prospective Cohort | Adults with right-heart catheterization (RHC)-confirmed WHO Group 1 pulmonary arterial hypertension (PAH) consecutively enrolled at participating Chinese centers and followed prospectively with standardized nocturnal sleep/cardiorespiratory phenotyping and longitudinal PAH assessments. Receives: Diagnostic Test: Standardized Overnight Sleep and Cardiorespiratory Monitoring |
What is being measured
The primary outcome is the main question the study is designed to answer.
Prevalence and phenotypic distribution of sleep-disordered breathing and nocturnal hypoxemia
Proportion of participants with sleep-disordered breathing (SDB) and its phenotypes, including obstructive sleep apnea (OSA) and central sleep apnea (CSA), together with the distribution of nocturnal hypoxemia and multidimensional sleep physiological burden. Core measures will include the apnea-hypopnea index (AHI) or respiratory event index (REI), obstructive and central respiratory event indices, oxygen desaturation index (ODI), percentage of recording time with peripheral oxygen saturation below 90% (T90), mean and minimum peripheral oxygen saturation (SpO₂), and prespecified hypoxic-burden metrics. Prevalence estimates will be reported with 95% confidence intervals.
Measured: Baseline
Time to first clinical worsening event
Time from enrollment to the first adjudicated clinical worsening event. The primary composite is recommended to include all-cause death, lung or heart-lung transplantation, PAH-related unplanned hospitalization, atrial septostomy, or clinically driven major PAH treatment escalation/rescue therapy because of documented disease worsening. A sensitivity definition limited to hard outcomes will also be analyzed.
Measured: From enrollment through 5 years of follow-up
Secondary outcomes (24)
All-cause mortality
Time from enrollment to death from any cause
Measured: From enrollment through 5 years of follow-up
Transplant-free survival
Time to death or lung/heart-lung transplantation
Measured: From enrollment through 5 years of follow-up
PAH-related hospitalization
Time to first PAH-related unplanned hospitalization and recurrent hospitalization burden
Measured: From enrollment through 5 years of follow-up
Change From Baseline in REVEAL 2.0 Risk Score
The REVEAL 2.0 risk score will be calculated using available clinical variables according to the established REVEAL 2.0 algorithm. Higher scores indicate greater predicted mortality risk. Change from baseline will be evaluated at available follow-up assessments.
Measured: Baseline to longitudinal follow-up through 5 years
Change From Baseline in ESC/ERS Four-Strata Risk Status
PAH risk status will be assessed using the ESC/ERS four-strata risk assessment approach and classified as low risk, intermediate-low risk, intermediate-high risk, or high risk. For longitudinal analyses, the four categories will be coded ordinally from 1 to 4, with higher values indicating greater estimated risk. Changes from baseline will be assessed during follow-up.
Measured: Baseline to longitudinal follow-up through 5 years
Change From Baseline in WHO Functional Class
WHO functional class will be assessed according to the World Health Organization functional classification for pulmonary hypertension, ranging from Class I to Class IV. A higher class indicates greater functional limitation.
Measured: Baseline to 3-6 months, 12 months, and annual follow-up through 5 years.
Change From Baseline in 6-Minute Walk Distance
Exercise capacity will be assessed using the 6-minute walk distance performed according to standardized clinical procedures. Change from baseline in walking distance will be evaluated during follow-up.
Measured: Baseline to 3-6 months, 12 months, and annual follow-up through 5 years.
Change From Baseline in N-Terminal Pro-B-Type Natriuretic Peptide
Plasma N-terminal pro-B-type natriuretic peptide concentration will be recorded when measured as part of routine clinical assessment. Change from baseline will be evaluated at available follow-up assessments.
Measured: Baseline to 3-6 months, 12 months, and annual follow-up through 5 years.
Change From Baseline in Right Atrial Pressure
Right atrial pressure will be measured by right-heart catheterization. Longitudinal change will be evaluated in participants who undergo clinically indicated repeat right-heart catheterization.
Measured: Baseline to repeat right-heart catheterization during follow-up, up to 5 years
Change From Baseline in Mean Pulmonary Artery Pressure
Mean pulmonary artery pressure will be measured by right-heart catheterization. Longitudinal change will be evaluated when repeat right-heart catheterization data are available.
Measured: Baseline to repeat right-heart catheterization during follow-up, up to 5 years
Change From Baseline in Pulmonary Arterial Wedge Pressure
Pulmonary arterial wedge pressure will be measured during right-heart catheterization.
Measured: Baseline to repeat right-heart catheterization during follow-up, up to 5 years
Change From Baseline in Cardiac Index
Cardiac output will be determined during right-heart catheterization according to the standardized method used at the participating center. Cardiac index will be calculated as cardiac output indexed to body surface area.
Measured: Baseline to repeat right-heart catheterization during follow-up, up to 5 years
Change From Baseline in Pulmonary Vascular Resistance
Pulmonary vascular resistance will be calculated from invasive hemodynamic measurements obtained during right-heart catheterization.
Measured: Baseline to repeat right-heart catheterization during follow-up, up to 5 years
Change From Baseline in Respiratory Event Index
Respiratory event index will be calculated as the number of scored respiratory events per hour of valid recording time in participants assessed using portable cardiorespiratory monitoring.
Measured: Baseline to repeat sleep monitoring during follow-up, up to 5 years
Change From Baseline in Apnea-Hypopnea Index
Apnea-hypopnea index will be calculated as the number of apneas and hypopneas per hour of total sleep time in participants undergoing polysomnography.
Measured: Baseline to repeat polysomnography during follow-up, up to 5 years
Change From Baseline in Oxygen Desaturation Index
Oxygen desaturation index will be calculated as the number of qualifying oxygen desaturation events per hour of valid recording time according to the prespecified scoring criteria.
Measured: Baseline to repeat sleep monitoring during follow-up, up to 5 years
Change From Baseline in Percentage of Recording Time With Oxygen Saturation Below 90% (T90)
T90 will be defined as the percentage of valid overnight recording time during which peripheral oxygen saturation is below 90%.
Measured: Baseline to repeat sleep monitoring during follow-up, up to 5 years
Change From Baseline in Mean Overnight Oxygen Saturation
Mean peripheral oxygen saturation will be calculated across the valid overnight recording period.
Measured: Baseline to repeat sleep monitoring during follow-up, up to 5 years
Change From Baseline in Minimum Overnight Oxygen Saturation
Minimum peripheral oxygen saturation will be defined as the lowest valid oxygen saturation value recorded during the overnight monitoring period after signal-quality control.
Measured: Baseline to repeat sleep monitoring during follow-up, up to 5 years
Change From Baseline in Respiratory Event-Associated Hypoxic Burden
Respiratory event-associated hypoxic burden will quantify the cumulative area under oxygen desaturation curves associated with scored respiratory events, normalized by recording duration.
Measured: Baseline to repeat sleep monitoring during follow-up, up to 5 years
Change From Baseline in Mean Event-Related Heart-Rate Surge
Event-related heart-rate surge will be calculated as the increase from the pre-event heart-rate baseline to the post-event peak heart rate for each qualifying respiratory event. The participant-level mean event-related heart-rate surge will be used for longitudinal analysis.
Measured: Baseline to repeat sleep monitoring during follow-up, up to 5 years
Change From Baseline in Tricuspid Annular Plane Systolic Excursion
Tricuspid annular plane systolic excursion (TAPSE) will be measured by echocardiography as an index of right ventricular longitudinal systolic function. Change from baseline will be evaluated during longitudinal follow-up.
Measured: Baseline to annual follow-up through 5 years.
Change From Baseline in Right Ventricular Fractional Area Change
Right ventricular fractional area change (RV FAC) will be assessed by echocardiography as an index of right ventricular systolic function. Change from baseline will be evaluated during longitudinal follow-up.
Measured: Baseline to annual follow-up through 5 years.
Change From Baseline in TAPSE/sPAP Ratio
The ratio of tricuspid annular plane systolic excursion to systolic pulmonary artery pressure (TAPSE/sPAP) will be calculated from echocardiographic measurements as a noninvasive marker of right ventricular-pulmonary arterial coupling. Change from baseline will be evaluated during longitudinal follow-up.
Measured: Baseline to annual follow-up through 5 years.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted1 Oct 2026
- Study start1 Oct 2026 (estimated)
- Primary completion31 Dec 2031 (estimated)
- Study completion31 Dec 2032 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (14)Papers the sponsor has linked to this study.
- Other trials for Pulmonary Arterial Hypertension (PAH)Studies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 1,500 participants (estimated)
- Target duration
- 5 Years
Sponsor and investigators
- Lead sponsor
- Chinese Pulmonary Vascular Disease Research Group
- Sponsor type
- University, hospital or other
- Collaborators
- Chinese Academy of Medical Sciences, Fuwai Hospital
- Responsible party
- Principal investigator, Zhihong Liu, Chinese Pulmonary Vascular Disease Research Group
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07852403
- Sponsor's protocol ID
- PAH-SDB Study
- Acronym
- PAH-SDB
- Status last verified
- Sep 2026
- First submitted
- 15 Sep 2026
- Last updated
- 1 Oct 2026
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Yes: De-identified participant-level data and a data dictionary may be shared with qualified academic investigators for scientifically sound, non-commercial research after approval by the registry Steering Committee and relevant ethics/data-governance bodies, subject to a data-use agreement and applicable Chinese regulations. Data that could enable participant re-identification will not be shared.
Publications
American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events, Version 3. Released 2023; current online scoring reference.
Adir Y, Humbert M, Chaouat A. Sleep-related breathing disorders and pulmonary hypertension. Eur Respir J. 2021 Jan 5;57(1):2002258. doi: 10.1183/13993003.02258-2020. Print 2021 Jan.
PubMed 32747397Spiesshoefer J, Herkenrath S, Harre K, Kahles F, Florian A, Yilmaz A, Mohr M, Naughton M, Randerath W, Emdin M, Passino C, Regmi B, Dreher M, Boentert M, Giannoni A. Sleep-Disordered Breathing and Nocturnal Hypoxemia in Precapillary Pulmonary Hypertension: Prevalence, Pathophysiological Determinants, and Clinical Consequences. Respiration. 2021;100(9):865-876. doi: 10.1159/000515602. Epub 2021 Apr 28.
PubMed 33910200Nagaoka M, Goda A, Takeuchi K, Kikuchi H, Finger M, Inami T, Soejima K, Satoh T. Nocturnal Hypoxemia, But Not Sleep Apnea, Is Associated With a Poor Prognosis in Patients With Pulmonary Arterial Hypertension. Circ J. 2018 Nov 24;82(12):3076-3081. doi: 10.1253/circj.CJ-18-0636. Epub 2018 Oct 16.
PubMed 30333436Huang Z, Duan A, Zhao Z, Zhao Q, Zhang Y, Li X, Zhang S, Gao L, An C, Luo Q, Liu Z. Sleep-disordered breathing patterns and prognosis in pulmonary arterial hypertension: A cluster analysis of nocturnal cardiorespiratory signals. Sleep Med. 2024 Jan;113:61-69. doi: 10.1016/j.sleep.2023.11.016. Epub 2023 Nov 13.
PubMed 37984019Javaheri S, Somers VK. Sleep, Hypoxia, and Survival in Group 1 Pulmonary Arterial Hypertension: What to Do? J Am Coll Cardiol. 2023 Nov 21;82(21):2006-2008. doi: 10.1016/j.jacc.2023.10.005. No abstract available.
PubMed 37968018Lowery MM, Hill NS, Wang L, Rosenzweig EB, Bhat A, Erzurum S, Finet JE, Jellis CL, Kaur S, Kwon DH, Nawabit R, Radeva M, Beck GJ, Frantz RP, Hassoun PM, Hemnes AR, Horn EM, Leopold JA, Rischard FP, Mehra R; Pulmonary Vascular Disease Phenomics (PVDOMICS) Study Group. Sleep-Related Hypoxia, Right Ventricular Dysfunction, and Survival in Patients With Group 1 Pulmonary Arterial Hypertension. J Am Coll Cardiol. 2023 Nov 21;82(21):1989-2005. doi: 10.1016/j.jacc.2023.09.806.
PubMed 37968017Humbert M, McLaughlin VV, Badesch DB, Ghofrani HA, Gibbs JSR, Gomberg-Maitland M, Preston IR, Souza R, Waxman AB, Moles VM, Savale L, Vizza CD, Rosenkranz S, Shi Y, Miller B, Mackenzie HS, Kim SS, Loureiro MJ, Patel MJ, Koglin J, Cornell AG, Hoeper MM; ZENITH Trial Investigators. Sotatercept in Patients with Pulmonary Arterial Hypertension at High Risk for Death. N Engl J Med. 2025 May 29;392(20):1987-2000. doi: 10.1056/NEJMoa2415160. Epub 2025 Mar 31.
PubMed 40167274McLaughlin VV, Hoeper MM, Badesch DB, Ghofrani HA, Gibbs JSR, Gomberg-Maitland M, Preston IR, Souza R, Waxman AB, Kopec G, Meyer G, Olsson KM, Fu W, Shi Y, Miller B, Kim SS, Mackenzie HS, Brambatti M, Patel MJ, Koglin J, Cornell AG, Humbert M; HYPERION Trial Investigators. Sotatercept for Pulmonary Arterial Hypertension within the First Year after Diagnosis. N Engl J Med. 2025 Oct 23;393(16):1599-1611. doi: 10.1056/NEJMoa2508170. Epub 2025 Sep 30.
PubMed 41025556Weatherald J, Fleming TR, Wilkins MR, Cascino TM, Psotka MA, Zamanian R, Seeger W, Galie N, Gomberg-Maitland M. Clinical trial design, end-points, and emerging therapies in pulmonary arterial hypertension. Eur Respir J. 2024 Oct 31;64(4):2401205. doi: 10.1183/13993003.01205-2024. Print 2024 Oct.
PubMed 39209468Chin KM, Gaine SP, Gerges C, Jing ZC, Mathai SC, Tamura Y, McLaughlin VV, Sitbon O. Treatment algorithm for pulmonary arterial hypertension. Eur Respir J. 2024 Oct 31;64(4):2401325. doi: 10.1183/13993003.01325-2024. Print 2024 Oct.
PubMed 39209476Dardi F, Boucly A, Benza R, Frantz R, Mercurio V, Olschewski H, Radegran G, Rubin LJ, Hoeper MM. Risk stratification and treatment goals in pulmonary arterial hypertension. Eur Respir J. 2024 Oct 31;64(4):2401323. doi: 10.1183/13993003.01323-2024. Print 2024 Oct.
PubMed 39209472Kovacs G, Bartolome S, Denton CP, Gatzoulis MA, Gu S, Khanna D, Badesch D, Montani D. Definition, classification and diagnosis of pulmonary hypertension. Eur Respir J. 2024 Oct 31;64(4):2401324. doi: 10.1183/13993003.01324-2024. Print 2024 Oct.
PubMed 39209475Humbert M, Kovacs G, Hoeper MM, Badagliacca R, Berger RMF, Brida M, Carlsen J, Coats AJS, Escribano-Subias P, Ferrari P, Ferreira DS, Ghofrani HA, Giannakoulas G, Kiely DG, Mayer E, Meszaros G, Nagavci B, Olsson KM, Pepke-Zaba J, Quint JK, Radegran G, Simonneau G, Sitbon O, Tonia T, Toshner M, Vachiery JL, Vonk Noordegraaf A, Delcroix M, Rosenkranz S; ESC/ERS Scientific Document Group. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J. 2022 Oct 11;43(38):3618-3731. doi: 10.1093/eurheartj/ehac237. No abstract available.
PubMed 36017548