{"doi":"10.1002/ejhf.2774","title":"Invasive Exercise Haemodynamics: An Oracle in Heart Failure with Preserved Ejection Fraction Diagnosis and Prognostication","abstract":"This article refers to ‘Central haemodynamic abnormalities and outcome in patients with unexplained dyspnoea’ by K. Omote et al., published in this issue on pages 185–196. Patients with unexplained dyspnoea on exertion represent a diagnostically challenging population. Reliance on cardiopulmonary diagnostic testing solely performed at rest poses significant risk of overlooking physiologic abnormalities unmasked by exercise. Exercise invasive haemodynamic measurements have emerged as an important modality for assessment and differentiation of cardiac versus non-cardiac dyspnoea and their value is increasingly recognized by guidelines and major consensus documents.1-3 In the current issue of the Journal, Omote et al.4 expand the knowledge base underlying the importance of pulmonary arterial catheter-based haemodynamic measurements in the evaluation of suspected heart failure with preserved ejection fraction (HFpEF). The authors investigated whether abnormal invasive haemodynamic parameters derived during clinically-indicated supine cardiopulmonary exercise testing (CPET) predict heart failure-related hospitalizations or death. This retrospective analysis of 764 patients with unexplained dyspnoea included three groups: (i) patients with haemodynamic evidence of HFpEF at rest based on pulmonary arterial wedge pressure ≥15 mmHg (rPAWP≥15, n = 384); (ii) patients with haemodynamic evidence of HFpEF defined by a supine peak exercise PAWP ≥25 mmHg (exPAWP≥25, n = 187); and (iii) patients with ‘non-cardiac dyspnoea’ (NCD) based on not only having rPAWP <15 mmHg and exPAWP <25 mmHg but also having resting mean pulmonary arterial pressure (PAP) <20 mmHg as well as pulmonary vascular resistance (PVR) <3 Wood units (WU) at rest and mean PAP ≤30 mmHg or PVR <3 WU with exercise. This grouping clusters those with abnormal pre-capillary pulmonary haemodynamics exclusively with the two elevated PAWP groups, arguably enriching for adverse outcomes in comparison to the NCD group. Over a median follow-up period of 2.7 years, 117 events were identified. The authors found that: (i) the rPAWP≥15 group demonstrated increased risk of combined outcomes compared to rPAWP <15 mmHg with exPAWP≥25 (hazard ratio [HR] 2.24; 95% confidence interval [CI] 1.38–3.65), and (ii) the exPAWP≥25 group demonstrated increased risk for adverse events compared to NCD (HR 2.44; 95% CI 1.11–5.36). Importantly, lower cardiac output (CO) during exercise also predicted increased risk for adverse outcomes (HR 2.35; 95% CI 1.50–3.68; p = 0.0002). When examined as continuous variables, one standard deviation increase in exPAWP and decrease in exercise CO resulted in 30% (HR 1.30; 95% CI 1.05–1.62) and 33% (HR 0.67; 95% CI 0.51–0.89) increase in combined outcomes, respectively. The integrated measure PAWP/CO slope also predicted adverse outcomes (log PAWP/CO slope, HR 1.20; 95% CI 1.02–1.41). Overall, the authors should be commended on this comprehensive and in-depth analysis. First, they extensively evaluated the prognostic impact of multiple pertinent haemodynamic parameters including PAWP, PAP, right atrial pressure (RAP), PVR, pulmonary artery compliance (PAC), CO, as well as PAWP/CO and mean PAP/CO slopes, more parameters than any previous exercise haemodynamic study.4-8 In addition, they used echocardiography to exclude patients with underlying conditions that could manifest with HFpEF symptoms, thus further refining the focus on HFpEF. The present study further establishes the role of exercise haemodynamic measurements to both diagnose and risk stratify patients with suspected HFpEF. This analysis complements previous studies (Table 1) in which normal rPAWP with a steep increment in PAWP in response to exercise purports an intermediate prognosis between those with normal rest and exPAWP and those with elevated resting and exPAWP.5-7, 9 NYHA class II or III 61.2 ± 11 years, 33.8% male BMI 27.8 ± 4.5 kg/m2 rPAWP >12 PAWPL >25.5 Both 2.21 [1.14–4.17]a 5.44 [2.88–10.29] 4.75 [1","journal":"European Journal of Heart Failure","year":2023,"id":379477,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9567,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2023-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1103653,"name":"Joseph Campain","orcid":null,"position":1,"is_corresponding":false},{"id":255092,"name":"Gregory D. Lewis","orcid":"0000-0001-8108-8240","position":2,"is_corresponding":false},{"id":767873,"name":"Ioannis Mastoris","orcid":"0000-0002-1779-6629","position":0,"is_corresponding":true}],"reference_count":18,"raw_metadata":null,"created_at":"2026-07-19T01:16:56.650289Z","pmid":"36644824","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}