{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T16:12:47Z","timestamp":1782922367814,"version":"3.54.5"},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"abstract":"\n Background<\/jats:title>\n The association between raised pulmonary artery pressures, pulmonary vascular resistance (PVR), and right\u2010sided heart dysfunction is well recognized. The added value of pulsatile indices, specifically pulmonary arterial compliance (PAC) and characteristic impedance, remains unclear. This study aimed to identify the optimal vascular afterload model for predicting right\u2010sided heart dysfunction in newly diagnosed pulmonary hypertension (PH).<\/jats:p>\n <\/jats:sec>\n \n METHODS AND RESULTS<\/jats:title>\n \n This was a prospective cohort study of 86 patients with suspected PH (60\u00b116\u2009years; 66 women) who underwent right\u2010sided heart catheterization and cardiac magnetic resonance imaging. Right ventricular end\u2010diastolic volume index (RVEDVi) and right atrial (RA) volume index were measured using cardiac magnetic resonance imaging. Vascular resistance, PAC, and characteristic impedance were measured using pulmonary artery pressure from right\u2010sided heart catheterization and pulmonary artery flow from cardiac magnetic resonance imaging. Optimal model fit was determined by the lowest Akaike Information Criterion value. A total of 58% of patients had a right ventricular ejection fraction <50%, 63% had an increased RVEDVi, and 56% had an increased RA volume index. Overall, PVR was the best predictor of right ventricular ejection fraction <50% (\n P<\/jats:italic>\n <0.01), increased RVEDVi (\n P<\/jats:italic>\n <0.01), and RA volume index (\n P<\/jats:italic>\n =0.02). However, for patients with a PVR <240\n dynes.s.cm<\/jats:ext-link>\n \u22125<\/jats:sup>\n , PAC\n clinical<\/jats:sub>\n outperformed PVR in predicting right ventricular ejection fraction <50% (\n P<\/jats:italic>\n =0.02) and increased RVEDVi (\n P<\/jats:italic>\n =0.05). A 3\u2010component model (PVR, PAC\n clinical<\/jats:sub>\n , and characteristic impedance) best predicted RA dilatation (\n P<\/jats:italic>\n =0.05). In paired analysis, alternative methods of PAC quantification better predicted increased RVEDVi (PAC\n decay<\/jats:sub>\n P<\/jats:italic>\n =0.02) and RA volume index (PAC\n area<\/jats:sub>\n P<\/jats:italic>\n =0.02). PAC\n clinical<\/jats:sub>\n <2.3\u2009mL\/mm\u2009Hg optimally predicted right\u2010sided heart dysfunction (area under the curve, 0.768) and increased the AUC for PVR in undifferentiated\/left\u2010sided PH (0.89 versus 0.72).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Pulsatile vascular afterload measurement improves right\u2010sided heart dysfunction prediction in undifferentiated\/left\u2010sided PH. More accurate PAC measurement methods could further enhance prognostic accuracy, while a PVR \u2265240\n dynes.s.cm<\/jats:ext-link>\n \u22125<\/jats:sup>\n remains a valuable threshold for precapillary PH.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/jaha.124.034684","type":"journal-article","created":{"date-parts":[[2024,11,22]],"date-time":"2024-11-22T11:34:01Z","timestamp":1732275241000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["Pulsatile Vascular Afterload Measurement Improves Prediction of Right\u2010Sided Heart Dysfunction in Undifferentiated and Left\u2010Sided Pulmonary Hypertension"],"prefix":"10.1161","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0040-7719","authenticated-orcid":false,"given":"Sara Louise","family":"Hungerford","sequence":"first","affiliation":[{"name":"Faculty of Health and Medicine The University of New South Wales Sydney Australia"},{"name":"Department of Cardiology Royal 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Chang Cardiac Research Institute Sydney Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5949-0812","authenticated-orcid":false,"given":"Kay","family":"Everett","sequence":"additional","affiliation":[{"name":"The CardioVascular Center Tufts Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7701-0878","authenticated-orcid":false,"given":"Gaurav","family":"Gulati","sequence":"additional","affiliation":[{"name":"The CardioVascular Center Tufts Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7990-3197","authenticated-orcid":false,"given":"Nicholas","family":"Olsen","sequence":"additional","affiliation":[{"name":"Faculty of Health and Medicine The University of New South Wales Sydney Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edmund","family":"Lau","sequence":"additional","affiliation":[{"name":"Department of Respiratory Medicine Royal Prince Alfred Hospital Sydney Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9219-5524","authenticated-orcid":false,"given":"Andrew","family":"Jabbour","sequence":"additional","affiliation":[{"name":"Faculty of Health and Medicine The University of New South Wales Sydney Australia"},{"name":"Victor Chang Cardiac Research Institute Sydney Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3546-0758","authenticated-orcid":false,"given":"Nicole","family":"Bart","sequence":"additional","affiliation":[{"name":"Faculty of Health and Medicine The University of New South Wales Sydney Australia"},{"name":"Victor Chang Cardiac Research Institute Sydney Australia"},{"name":"Harvard University Boston 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