275  Role of right ventricle in acute heart failure with preserved ejection fraction: a comparison between hypertensive pulmonary edema and decompensated heart failure. (17th December 2020)

• Record Type: Journal Article
• Authors: Abete, Raffaele; Iacovoni, Attilio; Vecchi, Andrea Lorenzo; Palmieri, Vittorio; De Ponti, Roberto; Mortara, Andrea; Senni, Michele
• Is Part Of: European heart journal supplements. Volume 22(2020)Supplement N
• Page Start: N88
• Page End: N102
• Publication Date: 2020-12-17
• Subjects: Cardiology -- Periodicals; Cardiology -- Europe -- Periodicals; 616.12005
• DOI: 10.1093/eurheartj/suaa202
• Languages: English
• ISSNs: 1520-765X

Abstract

Abstract: Aims: Limited data are available on the pathophysiological role of the right ventricle (RV) in patients with acute heart failure with preserved ejection fraction (AHF-PEF) and its impact on the main clinical manifestation such as pulmonary oedema or peripheral congestion. Mainly through right-to-left stroke volume mismatch and ventricular-arterial decoupling, right chambers size and function may play a key role leading to fluid overload or maldistributed phenotypes. Methods and results: In this monocenter, prospective, observational study 80 consecutive patients with AHF-PEF were enrolled. A complete echocardiographic examination was performed within 6 hours from emergency department admission; multiparametric RV function was carefully evaluated in the very acute phase. Focusing on hypertensive pulmonary oedema (H-AHF) and decompensated AHF without pulmonary oedema (D-AHF) phenotypes, the study aims to analyze the echocardiographic peculiarities of these clinical entities in the early phase of admission and its modification at discharge (D-AHF n = 58, H-AHF n = 22). Baseline clinical characteristics were comparable in both groups, except for coronary artery disease more prevalent in H-AHF and atrial fibrillation more prevalent in D-AHF. D-AHF patients showed dilated and dysfunctional right chambers compared to H-AHF. Regarding systolic function, normal values of fractional area change (FAC) and tricuspid annular plane systolic excursion (TAPSE) were registered in H-AHF at admission and at discharge. D-AHF showed greater systolic pulmonary artery pressure (sPAP) and lower TAPSE/sPAP ratio. Left ventricular dimensions and function were comparable in both groups. Conversely, E/e' ratio was significantly higher in H-AHF at admission. Data are summarized in the tables and figures below. Conclusion: D-AHF and H-AHF represent different phenotypes of AHF-PEF. Right heart structure and function and ventricular-arterial coupling could play a crucial role in their pathophysiology. Non dilated RV with preserved systolic function seems to be crucial to develop pulmonary oedema without signs of peripheral congestion. Further investigations are needed to corroborate the hypothesis of interventricular stroke volume mismatch in the complex AHF-PEF clinical scenario.