000102243 001__ 102243
000102243 005__ 20240118091946.0
000102243 0247_ $$2doi$$a10.1007/s00380-020-01634-9
000102243 0248_ $$2sideral$$a118203
000102243 037__ $$aART-2020-118203
000102243 041__ $$aeng
000102243 100__ $$0(orcid)0000-0002-4769-7154$$aRubio-Gracia, J.$$uUniversidad de Zaragoza
000102243 245__ $$aIntra-abdominal pressure and its relationship with markers of congestion in patients admitted for acute decompensated heart failure
000102243 260__ $$c2020
000102243 5060_ $$aAccess copy available to the general public$$fUnrestricted
000102243 5203_ $$aSystemic congestion is one of the mechanisms involved in acute decompensated heart failure (ADHF). Increased intra-abdominal pressure (IAP), elicited by abdominal congestion, has been related to acute kidney injury and prognosis. Nonetheless, the link between diuretic response, surrogate markers of congestion and renal function remains poorly understood. We measured IAP in 43 patients from a non-interventional, exploratory, prospective, single center study carried out in patients admitted for ADHF. IAP was measured with a calibrated electronic manometer through a catheter inserted in the bladder. Normal IAP was defined as < 12 mmHg. At baseline, median IAP was 15 mmHg, with a reduction over the next 72 h to a median of 12 mmHg. A higher IAP at admission was associated with higher baseline blood urea (83 mg/dL [62–138] vs. 50 mg/dL [35–65]; p = 0.007) and creatinine (1.30 mg/dL vs. 0.95 mg/dL; p = 0.027), and with poorer diuretic response 72 h after admission, either measured by diuresis (14.4 mL/mg vs. 21.6 mL/mg; [p = 0.005]) or natriuresis (1.2 mEqNa/mg vs. 2.0 mEqNa/mg; [p = 0.008]). A higher incidence for 1-year all-cause mortality (45.0% vs. 16.7%; log-rank test = 0.041) was observed among those patients with IAP > 12 mmHg at 72 h. In patients with ADHF, higher IAP at admission is associated with poorer baseline renal function and impaired diuretic response. The persistence of IAP at 72 h above 12 mmHg associates to longer length of hospital stay and higher 1-year all-cause mortality.
000102243 536__ $$9info:eu-repo/grantAgreement/ES/DGA/B17-R07
000102243 540__ $$9info:eu-repo/semantics/openAccess$$aAll rights reserved$$uhttp://www.europeana.eu/rights/rr-f/
000102243 590__ $$a2.037$$b2020
000102243 591__ $$aCARDIAC & CARDIOVASCULAR SYSTEMS$$b105 / 141 = 0.745$$c2020$$dQ3$$eT3
000102243 591__ $$aPERIPHERAL VASCULAR DISEASE$$b52 / 65 = 0.8$$c2020$$dQ4$$eT3
000102243 592__ $$a0.624$$b2020
000102243 593__ $$aCardiology and Cardiovascular Medicine$$c2020$$dQ2
000102243 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/acceptedVersion
000102243 700__ $$0(orcid)0000-0002-6043-4869$$aGiménez-López, I.$$uUniversidad de Zaragoza
000102243 700__ $$0(orcid)0000-0002-2338-7637$$aSánchez-Marteles, M.$$uUniversidad de Zaragoza
000102243 700__ $$0(orcid)0000-0002-8328-9836$$aJosa-Laorden, C.$$uUniversidad de Zaragoza
000102243 700__ $$0(orcid)0000-0003-2361-9941$$aPérez-Calvo, J.I.$$uUniversidad de Zaragoza
000102243 7102_ $$11012$$2410$$aUniversidad de Zaragoza$$bDpto. Farmac.Fisiol.y Med.L.F.$$cÁrea Fisiología
000102243 7102_ $$11007$$2610$$aUniversidad de Zaragoza$$bDpto. Medicina, Psiqu. y Derm.$$cArea Medicina
000102243 773__ $$g35 (2020), 1545–1556$$pHeart vessels$$tHeart and Vessels$$x0910-8327
000102243 8564_ $$s624327$$uhttps://zaguan.unizar.es/record/102243/files/texto_completo.pdf$$yPostprint
000102243 8564_ $$s550477$$uhttps://zaguan.unizar.es/record/102243/files/texto_completo.jpg?subformat=icon$$xicon$$yPostprint
000102243 909CO $$ooai:zaguan.unizar.es:102243$$particulos$$pdriver
000102243 951__ $$a2024-01-18-09:11:09
000102243 980__ $$aARTICLE