Jan Biegus1, Sylwia Nawrocka-Millward2, Robert Zymliński3, Marat Fudim4, Jeffrey Testani5, Dominik Marciniak6, Marta Rosiek-Biegus7, Barbara Ponikowska8, Mateusz Guzik2, Mateusz Garus2, Piotr Ponikowski3. 1. Institute of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland; Institute of Heart Diseases, University Hospital, Wroclaw, Poland. Electronic address: jan.biegus@umw.edu.pl. 2. Institute of Heart Diseases, University Hospital, Wroclaw, Poland. 3. Institute of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland; Institute of Heart Diseases, University Hospital, Wroclaw, Poland. 4. Division of Cardiology, Duke University Medical Center, Durham, NC, USA; Duke Clinical Research Institute, Durham, NC, USA. 5. Department of Medicine, Yale University, New Haven, CT, USA. 6. Department of Drugs Form Technology, Faculty of Pharmacy, Medical University, Wroclaw, Poland. 7. Department of Internal Medicine, Pneumology and Allergology, Medical University, Wroclaw, Poland. 8. Student Scientific Club, Department of Heart Diseases, Medical University, Wroclaw, Poland.
Abstract
BACKGROUND: Although renin-angiotensin-aldosterone system (RAAS) activation is believed to be the major driver of acute heart failure (AHF) episodes our understanding of its prevalence and clinical relevance in contemporary settings is incomplete. METHODS: Serum renin and aldosterone were measured at day-1 and at discharge in patients (n = 211) that were hospitalized between 2016 and 2017 for AHF in a single cardiology center. The population was profiled based on upper limits of normal (ULN) of both biomarkers assessed at day-1 and linked with the clinical course and outcomes. RESULTS: The study population constituted of three profiles: RAAS-/- (n = 121 [57%]); RAAS+/- (n = 60 [28%]); and RAAS+/+ (n = 30 [14%]). The RAAS+/+ profile had the lowest blood pressure and serum sodium at admission, day-2 and discharge compared to the other profiles (p < 0.001). The RAAS+/+ patients had significantly lower urine Na+ at admission (57.8 ± 36.7 vs 97.3 ± 31.3 and 86.4 ± 35.0), day-1 (52.7 ± 32.7 vs 85.3 ± 36.3 and 75.5 ± 33.9) mmol/l, vs RAAS-/- and RAAS+/- profiles, respectively, all p < 0.001. There was also a gradual decrease of renal function across increasing RAAS profiles. The RAAS+/+ profile received higher dose of furosemide at discharge 120 [80-160] vs the other profiles 80 [40-120] mg, p < 0.01. The risks of one year mortality or HF rehospitalization increased across the RAAS profiles (p < 0.001). The trajectory of renin or aldosterone change during hospitalization was not related to outcomes. CONCLUSIONS: The RAAS overactivity is not essential for development of AHF. However, elevated RAAS is a marker of more advanced stages of heart failure, is related to low natriuresis and adverse clinical outcomes.
BACKGROUND: Although renin-angiotensin-aldosterone system (RAAS) activation is believed to be the major driver of acute heart failure (AHF) episodes our understanding of its prevalence and clinical relevance in contemporary settings is incomplete. METHODS: Serum renin and aldosterone were measured at day-1 and at discharge in patients (n = 211) that were hospitalized between 2016 and 2017 for AHF in a single cardiology center. The population was profiled based on upper limits of normal (ULN) of both biomarkers assessed at day-1 and linked with the clinical course and outcomes. RESULTS: The study population constituted of three profiles: RAAS-/- (n = 121 [57%]); RAAS+/- (n = 60 [28%]); and RAAS+/+ (n = 30 [14%]). The RAAS+/+ profile had the lowest blood pressure and serum sodium at admission, day-2 and discharge compared to the other profiles (p < 0.001). The RAAS+/+ patients had significantly lower urine Na+ at admission (57.8 ± 36.7 vs 97.3 ± 31.3 and 86.4 ± 35.0), day-1 (52.7 ± 32.7 vs 85.3 ± 36.3 and 75.5 ± 33.9) mmol/l, vs RAAS-/- and RAAS+/- profiles, respectively, all p < 0.001. There was also a gradual decrease of renal function across increasing RAAS profiles. The RAAS+/+ profile received higher dose of furosemide at discharge 120 [80-160] vs the other profiles 80 [40-120] mg, p < 0.01. The risks of one year mortality or HF rehospitalization increased across the RAAS profiles (p < 0.001). The trajectory of renin or aldosterone change during hospitalization was not related to outcomes. CONCLUSIONS: The RAAS overactivity is not essential for development of AHF. However, elevated RAAS is a marker of more advanced stages of heart failure, is related to low natriuresis and adverse clinical outcomes.
Authors: Agata Zdanowicz; Szymon Urban; Barbara Ponikowska; Gracjan Iwanek; Robert Zymliński; Piotr Ponikowski; Jan Biegus Journal: J Pers Med Date: 2022-05-29