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Curso de Atualização em Medicina Cardiovascular 2019
Reunião Anual Conjunta dos Grupos de Estudo de Cirurgia Cardíaca, Doenças Valvulares e Ecocardiografia da SPC
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A. Basics
B. Imaging
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01. History of Cardiology
02. Clinical Skills
03. Imaging
04. Arrhythmias, General
05. Atrial Fibrillation
06. Supraventricular Tachycardia (non-AF)
07. Syncope and Bradycardia
08. Ventricular Arrhythmias and Sudden Cardiac Death (SCD)
09. Device Therapy
10. Chronic Heart Failure
11. Acute Heart Failure
12. Coronary Artery Disease (Chronic)
13. Acute Coronary Syndromes
14. Acute Cardiac Care
15. Valvular Heart Disease
16. Infective Endocarditis
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19. Tumors of the Heart
20. Congenital Heart Disease and Pediatric Cardiology
21. Pulmonary Circulation, Pulmonary Embolism, Right Heart Failure
22. Aortic Disease
23. Peripheral Vascular and Cerebrovascular Disease
24. Stroke
25. Interventional Cardiology
26. Cardiovascular Surgery
27. Hypertension
28. Risk Factors and Prevention
29. Rehabilitation and Sports Cardiology
30. Cardiovascular Disease in Special Populations
31. Pharmacology and Pharmacotherapy
32. Cardiovascular Nursing
33. e-Cardiology / Digital Health
34. Public Health and Health Economics
35. Research Methodology
36. Basic Science
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Angiotensinogen and hydrogen peroxide in human acute heart failure
Session:
Posters 4 - Écran 1 - Doença Coronária
Speaker:
MARTA FERNANDA REINA COUTO
Congress:
CPC 2019
Topic:
E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Theme:
14. Acute Cardiac Care
Subtheme:
14.4 Acute Cardiac Care – Cardiogenic Shock
Session Type:
Posters
FP Number:
---
Authors:
Marta Couto; Cruz, Rita; Serrão, Paula ; Afonso, Joana ; Roncon de Albuquerque; Paiva, José A. ; Albino-Teixeira, António ; Morato, Manuela ; Sousa, Teresa
Abstract
<p>Introduction and aims: Acute heart failure (AHF) is the most common cause of unscheduled hospital admissions. The renin-angiotensin-aldosterone system (RAAS) and hydrogen peroxide (H2O2) contribute to the pathophysiology of AHF, where H2O2 may function either as downstream mediator or as upstream regulator of RAAS. Since heart dysfunction negatively affects the kidney and vice versa, we aimed to evaluate the urinary excretion of angiotensinogen (U-AGT, a marker of intrarenal RAAS) and H2O2 (U-H2O2), as well as their correlation with each other and with cardiac biomarkers in acute heart failure (AHF) and cardiogenic shock (CS).</p> <p>Methods: This study was approved by the Health Ethics Committee of our hospital. Blood and urine samples were collected from patients with AHF (n=9), CS (n=7) or non-cardiogenic shock (NCS) (n=6) at admission, days 3-4 and days 5-7 of the hospitalization period. Samples from healthy volunteers (controls) (n=8) were collected at a single time point. U-AGT and U-H2O2 were quantified by ELISA and a fluorimetric assay, respectively and B-type natriuretic peptide (BNP), high-sensitivity troponin I (hs-trop I) using automated analyzers.</p> <p>Results: U-AGT (ng/mg creatinine) at admission was higher in all patients groups, being markedly higher in CS and NCS (controls:3.6±0.8; AHF:18.8±5.9; CS:106.6±32.6; NCS:491.1±244.0; CS and NCS vs. controls, p<0.01 and p<0.001, respectively). In most shock patients, U-AGT increased during hospitalization. U-H2O2 values (nmol/mg creatinine) at admission were lower in patients groups, particularly in those with shock (controls: 6.3±1.1; AHF: 1.7±0.8; CS: 0.6±0.4; NCS: 0.9±0.5; CS and NCS vs. controls, p<0.01). There was a significant inverse correlation between U-AGT and U-H2O2 at admission (r=-0.55, p=0.002), when considering all groups. U-AGT or U-H2O2 were not correlated with cardiac biomarkers like BNP or hs-trop I or even with APACHE II and SAPS II scores.</p> <p>Conclusion: At admission, U-AGT is higher and U-H2O2 is lower in all patients groups, being more markedly altered in shock patients, although no changes in renal function were observed in these groups, probably reflecting intrarenal RAAS activation, with increased local AGT production. The inverse correlation between U-AGT and U-H2O2 suggests the existence of a counterregulatory mechanism between these markers. [Funded by FCT/FEDER (COMPETE, Portugal 2020), PTDC/MEC-CAR/32188/2017]</p>
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