Abstract
The progression of heart failure is the result of the interaction of several pathogenetic processes that involve the activation of biomarkers belonging to the renin angiotensin aldosterone system (RAAS), to its counterregulatory mechanisms, to the sympathetic nervous system and inflammation, and to oxidative stress. This study is aimed at determining the prognostic role of biomarkers in the evolution of patients with heart failure. These biomarkers are representative of different pathogenetic pathways involved in the progression of heart failure and the possible interrelationships between them and heart remodelling. Method. This is a progressive observational study on 53 hospitalized patients with low ejection fraction heart failure, who were followed up for 12 months. The aetiology of heart failure was ischemic heart disease and dilated cardiomyopathy. The patients were clinically and biochemically evaluated by EKG (echocardiography) on admission and at 6 and 12 months. The biomarkers included in the present study were angiotensin-converting enzyme type 2 (ACE2), apelin-13, NT-proBNP (biomarkers involved in the counterregulation of RAAS), interleukin 17 (IL-17), hsCRP (inflammatory biomarkers), and urinary 8-iso-PGF2α (oxidative stress biomarker). The evolution was considered unfavourable if the patients presented complications during hospitalization, were readmitted for decompensated heart failure, or died. Results. From the study group, 14 patients (24.52%) presented an unfavourable clinical evolution. The biomarkers that were associated with the evolution of patients during hospitalization were ACE2, apelin-13, NT-proBNP, and hsCRP. Multivariate logistic regression analysis identified ACE2 and apelin-13 as independent, predictive biomarkers for the unfavourable evolution of patients over the study period. Values of ACE2 above 4000.75 pg/mL and of apelin-13 less than 402.5 pg/mL were associated with an unfavourable evolution (poor clinical outcomes). Conclusion. The serum values of ACE2 and apelin-13 correlate with the unfavourable evolution of patients with reduced ejection fraction heart failure.
Highlights
In patients with heart failure, congestion is the dominant clinical profile and the main pathophysiological mechanism that causes organic dysfunction [1].The therapeutic reduction of the congestion leads to improved organ function and improved patient prognosis [1].The identification of blood and urine biomarkers, which are closely linked to the functional damage of the organs affected in congestive heart failure, is important for a better stratification of the prognosis of patients and for the development of new therapeutic methods [2, 3].The renin angiotensin aldosterone system (RAAS) is a key pathophysiological mechanism in the development and Disease Markers progression of heart failure
Analysing the value of the area under the curve (AUC), it was observed that only angiotensin-converting enzyme type 2 (ACE2), apelin-13, NT-proBNP, and hsCRP presented statistically significant values indicating that they have an ability to predict evolution (Table 2)
The area under the curve (AUC) was 0.796 indicating that the variable can be used to predict the evolution of the patient (Figure 1)
Summary
In patients with heart failure, congestion is the dominant clinical profile and the main pathophysiological mechanism that causes organic dysfunction [1].The therapeutic reduction of the congestion leads to improved organ function and improved patient prognosis [1].The identification of blood and urine biomarkers, which are closely linked to the functional damage of the organs affected in congestive heart failure, is important for a better stratification of the prognosis of patients and for the development of new therapeutic methods [2, 3].The renin angiotensin aldosterone system (RAAS) is a key pathophysiological mechanism in the development and Disease Markers progression of heart failure. In patients with heart failure, congestion is the dominant clinical profile and the main pathophysiological mechanism that causes organic dysfunction [1]. The identification of blood and urine biomarkers, which are closely linked to the functional damage of the organs affected in congestive heart failure, is important for a better stratification of the prognosis of patients and for the development of new therapeutic methods [2, 3]. RAAS is activated together with the sympathetic system in patients with heart failure as a compensatory mechanism to decrease cardiac output. It contributes to maintaining cardiac output through water and salt retention, peripheral vasoconstriction, increased cardiac contractility, and myocardial hypertrophy [4]
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