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PROGNOSTIC SIGNIFICANCE OF SST2 IN HEART FAILURE WITH REDUCED EJECTION FRACTION, A BIOMARKER OF CARDIOVASCULAR MORTALITY AND REHOSPITALIZATION.

射血分数 心力衰竭 生物标志物 心脏病学 内科学 医学 生物 生物化学
作者
Tamar Shengelia,B Tsinamdzgvrishvili,Kakha Nadaraia,K Liluashvili,T Talakvadze
出处
期刊:PubMed 卷期号: (356): 6-12
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摘要

Heart failure (HF) poses a substantial burden on healthcare systems and society, necessitating effective diagnostic tools for enhanced patient management. The soluble suppression of tumorigenesis 2 protein (Soluble Suppression of Tumorigenesis 2 (sST2)) has emerged as a promising biomarker linked to cardiac remodeling and fibrosis. This study investigates Soluble Suppression of Tumorigenesis 2 (sST2)'s potential as a diagnostic and prognostic marker for chronic heart failure (CHF) and explores its clinical utility in predicting outcomes. To evaluate the utility of Soluble Suppression of Tumorigenesis 2 (sST2) as a predictive and diagnostic marker in patients with heart failure with reduced ejection fraction (HFrEF). The study aims to explore the connection between Soluble Suppression of Tumorigenesis 2 (sST2) levels and cardiovascular (CV) mortality in patients suffering from chronic heart failure (CHF), providing insights into how Soluble Suppression of Tumorigenesis 2 (sST2) levels correlate with patient outcomes. Additionally, it seeks to assess the ability of Soluble Suppression of Tumorigenesis 2 (sST2) to predict critical clinical events such as hospital readmissions and adverse 02composite outcomes, offering a deeper understanding of its potential role in disease management. Furthermore, the research compares the prognostic accuracy of Soluble Suppression of Tumorigenesis 2 (sST2) with NT-proBNP, a well-established biomarker, to determine which marker is more reliable and informative for predicting the progression and severity of CHF. This prospective cohort study included 111 CHF patients enrolled from May 2020 to January 2022. Participants were classified into two groups based on their Soluble Suppression of Tumorigenesis 2 (sST2) concentrations (<35 ng/mL and >35 ng/mL) and monitored over a year. Comprehensive demographic, clinical, and echocardiographic data were collected, alongside blood samples for Soluble Suppression of Tumorigenesis 2 (sST2) and NT-proBNP analysis. Kaplan-Meier survival analysis, Cox regression modeling, and chi-square tests were employed, with statistical significance defined as P < 0.05. Patients with Soluble Suppression of Tumorigenesis 2 (sST2) levels above 35 ng/mL experienced a markedly higher one-year cardiovascular (CV) mortality rate of 27.3%, compared to just 2.2% in those with lower levels. Similarly, elevated Soluble Suppression of Tumorigenesis 2 (sST2) levels were strongly associated with an increased risk of hospital readmissions, as 27.3% of high-Soluble Suppression of Tumorigenesis 2 (sST2) patients required multiple hospitalizations within a year, compared to only 2.3% in the low-Soluble Suppression of Tumorigenesis 2 (sST2) group. In contrast to NT-proBNP, Soluble Suppression of Tumorigenesis 2 (sST2) levels were not affected by factors like age or kidney function, making it a more reliable and consistent marker of cardiac remodeling. Additionally, patients who did not show a reduction in Soluble Suppression of Tumorigenesis 2 (sST2) levels were significantly more likely to face adverse composite outcomes, with 45.5% affected, compared to 12.4% among those whose levels decreased. Soluble Suppression of Tumorigenesis 2 (sST2) has emerged as a valuable prognostic biomarker for CHF, offering advantages over NT-proBNP due to its independence from confounding factors such as renal function and atrial rhythm. Elevated Soluble Suppression of Tumorigenesis 2 (sST2) levels are strongly correlated with increased mortality, hospitalizations, and adverse outcomes. While baseline Soluble Suppression of Tumorigenesis 2 (sST2) levels provide meaningful insights into disease severity, short-term changes are less indicative of prognosis. Integrating Soluble Suppression of Tumorigenesis 2 (sST2) into routine clinical practice could improve CHF management by enabling early identification of high-risk patients and guiding personalized treatment strategies.

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