Abstract 14206: Cross-Sectional, Exploratory Assessment of Biomarkers in Patients With Decompensated Heart Failure and Underlying Coronary Artery Disease (abide-hf)

Abstract

Introduction: Heart failure (HF) is a key contributor to high mortality and economic burden associated with cardiovascular diseases. Understanding the factors responsible for accelerated HF progression due to comorbid conditions is important in HF management. Hypothesis: The hypothesis of this study was that specific biomarkers related to thrombosis, inflammation, cardiac injury, and remodeling in patients with reduced ejection fraction (HFrEF) and coronary artery disease (CAD) may inform disease progression and aid in evaluating therapeutic efficacy. Methods: This study was a cross-sectional, exploratory assessment of biomarkers related to thrombosis, inflammation, and cardiac injury/remodeling in decompensated heart failure patients with reduced ejection fraction and underlying CAD. Symptomatic HF patients (n=74) with reduced left ventricular ejection fraction (LVEF ≤40%, HF ≥3 months) and significant underlying CAD as evidenced by previous myocardial infarction, prior coronary artery bypass graft, 50% coronary stenosis of one or more arteries, and history of percutaneous coronary intervention with or without stenting were enrolled in the study, and age-matched healthy subjects (n=20) were enrolled for comparative analysis of biomarkers. Results: Significant differences between HF+CAD and Controls were observed for thrombosis biomarkers (TM, p =0.0002, TGA [lag time, p =0.003; endogenous thrombin potential p =0.048], inflammatory biomarkers (CD62P, p =0.006; hsCRP, p= 0.0064; S100β, p =0.0004), and cardiac injury/remodeling (GDF-15, p =0.0002; NTproBNP, p <0.0001). Conclusions: Elevated levels of hsCRP and GDF-15 demonstrate heightened systemic inflammation in HF and CAD, and support the hypothesis that targeting inflammation may provide additional treatment options for this patient population. A novel finding of this study was that S100β, previously identified to play a role in maladaptive compensatory mechanisms, was higher in HF+CAD patients and correlated with multiple biomarkers including, CD62P, NTproBNP, and TM. (ClinicalTrials.gov Identifier: NCT03551756).