Heart failure (HF) is a clinical manifestation caused by various cardiovascular pathologies. It is characterized by the heart's inability to pump sufficient oxygenated blood to the body. HF is associated with a general deterioration in quality of life and a high rate of hospitalization and mortality. HF Severity is classified according to the New York Heart Association (NYHA) classification groups:
HF can be further divided into subcategories based on the patient's ejection fraction (EF). Three subcategories have been accepted to date: Heart failure with reduced ejection fraction (HFrEF), heart failure with intermediate ejection fraction (HFmrEF), and heart failure with preserved ejection fraction (HFpEF). For HFrEF, and to some extent HFmrEF, there are well-established treatment strategies that effectively reduce morbidity and outcome. Conversely, specific biomarkers and treatments for HFpEF patients are urgently needed.
The most common causes of HF, regardless of subtype, include coronary artery disease, previous myocardial infarction(s), hypertension, arrhythmia, and cardiomyopathy.
Cardiac fibrosis is an underlying process in all types of HF. HF often develops in patients with previous MI. MI is characterized by a reparative phase after the event, leading to increased deposition of collagen and other ECM proteins in the myocardium. Cardiac fibrosis, characterized by dynamic remodeling of extracellular matrix (ECM) proteins (Figure 1), plays an important role in the pathogenesis of HFpEF. Therefore, understanding the balance of ECM protein formation and degradation in HF is critical.
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