Cardiovascular Biomarkers: Tools for Precision Diagnosis and Prognosis

Abstract

The present study provides a detailed review of cardiovascular biomarkers critical for the diagnosis, prognosis, and pathophysiology of cardiovascular diseases, the leading cause of global morbidity and mortality. These biomarkers aid in detecting disease onset, progression, and therapeutic responses, providing insights into molecular mechanisms. Enzyme markers like AST, CK-MB, LDH, CA-III, and HBDH are pivotal for detecting myocardial injury during acute events. Protein markers such as CRP, H-FABP, and MPO shed light on inflammation and oxidative stress. Cardiac Troponins, the gold standard for myocardial infarction diagnosis, exhibit high specificity and sensitivity, while IMA and GPBB indicate ischemia and early myocardial damage. Peptide markers, including BNP and NT-proBNP, are crucial for heart failure diagnosis and management, reflecting ventricular stress and remodeling. Novel peptides like MR-proANP and MR-proADM aid in assessing disease severity. Lipid markers such as lipoprotein-associated phospholipase A2 and oxylipins provide insights into lipid metabolism and atherosclerosis. Inflammatory and stress-related biomarkers, including TNFα, IL-6, GDF-15, and Pentraxin 3, illuminate chronic inflammation in CVDs. Hormonal markers like copeptin and endothelin-1 highlight neurohormonal activation, while emerging markers such as ST2, galectin-3, PAPP-A, and TMAO elucidate fibrosis, remodeling, and metabolic dysregulation. The inclusion of microRNAs and long non-coding RNAs represents a breakthrough in biomarker research, offering sensitive tools for early detection, risk stratification, and therapeutic targeting. This review emphasizes the diagnostic and prognostic utility of these biomarkers, advancing cardiovascular care through personalized medicine.

Keywords: IL-6; TNFα; cardiac troponins; cardiovascular biomarkers; copeptin and endothelin-1; heart failure biomarkers; miRNAs.

Figure 1

Schematic illustration of various cardiovascular diseases. Figure was created using app.biorender.com.

Figure 2

Schematic representation of the role of H-FABP in cardiac injury, metabolism, and therapeutic modulation. Under physiological conditions, H-FABP functions as a transport protein in cellular metabolism, reversibly binding fatty acids and activating peroxisome proliferator-activated receptors (PPARs), thereby contributing to lipid metabolism and energy homeostasis. The expression of H-FABP is regulated by microRNA-1 (miR-1). In response to cardiac injury, H-FABP is rapidly released into the bloodstream, where it can be quantified as a biomarker. Increased H-FABP levels are associated with ischemia, inflammation, fibrosis, and strain, ultimately leading to heart failure. Physical training and pharmacological interventions, such as anti-tachycardic therapy, have been shown to reduce plasma H-FABP levels, supporting their role in therapy. Figure is adapted from Rezar et al. [23].

Figure 3

Mechanisms of CRP in atherosclerotic CVD. CRP, synthesized in the liver in response to IL-6, IL-1β, and TNF, binds to DAMPs and PAMPs, activating the complement cascade and macrophages. This inflammatory response promotes oxidized LDL deposition, foam cell formation, and inflammasome activation, increasing IL-1β and IL-18 production. The resulting endothelial dysfunction and chronic inflammation contribute to an increased atherosclerotic burden and the progression of CAD. Figure is adapted from Amezcua-Castillo E et al. [24].

Figure 4

Diagram illustrating the structural domains of MMPs and TIMPs, categorized by sequence similarity and cellular location. Secreted MMPs include matrilysins, gelatinases, stromelysins, and collagenases, whereas MT-MMPs and GPI-anchored proteinases remain membrane-bound. The gray box highlights the specific domains of MMPs and TIMPs. Figure is adapted from Molière et al. [33].

Figure 5

The role of ET-1 in the pathogenesis of AHF. ET-1 induces systemic and pulmonary vasoconstriction, promotes cardiac remodeling and neurohormonal activation, and worsens renal function, thereby contributing to vascular and cardiac dysfunction. Figure is adapted from Dmour et al. [62].

Figure 6

Demonstrates the role of IL-6 in atherosclerosis, myocardial infarction, and vascular calcification. IL-6 trans-signaling activates the JAK/STAT pathway, inducing chronic inflammation, endothelial dysfunction, and lipid deposition, which drive plaque formation and rupture. IL-6 also upregulates RUNX2 and RANKL, promoting vascular smooth muscle cell differentiation into osteoblasts, contributing to vascular calcification. Figure is adapted from Feng et al. [72].

Figure 7

Structure, physiological functions, and clinical applications of AVP and copeptin were represented. Figure is adapted from Mu et al. [90].