The Right Approach: Power of Biomarkers in the Assessment and Management of Right Ventricular Dysfunction

Abstract

Right ventricular (RV) dysfunction is common and linked to poor outcomes across conditions such as heart failure (HF), acute coronary syndromes, pulmonary embolism, and pulmonary hypertension. While imaging, electrocardiogram (ECG), and invasive tests remain central to RV assessment, circulating biomarkers offer a rapid, non-invasive, and reliable alternative. These biomarkers reflect key pathophysiological processes, including myocardial injury, stress, fibrosis, inflammation, congestion, and multiorgan involvement. High-sensitivity troponins and natriuretic peptides (BNP, NT-proBNP) are already widely used, while emerging biomarkers-such as CA125, copeptin, galectin-3, and others-may enhance diagnostic accuracy and risk stratification. Some, like CA125 and NT-proBNP, have shown promise in guiding post-discharge therapy. However, challenges remain regarding the specificity of biomarkers for RV dysfunction and their role across different clinical contexts. This review provides an integrated overview of RV dysfunction, with a focus on the diagnostic and therapeutic potential of both established and novel biomarkers.

Keywords: acute myocardial infarction; biomarker; cardiovascular disease; diagnosis; dysfunction; heart failure; pulmonary embolism; pulmonary hypertension; right ventricle; risk stratification; therapy.

Figure 1

Aetiologias and mechanisms of right ventricular dysfunction. CIED—cardiac implantable devices, LV—left ventricular, LAVD—left ventricular assist device, RV—right ventricular, TR—tricuspid regurgitation. Note: RV dysfunction results from the interplay of increased afterload, reduced contractility, and excessive preload. Acute or chronic pressure overload leads to dilation, hypertrophy, and secondary ventricular tricuspid regurgitation. Reduced contractility leads to RV dilatation and secondary ventricular tricuspid regurgitation, which increased RV preload and exacerbates RV dysfunction. Excessive preload further strains the RV. Secondary tricuspid regurgitation amplifies all mechanisms, fueling congestion and creating a vicious cycle of RV failure. Interconnecting arrows depict how these mechanisms interact and collectively contribute to RV dysfunction progression.

Figure 2

Established and emerging biomarkers reflecting pathophysiological processes relevant for RV dysfunction. ALT—alanine aminotransferase, ALP—alkaline phosphatase, AST—aspartate aminotransferase, Bio-ADM—biologically active adrenomedullin, BNP—B-type natriuretic peptide, CA-125—carbohydrate antigen 125, DPP3—dipeptidyl peptidase-3, eGFR—estimated glomerular filtration rate, FGF23—fibroblast growth factor 23, GDF-15—growth differentiation factor-15, GGT—gamma-glutamyl transferase hs-CRP—high sensitivity C-reactive protein, LDH—lactate dehydrogenase, LP-PLA2—lipoprotein-associated phospholipase A2, micro-RNAs—micro ribonucleic acids, MR-proANP—midregional pro-atrial natriuretic peptide, NGAL—neutrophil gelatinase-associated lipocalin, NT-proBNP—N-terminal pro-B type natriuretic peptide, oxLDL—oxidised low density lipoprotein, TNFα—tumour necrosis factor alfa, SPARCL1—SPARC-like protein 1, sST2—soluble suppression of tumorigenicity-2. Note: Established biomarkers with the strongest validation for diagnosis, prognosis, or therapy are shown in red; those with established but less robust validation in black; and emerging biomarkers in blue.