Inflammatory and fibrotic biomarkers in relation to left ventricular mass index among hypertensive patients evaluated in a cardiology setting

Abstract Left ventricular hypertrophy, expressed as an increased left ventricular mass index (LVMI), is a common manifestation of hypertensive heart disease and may be influenced by inflammatory and fibrotic pathways. To evaluate the association and within-sample discriminatory performance of inflammatory and fibrotic biomarkers, including high-sensitivity C-reactive protein (hs-CRP), galectin-3, propeptide of type III procollagen (PIIINP), and suppression of tumorigenicity 2 (ST2), in relation to abnormal left ventricular mass index (LVMI) among hypertensive patients evaluated in a cardiology setting. A cross-sectional study with prospective enrollment was conducted from January to December 2025. The participants underwent clinical assessment, laboratory testing (hs-CRP, galectin-3, PIIINP, and ST2), and transthoracic echocardiography, and the LV mass was calculated via the Devereux formula and indexed to the body surface area (BSA). Patients were classified as normal vs. abnormal (enlarged) for LVMI. Receiver operating characteristic (ROC) curves were used to assess within-sample discrimination between patients with normal and abnormal LVMI. Compared with patients with normal LVMI, those with abnormal LVMI were older, had higher body mass index, longer hypertension duration, higher creatinine, and lower estimated glomerular filtration rate. Biomarker levels, including PIIINP (210.52 ± 100.77 vs. 124.38 ± 45.10 ng/mL), hs-CRP (3.53 ± 0.18 vs. 1.20 ± 0.15 mg/L), and galectin-3 (27.65 ± 8.08 vs. 15.80 ± 4.96 ng/mL), were significantly greater in the abnormal LVMI group (all p < 0.001). In the exploratory multivariable model, PIIINP (OR = 1.03, p = 0.021), hs-CRP (OR = 4.34, p < 0.001), and galectin-3 (OR = 1.44, p < 0.001) were associated with abnormal LVMI. Galectin-3 showed the highest within-sample discriminatory performance (AUC = 0.904), followed by PIIINP (AUC = 0.797) and hs-CRP (AUC = 0.749). LVMI was positively correlated with galectin-3 ( r = 0.454), PIIINP ( r = 0.393), and hs-CRP ( r = 0.251). Among hypertensive patients evaluated in a cardiology setting, abnormal LVMI was associated with older age, higher BMI, longer hypertension duration, impaired renal indices, and higher levels of selected fibrotic and inflammatory biomarkers. Because the cohort included patients with reduced systolic function and incomplete heart failure phenotyping, these associations should not be interpreted as reflecting hypertension-mediated remodeling alone. Rather, the findings describe exploratory biomarker–LVMI relationships within a clinically heterogeneous hypertensive cardiology cohort, potentially reflecting overlapping contributions from hypertension, reduced systolic function, renal impairment, and broader cardiometabolic comorbidity. Validation in prospective studies with detailed heart failure characterization is required.