Journal of electrocardiology · 2026
Relationship between fragmented QRS and serum fibroblast growth factor-23 in hypertensive patients with left ventricular hypertrophy.
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Bebek Berkant, Karabulut Alpaslan, Eser Barış, Sarıhan Abdullah, Birgün Abdülmelik, Özden Muharrem, Yetim Mucahit, Kalçık Macit, Bekar Lütfü, Biter Burak
Аннотация
BACKGROUND: Hypertensive heart disease is frequently accompanied by left ventricular hypertrophy (LVH) and myocardial fibrosis, which contribute to diastolic dysfunction and adverse cardiovascular outcomes. Fragmented QRS (fQRS) on surface electrocardiography has been associated with myocardial fibrosis and is considered a potential noninvasive marker of myocardial fibrosis. Fibroblast growth factor-23 (FGF-23), a key regulator of mineral metabolism, has been implicated in myocardial remodeling and fibrosis; however, its relationship with fQRS in hypertensive patients with LVH has not been fully elucidated.
METHODS: In this cross-sectional, single-center study, 265 patients with isolated hypertension and echocardiographically confirmed LVH were enrolled. All participants underwent clinical evaluation, laboratory testing, transthoracic echocardiography, and 12‑lead electrocardiography. Serum FGF-23 levels were measured using a sandwich enzyme-linked immunosorbent assay. Patients were compared according to the presence or absence of fQRS. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the discriminative ability of FGF-23 and left ventricular mass index (LVMI) for predicting fQRS.
RESULTS: Fragmented QRS was present in 55 patients (20.8%). Patients with fQRS had significantly higher serum FGF-23 levels compared with those without fQRS (835.1 ± 153.4 vs. 670.7 ± 223.7 pg/mL, p < 0.001). The fQRS-positive group also exhibited higher LVMI and a lower E/A ratio, indicating impaired diastolic function (all p < 0.01). ROC analysis demonstrated that FGF-23 had a moderate ability to predict the presence of fQRS (AUC = 0.734, 95% CI: 0.661-0.808), exceeding that of LVMI (AUC = 0.654, 95% CI: 0.574-0.735).
CONCLUSIONS: In hypertensive patients with LVH, the presence of fQRS is associated with elevated serum FGF-23 levels, increased LVMI, and impaired diastolic function. These findings suggest a potential link between FGF-23-related pathways and possible myocardial fibrotic remodeling, and support the complementary value of FGF-23 alongside electrocardiographic markers in risk stratification.
METHODS: In this cross-sectional, single-center study, 265 patients with isolated hypertension and echocardiographically confirmed LVH were enrolled. All participants underwent clinical evaluation, laboratory testing, transthoracic echocardiography, and 12‑lead electrocardiography. Serum FGF-23 levels were measured using a sandwich enzyme-linked immunosorbent assay. Patients were compared according to the presence or absence of fQRS. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the discriminative ability of FGF-23 and left ventricular mass index (LVMI) for predicting fQRS.
RESULTS: Fragmented QRS was present in 55 patients (20.8%). Patients with fQRS had significantly higher serum FGF-23 levels compared with those without fQRS (835.1 ± 153.4 vs. 670.7 ± 223.7 pg/mL, p < 0.001). The fQRS-positive group also exhibited higher LVMI and a lower E/A ratio, indicating impaired diastolic function (all p < 0.01). ROC analysis demonstrated that FGF-23 had a moderate ability to predict the presence of fQRS (AUC = 0.734, 95% CI: 0.661-0.808), exceeding that of LVMI (AUC = 0.654, 95% CI: 0.574-0.735).
CONCLUSIONS: In hypertensive patients with LVH, the presence of fQRS is associated with elevated serum FGF-23 levels, increased LVMI, and impaired diastolic function. These findings suggest a potential link between FGF-23-related pathways and possible myocardial fibrotic remodeling, and support the complementary value of FGF-23 alongside electrocardiographic markers in risk stratification.