Heart rhythm · 2025
Associations between biomarkers and P-wave indices in relation to atrial fibrillation development in heart failure patients.
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Nezami Zainu, Jujic Amra, Ohlsson Marcus, Magnusson Martin, Isholth Hannes Holm, Platonov Pyotr G
Аннотация
BACKGROUND: The predictive value of atrial conduction abnormalities, reflected by P-wave indices (PWIs), and their association with biomarkers signaling fibrosis for the development of atrial fibrillation (AF) in patients with heart failure (HF) remains underexplored.
OBJECTIVE: We aimed to investigate the associations among PWIs, fibrosis biomarkers, and the risk of incident AF in patients with HF.
METHODS: A total of 476 patients (mean age 74.6 years; 68% male) with new-onset or worsening HF were followed for 5 years. Fibrosis-associated biomarkers (tissue inhibitor of metalloproteinase 4, matrix metalloproteinase 2 [MMP-2], matrix metalloproteinase 3, matrix metalloproteinase 9, suppression of tumorigenicity 2, growth/differentiation factor 15 [GDF-15], galectin-3) were analyzed using the proximity extension assay. PWIs, including P-wave duration, P-wave amplitude in lead I, P-wave terminal force in lead V1, axis, and morphology, were derived from electrocardiograms processed with the Glasgow algorithm. Cox regression assessed associations among the biomarkers, PWIs, and incident AF.
RESULTS: During follow-up, 41 developed AF over 5 years. Low P-wave amplitude correlated negatively with GDF-15 (P < .001) and MMP-2 (P = .037) in leads I and II. 6 biomarkers were significantly associated with incident AF in adjusted analysis: tissue inhibitor of metalloproteinase 4 (P = .007), MMP-2 (P = .046), matrix metalloproteinase 3 (P = .007), suppression of tumorigenicity 2 (P = .003), GDF-15 (P = .001), and galectin-3 (P = .048). Among PWIs, P-wave axis of <0° (P = .021) and low P-wave amplitude in lead I (P = .036) were significantly associated with incident AF.
CONCLUSION: In patients with advanced HF, fibrotic biomarkers were associated with incident AF. Low P-wave amplitude and abnormal P-wave axis (<0°) were associated with incident AF. This may reflect an abnormal LA-conduction pathway and a displaced intra-atrial conduction pattern in advanced HF.
OBJECTIVE: We aimed to investigate the associations among PWIs, fibrosis biomarkers, and the risk of incident AF in patients with HF.
METHODS: A total of 476 patients (mean age 74.6 years; 68% male) with new-onset or worsening HF were followed for 5 years. Fibrosis-associated biomarkers (tissue inhibitor of metalloproteinase 4, matrix metalloproteinase 2 [MMP-2], matrix metalloproteinase 3, matrix metalloproteinase 9, suppression of tumorigenicity 2, growth/differentiation factor 15 [GDF-15], galectin-3) were analyzed using the proximity extension assay. PWIs, including P-wave duration, P-wave amplitude in lead I, P-wave terminal force in lead V1, axis, and morphology, were derived from electrocardiograms processed with the Glasgow algorithm. Cox regression assessed associations among the biomarkers, PWIs, and incident AF.
RESULTS: During follow-up, 41 developed AF over 5 years. Low P-wave amplitude correlated negatively with GDF-15 (P < .001) and MMP-2 (P = .037) in leads I and II. 6 biomarkers were significantly associated with incident AF in adjusted analysis: tissue inhibitor of metalloproteinase 4 (P = .007), MMP-2 (P = .046), matrix metalloproteinase 3 (P = .007), suppression of tumorigenicity 2 (P = .003), GDF-15 (P = .001), and galectin-3 (P = .048). Among PWIs, P-wave axis of <0° (P = .021) and low P-wave amplitude in lead I (P = .036) were significantly associated with incident AF.
CONCLUSION: In patients with advanced HF, fibrotic biomarkers were associated with incident AF. Low P-wave amplitude and abnormal P-wave axis (<0°) were associated with incident AF. This may reflect an abnormal LA-conduction pathway and a displaced intra-atrial conduction pattern in advanced HF.