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Peer-reviewedCC BY 4.0International Journal of Hypertension

Association Between β1‐Selective Beta‐Blocker Use and P‐Wave Terminal Force in Lead V1 in Hypertensive Patients With Left Ventricular Hypertrophy

  1. 1Department of Cardiology Faculty of Medicine İzmir Demokrasi University İzmir Türkiye
  2. 2Department of Cardiology Buca Seyfi Demirsoy Training and Research Hospital İzmir Türkiye

Abstract

Background: P‐wave terminal force in lead V1 (PTFV1) is an electrocardiographic marker of atrial electrical abnormality. We investigated whether β1‐selective beta‐blocker use was associated with PTFV1 in hypertensive patients with echocardiographically confirmed left ventricular hypertrophy (LVH).

Methods: This retrospective study included 182 eligible patients with essential hypertension and LVH selected from 1372 screened patients. Patients were classified as β1‐selective beta‐blocker users (n = 82) or nonusers (n = 100). Abnormal PTFV1 was defined as ≥ 0.04 mm s. Multivariable regression and sensitivity analyses were performed.

Results: PTFV1 was lower in beta‐blocker users than in nonusers (0.024 [0.015–0.036] vs. 0.030 [0.020–0.048] mm s, p = 0.005). In the primary adjusted model, beta‐blocker use was associated with lower PTFV1 (B = −0.008, standardized β = −0.202, 95% CI −0.014 to −0.002, p = 0.009), although model explanatory capacity was limited (R 2 = 0.064; adjusted R 2 = 0.021; overall p = 0.168). In an extended sensitivity analysis additionally adjusting for diabetes, renal function, and concomitant antihypertensive therapies, beta‐blocker group status remained associated with lnPTFV1 (standardized β = 0.294, p < 0.001; R 2 = 0.147; adjusted R 2 = 0.081; overall p = 0.011). Beta‐blocker use was also associated with lower odds of abnormal PTFV1 (OR = 0.43, 95% CI 0.22–0.84, p = 0.013).

Conclusion: β1‐Selective beta‐blocker use was associated with lower PTFV1 and a lower likelihood of abnormal PTFV1. These findings suggest a more favorable atrial electrical profile but should be considered hypothesis‐generating given the retrospective design and modest model explanatory capacity.

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BibTeX
@article{alpaslan2026association,
  title = {{Association Between β1‐Selective Beta‐Blocker Use and P‐Wave Terminal Force in Lead V1 in Hypertensive Patients With Left Ventricular Hypertrophy}},
  author = {Erkan Alpaslan and Sedat Taş and Ümmü Taş and Mehmet Eyüboğlu and Ömer Özkan Duman and Onur Dalgıç and Lütfullah Candan and Ahmet Rıdvan Özdemir},
  journal = {International Journal of Hypertension},
  year = {2026},
  month = oct,
  doi = {10.1155/ijhy/2095472},
  url = {https://doi.org/10.1155/ijhy/2095472},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Association Between β1‐Selective Beta‐Blocker Use and P‐Wave Terminal Force in Lead V1 in Hypertensive Patients With Left Ventricular Hypertrophy
AU  - Erkan Alpaslan
AU  - Sedat Taş
AU  - Ümmü Taş
AU  - Mehmet Eyüboğlu
AU  - Ömer Özkan Duman
AU  - Onur Dalgıç
AU  - Lütfullah Candan
AU  - Ahmet Rıdvan Özdemir
PY  - 2026
DA  - 2026/10/26
JO  - International Journal of Hypertension
DO  - 10.1155/ijhy/2095472
UR  - https://doi.org/10.1155/ijhy/2095472
AB  - Background: P‐wave terminal force in lead V1 (PTFV1) is an electrocardiographic marker of atrial electrical abnormality. We investigated whether β1‐selective beta‐blocker use was associated with PTFV1 in hypertensive patients with echocardiographically confirmed left ventricular hypertrophy (LVH).  Methods: This retrospective study included 182 eligible patients with essential hypertension and LVH selected from 1372 screened patients. Patients were classified as β1‐selective beta‐blocker users (n = 82) or nonusers (n = 100). Abnormal PTFV1 was defined as ≥ 0.04 mm s. Multivariable regression and sensitivity analyses were performed.  Results: PTFV1 was lower in beta‐blocker users than in nonusers (0.024 [0.015–0.036] vs. 0.030 [0.020–0.048] mm s, p = 0.005). In the primary adjusted model, beta‐blocker use was associated with lower PTFV1 (B = −0.008, standardized β = −0.202, 95% CI −0.014 to −0.002, p = 0.009), although model explanatory capacity was limited (R 2 = 0.064; adjusted R 2 = 0.021; overall p = 0.168). In an extended sensitivity analysis additionally adjusting for diabetes, renal function, and concomitant antihypertensive therapies, beta‐blocker group status remained associated with lnPTFV1 (standardized β = 0.294, p < 0.001; R 2 = 0.147; adjusted R 2 = 0.081; overall p = 0.011). Beta‐blocker use was also associated with lower odds of abnormal PTFV1 (OR = 0.43, 95% CI 0.22–0.84, p = 0.013).  Conclusion: β1‐Selective beta‐blocker use was associated with lower PTFV1 and a lower likelihood of abnormal PTFV1. These findings suggest a more favorable atrial electrical profile but should be considered hypothesis‐generating given the retrospective design and modest model explanatory capacity.
SN  - 2090-0384
SN  - 2090-0392
ER  -