P wave terminal force V1 is associated with atrial myocardial inflammation, diastolic dysfunction and HFpEF in patients undergoing CABG

https://doi.org/10.1007/s00392-025-02737-x

Rosa Hultsch (Regensburg)1, C. Lochner (Regensburg)1, M. Wester (Regensburg)1, M. Tafelmeier (Regensburg)1, H. Heuer (Regensburg)2, B. Flörchinger (Regensburg)2, C. Schmid (Regensburg)2, L. S. Maier (Regensburg)1, S. Lebek (Regensburg)1, S. Wagner (Regensburg)1, M. Arzt (Regensburg)1, P. Hegner (Regensburg)1

1Universitätsklinikum Regensburg Klinik und Poliklinik für Innere Med. II, Kardiologie Regensburg, Deutschland; 2Universitätsklinikum Regensburg Herz-, Thorax- und herznahe Gefäßchirurgie Regensburg, Deutschland

 

Objective:

Cardiovascular high-risk patients with severe coronary artery disease are at increased risk for multiple comorbidities and secondary disorders. P wave terminal force in ECG lead V1 (PTFV1) is a noninvasive parameter associated with increased risk of atrial fibrillation (AF) and heart failure (HF). However, PTFV1 in HF with preserved ejection fraction (HFpEF) and underlying pathophysiologic mechanisms remain insufficiently studied.

Purpose:

We hypothesized that an increased PTFV1 is associated with HFpEF, increased myocardial inflammation in the atrium and elevated markers of congestion (NTproBNP).

Methods and Results:

We analyzed preoperative electrocardiograms and echocardiographic data of 106 patients undergoing elective coronary artery bypass grafting (CABG). Elevated PTFV1 was defined as > 4000 µV*ms. HFpEF was diagnosed according to ESC guideline criteria. Diastolic dysfunction was graded (none to III°) based on echocardiographic analysis. For 18 patients, atrial myocardial interleukin 1β mRNA expression was quantified (in %ACTB) from intraoperatively obtained right-atrial appendage biopsies using real-time qPCR.

Linear regression analysis determined a significant positive correlation between NTproBNP levels as surrogate for congestion and increased atrial pressure, and PTFV1 (r2=0.102, p=0.001, Figure A). This correlation was driven by the subgroup of HFpEF patients (r2=0.156, p=0.019, Figure B), and was not observed in patients without HFpEF (r2=0.004, p=n.s., not shown). Overall, patients with HFpEF also exhibited higher PTFV1 in comparison to those without (4088.9±1700.0 vs 2771.1±1463.9 µV*ms, p<0.001, Figure C). Similarly, echocardiographic diastolic dysfunction was associated with greater PTFV1 (3678.3 ± 2041.8 vs 2361.4± 963.7 µV*ms, p=0.004, Figure D). Furthermore, patients with an elevated PTFV1 were characterized by greater myocardial inflammation, indicated as higher interleukin-1β mRNA expression (0.184± 0.243 vs. 0.014± 0.007 %ACTB, p=0.002, Figure E).

Conclusion:

In this cohort of patients undergoing cardiac surgery, elevated PTFV1 was associated with HFpEF, increased atrial myocardial inflammation, elevated NTproBNP, and echocardiographic diastolic dysfunction. PTFV1 may serve as a non-invasive marker indicating pathophysiological mechanisms associated with HFpEF.

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