# Transthoracic Echocardiography as a Tool for Early Detection of Atrial Fibrillation in Patients Receiving Ibrutinib

**Authors:** Vittoria Gammaldi, Martina Pucci, Francesca La Rocca, Pasquale Megaro, Daniele Paoletta, Mariateresa Pontoriero, Luca Maria Capece, Roberto Luise, Marina Iacono, Roberta Esposito

PMC · DOI: 10.3390/life16020324 · 2026-02-13

## TL;DR

Transthoracic echocardiography can help identify patients at risk of developing atrial fibrillation while on ibrutinib treatment for chronic lymphocytic leukemia.

## Contribution

Baseline left atrial contractile function, as measured by echocardiography, may predict atrial fibrillation risk in ibrutinib-treated patients.

## Key findings

- Patients who developed atrial fibrillation had significantly lower baseline Peak Atrial Contraction Strain values.
- Left atrial functional parameters remained stable over 6 months despite a modest increase in indexed left atrial volume.
- Ibrutinib-related atrial fibrillation is likely due to pre-existing atrial vulnerability rather than early drug-induced dysfunction.

## Abstract

Background: Bruton’s tyrosine kinase inhibitors, particularly ibrutinib, have improved outcomes in patients with chronic lymphocytic leukemia but are associated with an increased risk of atrial fibrillation. The early identification of patients with increased susceptibility to atrial fibrillation remains a major challenge in cardio-oncology. Methods: This prospective pilot study included 45 patients with chronic lymphocytic leukemia treated with ibrutinib. All patients underwent comprehensive transthoracic echocardiography at baseline and after 6 months. Left atrial structure and function were assessed, with particular emphasis on speckle-tracking-derived left atrial strain parameters, including peak atrial longitudinal strain and peak atrial contraction strain. Results: At follow-up, a modest but significant increase in indexed left atrial volume was observed, while left atrial functional parameters remained stable. Patients who developed atrial fibrillation showed significantly lower baseline Peak Atrial Contraction Strain values compared with those who remained in sinus rhythm, whereas no significant differences in Peak Atrial Longitudinal Strain were detected. Conclusions: Ibrutinib-related atrial fibrillation appears to be driven primarily by pre-existing atrial vulnerability rather than early drug-induced atrial dysfunction. The baseline impairment of left atrial contractile function may represent a candidate echocardiographic marker of atrial functional vulnerability and may inform cardiovascular surveillance and monitoring strategies in patients treated with ibrutinib.

## Linked entities

- **Chemicals:** ibrutinib (PubChem CID 24821094)
- **Diseases:** atrial fibrillation (MONDO:0004981), chronic lymphocytic leukemia (MONDO:0004948)

## Full-text entities

- **Genes:** CSK (C-terminal Src kinase) [NCBI Gene 1445], AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, BTK (Bruton tyrosine kinase) [NCBI Gene 695] {aka AGMX1, AT, ATK, BPK, IGHD3, IMD1}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, TEC (tec protein tyrosine kinase) [NCBI Gene 7006] {aka PSCTK4}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** PACS (MESH:D013180), cardio-oncology toxicity (MESH:D000082802), ventricular systole (MESH:D018487), atrial structural and functional abnormalities (MESH:C566527), arrhythmia (MESH:D001145), bleeding (MESH:D006470), obesity (MESH:D009765), hematologic malignancies (MESH:D019337), arrhythmic (OMIM:212500), atrial impairment (MESH:D064752), dyslipidemia (MESH:D050171), chronic coronary syndrome (MESH:D054058), CLL (MESH:D015451), injury to (MESH:D014947), atrial disease (MESH:D004194), inflammation (MESH:D007249), atrial fibrosis (MESH:D005355), peripheral vascular disease (MESH:D016491), adult leukemia (MESH:D015459), atrial dysfunction (MESH:C538261), diabetes (MESH:D003920), cardiotoxic cancer (MESH:D009369), atrial enlargement (MESH:D006332), thromboembolic (MESH:D013923), cardiac complications (MESH:D006331), obstructive sleep apnea (MESH:D020181), atrial myocardial dysfunction (MESH:C563984), atrial functional impairment (MESH:D003072), systole (MESH:D000092244), Hypertension (MESH:D006973), anemia (MESH:D000740), drug toxicity (MESH:D064420), sudden death (MESH:D003645), cardiovascular (MESH:D002318), AF (MESH:D001281), endocrine disorders (MESH:D004700)
- **Chemicals:** Ibrutinib (MESH:C551803)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942086/full.md

---
Source: https://tomesphere.com/paper/PMC12942086