82-year-old woman comes to our clinical observation for worsening exertional dyspnea, with ECG evidence of atrial fibrillation (AF) with high ventricular response. Past medical history: previous right breast carcinoma treated in 1998 with quadrantectomy, radiotherapy and hormone therapy. Previous ischemic transitory attack. Hypertension. Dyslipidemia. The patient reports the first episode of paroxysmal AF in 2016, for which anticoagulant therapy with new oral anticoagulants NOACs was started for CHA2DS2VASc=6. During anticoagulant therapy episode of ocular haemorrhage for which the patient discontinued therapy with NOACs and used low-molecular-weight heparin LMWH "as needed" in the course of arrhythmic relapses. In July and August 2019 relapses of symptomatic paroxysmal AF. Multiple attempts to take different anticoagulants (Rivaroxaban, Edoxaban) poorly tolerated. The patient undergoes catheter ablation by isolation of the pulmonary veins (considered first line according to ESC guidelines for the control of symptoms in patients with paroxysmal AF) and percutaneous left atrial appendage occlusion (LAAO), with indication of anticoagulation therapy for at least 4 weeks after the procedure (Apixaban 2.5 mg bid, reduced dose due to the presence of age>80 years and weight<60 kg). At the entrance to our hospital, an ECG is performed with a finding of total arrhythmia from AF with a high ventricular response (HR 130 bpm), conducted with left bundle branch block (LBBB); cardiac echo-Doppler ultrasound is performed with a slight reduction in left ventricular systolic function (EF 45%), second degree diastolic dysfunction with increased filling pressures, moderate mitral valve insufficiency, severe left atrial dilatation (LAVi 125 ml/m2), moderate tricuspid valve insufficiency with moderate pulmonary arterial hypertension (PAPS 55 mmHg), right atrial dilatation, circumferential pericardial detachment, dilated inferior vena cava hyporeactive with breath acts. At blood tests: BNP 1022 pg/ml, sodium 145 mmol/l, potassium 3.5 mmol/l, creatinine 1.17 mg/dl with eGFR 43 ml/min/1.73mq. Rate control therapy with ß-blockers and Digoxin and diuretic therapy with Furosemide and Canrenone is set, with improvement of symptoms and clinical conditions. Anticoagulant therapy with LMWH is also undertaken but the patient shows poor adherence. After home discharge, the patient goes back to the emergency room for dyspnea. Further cardiac echo-Doppler ultrasound is performed with evidence of thrombotic formation in the left atrium of the size of 30×25 mm. Therapeutic dosage LMWH therapy is started with subsequent Warfarin embrication according to INR, obtaining complete resolution of the thrombotic formation. A systematic review of device-related thrombosis (DRT) after left atrial appendage occlusion (LAAO) proved that the overall incidence of DRT was 3.9% and the median time from procedure to diagnosis of DRT was 1.5 months. According to currently reported cases, most DRTs occur within one year after LAAO. This particular clinical case of DRT three years after LAAO underlines the importance of accurate assessment of the patient's risk profile: LAAO is a valid alternative to anticoagulant therapy in patients at high risk of bleeding but with low embolic risk profile. It's known that high CHA2DS2VASc values ​​and reduced cardiac function are recognized risk factors for thrombus formation, such as patient compliance with antithrombotic therapy. Surely additional studies are needed to determine if the current practice of antithrombotic regimens and duration after LAAO is sufficient.

Background Ibrutinib is a Bruton tyrosine kinase inhibitor, approved in the last few years for treatment as primary option for all subsets of chronic lymphocytic leukemia (CLL). Its use is associated with increased incidence of atrial fibrillation (AF). Objectives Aim of this study is to determine whether there are echocardiographic parameters that could identify patients at major risk of developing ibrutinib-related atrial fibrillation (IRAF). Methods We performed a retrospective review of 26 patients (mean age 70,34 ± 11,69; 27% females), admitted at our EchoLab in the last year, who underwent echocardiogram prior to Ibrutinib treatment. Echo-Doppler assessment was realized according to the standards of the European Association of Cardiovascular Imaging (EACVI) standardization of the echo report. Left atrial (LA) strain was measured with EchoPAC, obtaining peak atrial longitudinal strain (PALS) and peak atrial contraction strain (PACS) on 4-chambers and 2-chambers views. Continuous normally distributed variables were compared by using the Student t-test. A probability value < 0,05 was considered statistically significant. Analyses were performed with SPSS version 25 (IBM Corporation, Somers, New York). Results Six patients developed IRAF (23%). There weren't differences of clinical characteristics between the two groups (age, body mass index, arterial blood pressure, heart rate and diabetes, hypertension and cardiovascular diseases prevalence). It was noticed that IRAF's group had lower ejection fraction (EF) (54,67 ± 1,96 vs 60,90 ± 4,35, p-value < 0,0001), higher left atrium volume index (48,95 ± 16,31 vs 34,18 ± 9,07, p-value: 0,009), higher pulmonary arterial pressure values (PAPs) (44,16 ± 11,26 vs 32,89 ± 8,44, p-value: 0,015). Furthermore, it was noticed that peak atrial longitudinal strain (PALS) and peak atrial contraction strain (PACS) were reduced in patients who developed IRAF (PALS 4Ch: 18,89 ± 6,90 vs 29,40 ± 9,79, p-value 0,06; PACS 4Ch: 10,56 ± 5,66 vs 14,31 ± 5,72, p-value: 0,25; PALS 2Ch: 23,36 ± 5,02 vs 32,88 ± 16,57, p-value: 0,28; PACS 2Ch: 13,61 ± 8,16 vs 18,33 ± 9,87, p-value: 0,39), but not statistically significant, probably due to the sample size. Conclusions This is a preliminary pilot study which confirms the data already present in the literature. The importance of baseline evaluation by echocardiogram including measurement of atrial strain of patients before starting treatment with Ibrutinib is emphasized since, given the same anthropometric characteristics and risk factors, there are echocardiographic parameters that help us to identify patients at major risk of developing IRAF. Pharmacological intervention tailored on this type of basal echocardiographic evaluation could allow the reduction of IRAF's onset and improve patient outcomes in the long term. Certainly, further follow-up studies will be needed to confirm this hypothesis.

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