HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

BACKGROUND:
No known allergies. Cardiovascular risk factors (CVR): ex-smoker for 17 years.
Well-controlled arterial hypertension (AHT). Dyslipidaemia without medical treatment. Hyperuricaemia.
Obstructive sleep apnoea-hypopnoea syndrome (OSAHS) under treatment with continuous positive airway pressure (CPAP).
Haematological history: polyglobulia with periodic bleeding. In September 2017: diagnosed with lymphocytic lymphoma with p53 gene deletion. Degenerative shoulder arthropathy and acromioclavicular osteophytosis assessed by traumatology and rehabilitation.
Surgical interventions: inguinal hernia.
Usual treatment: enalapril/HCTZ 20/12.5 (1-0-0), allopurinol 300 mg 0-1-0, omeprazole 20 mg 1-0-0.
Preserved higher functions (SFB): independent for basic activities of daily living (BADL). Lives with his wife.

CURRENT ILLNESS:
During the first visit, the patient reports feeling tired, with more asthenia than usual. However, he denies dyspnoea, both on exertion and at rest, orthopnoea, oliguria or oedema in the lower limbs. There was no history of chest pain or palpitations.
An electrocardiogram (ECG) was performed and a blood test and echocardiogram were requested to complete the study.
Given the poor prognosis criteria associated with lymphocytic leukaemia, the haematology department decided to start treatment with ibrutinib (Bruton's tyrosine kinase inhibitor).
Approximately one month after starting treatment, the patient came to the emergency department with palpitations and a feeling of central thoracic oppression. On arrival, an
ECG showed a common atrial flutter with ventricular response at 150 bpm. There were no signs of heart failure on physical examination or chest X-ray. Treatment with beta-blockers was administered and spontaneously reverted to sinus rhythm after a few hours, and the patient was discharged and referred to outpatient cardio-oncohaematology consultations.

COMPLEMENTARY TESTS
ECG: sinus rhythm, complete right bundle branch block (RBBB) with secondary repolarisation abnormalities. No acute repolarisation alterations.
ANALYSIS: glucose 92 mg/dl, urea 117 mg/dl, creatinine 1.19 mg/dl, albumin 3.66 mg/dl, sodium 138 mmol/l, potassium 4.72 mmol/l, haemoglobin 12.4 g/dl, leukocytes 11,600 μL (N 68%), platelets 77000 μL.
ECOCARDIOGRAM: left ventricle (LV) not dilated or hypertrophic, with preserved global and segmental systolic function. Sclerocalcified aortic valve without functional alterations. Sclerosed mitral valve with mild regurgitation. Left atrium (LA) slightly dilated. Right ventricle (RV) not dilated with good function. Tricuspid insufficiency (TI) was not detected. The pulmonary acceleration curve does not suggest significant pulmonary hypertension. IVC not dilated. No pericardial effusion.
Emergency ECG: common atrial flutter with ventricular response at 150 bpm.
Chest X-ray: enlarged cardiac silhouette. No costophrenic sinus impingement or other signs of heart failure.

CLINICAL COURSE
After a first episode of atrial flutter, the patient met the criteria for anticoagulant treatment (CHA2DS2VASc: 3 due to age > 75 and hypertension), so treatment was started with rivaroxaban 15 mg, 1 tablet per day, and low-dose beta-blockers (bisoprolol 1.25 mg, 1 tablet per day).
One month later, he presented a new episode of palpitations together with dyspnoea on exertion and went to the emergency department. This time the ECG showed atrial fibrillation (AF) with rapid ventricular response. It was decided to apply a rate control strategy by administering digoxin and a higher dose of beta-blocker (bisoprolol 5 mg). Once the heart rate had been controlled and there were no congestive symptoms, the patient was discharged with an earlier cardio-oncohaematology appointment.
The patient was assessed one week later in the consultation room, where an ECG was performed showing sinus rhythm, so flecainide was started at low doses (50 mg at breakfast and 50 mg at dinner) and beta-blocker treatment was maintained (reducing the bisoprolol dose to 2.5 mg). Despite this treatment, the patient returned to the clinic 20 days later with palpitations of one week's duration, dyspnoea on medium exertion and oedema in the lower limbs. The ECG showed HF atrial flutter with ventricular response at 170 bpm, and the patient was admitted to the cardiology ward.
During admission, treatment with flecainide was suspended and a heart rate control strategy was initiated with high-dose beta-blockers (bisoprolol 10 mg per day) and digoxin, spontaneously reverting to sinus rhythm. Diuretic treatment was also started, with a good response and disappearance of the congestive signs, and the patient was discharged a week later.

DIAGNOSIS
AF - paroxysmal atrial flutter in the context of ibrutinib.
Episode of HF atrial flutter after taking flecainide.
Preserved biventricular function.
Lymphocytic lymphoma in treatment with ibrutinib.
