Ibrutinib and Bruton's Tyrosine Kinase Inhibitors in Chronic Lymphocytic Leukemia: Focus on Atrial Fibrillation and Ventricular Tachyarrhythmias/Sudden Cardiac Death.

Background: The natural history of chronic lymphocytic leukemia (CLL) was dramatically improved by the introduction of ibrutinib, a Bruton's tyrosine kinase (BTK) inhibitor. In this review, we aimed to summarize and critically evaluate the association between first- and second-generation BTK inhibitors and the risk of atrial fibrillation (AF) and ventricular arrhythmias (VA).

Summary: Since the first clinical experience, the development of AF was observed as the result of off-target effects that likely combined with patient's predisposing risk factors and concomitant cardiac morbidities.

[Optimal therapeutic management in the clinical journey of patients with heart failure].

Heart failure (HF) is still characterized by high mortality rates, despite the progress achieved in terms of treatment options. With regard to the treatment of HF with reduced ejection fraction (HFrEF), the 2016 European Society of Cardiology guidelines included in the therapeutic algorithm the angiotensin receptor-neprilysin inhibitor class, whose efficacy in modifying patient prognosis has been extensively proven in many clinical studies. Sacubitril/valsartan, the only representative of this drug class, can effectively affect the natural history of HF, thus reducing cardiovascular mortality (sudden death and death due to worsening cardiac function), total mortality, as well as first and recurrent hospitalization events, by improving renal function, cardiac remodeling, functional capacity and the patient's health-related quality of life.

Single coronary artery with anomalous origin of right coronary artery from left main stem.

We report the case of a 57-year-old man with unstable angina that was taken up for coronary angiography, which showed an anomalous right coronary artery originating from left main stem.

Provokable left ventricular outflow tract obstruction in a patient without hypertrophy.

Background: A 61-year-old man presented with shortness of breath and chest pain on exertion. He had been diagnosed as having hiatus hernia 2 years previously and was taking proton-pump inhibitors as necessary. He had a family history of ischemic heart disease and subarachnoid hemorrhage.