Clinical arrhythmology is an essential field for both electrophysiologists and cardiologists: in the case of the former to prevent the specialist from becoming a technician and in the case of the latter to fully understand the specialty. The clinical guidelines reaffirm this idea while also recommending an increasingly widespread interventional approach throughout the range of arrhythmias. This concept is clearly illustrated in the interaction between arrhythmia-cardiomyopathy and ventricular dysfunction. Between 10% and 50% of patients with heart failure have atrial fibrillation (AF), and the potential worsening of ventricular function due to inappropriate rate control is recognized. In patients with ventricular extrasystole (VE), who are often referred for electrophysiological assessment, several studies have shown an incidence of arrhythmia-induced cardiomyopathy of between 9% and 34%. Although knowledge of their pathophysiology is still incomplete, a fundamental factor is now recognized to be high total extrasystole burden, defined as more than 10 000 to 25 000 VE per day (10%-24% of the total number of complexes), as well as certain clinical characteristics (male sex, high body mass index), electrocardiographic characteristics (QRS width in VE > 153ms), and anatomic features (VE origin other than ventricular outflow tract).1 Although the incidence and prevalence of arrhythmia-induced cardiomyopathy is not known, early detection should be a priority, given the excellent response to treatment, which is generally interventional. The correlation between chronic consumption of caffeine-containing products and the degree of atrial and ventricular ectopy has still not been established.
The increasing prevalence of AF is a health challenge of the utmost importance. The 3 basic pillars of treatment include anticoagulation, rhythm control, and rate control.2 Recent evidence reflects the benefit of reducing or modifying risk factors, for example, substantially decreasing the arrhythmic load of AF by weight loss sustained in the long term. Along these lines, the CARDIO-FIT study analyzed the impact of cardiorespiratory fitness on arrhythmia recurrence in obese individuals with AF.3 The improvement in cardiorespiratory fitness achieved through a specific training program reduced recurrences, and this benefit was in addition to that obtained through weight loss: an increase of 1 metabolic equivalent corresponded to a 9% decrease in recurrences. Furthermore, several studies have confirmed the dose-dependent relationship between physical exercise and AF, as well as the additive effect of certain risk factors, and it was observed that more than 2000hours of high-intensity endurance training during the course of a lifetime, tall stature (> 179cm), abdominal obesity (> 102cm in men and 88cm in women), and sleep apnea syndrome were associated with AF.4 The role of intensive physical endurance training may also be proarrhythmic for the ventricle, and cause anatomical functional changes in the right ventricle in predisposed individuals. These changes can be detected by imaging techniques, particularly after exercise, and are associated with potentially fatal ventricular arrhythmias.
Oral anticoagulation in AF is becoming increasingly widespread, although this therapy is still underused in elderly patients and other subgroups with greater bleeding risk. In many cases, it is worth considering alternatives such as percutaneous closure of the left atrial appendage. In addition, the first specific reversal agent for dabigatran is now on the market (idarucizumab [Praxbind]). We do not know what the clinical impact of this availability will be.
Clinical history and the electrocardiogram (ECG) are the main source of information for stratification of arrhythmic risk: seek and you shall find. In patients with Brugada syndrome and no history of cardiac arrest, an S-wave ≥ 0.1 mV or duration ≥ 40 ms in lead I has been described as a marker of risk of sudden cardiac death.5 For this syndrome, the usefulness of quinidine in reducing malignant ventricular arrhythmias has also been confirmed. The term early repolarization has been used for more than 50 years now, but only in the last 10 has it been associated with sudden cardiac death. Finally, in 2015, a consensus was reached on its definition, thereby allowing appropriate characterization of this finding in the ECG for clinical investigation. Furthermore, progress in genetics is and will be important in the field of arrhythmology, and different studies continue to provide support for the clinical benefit of specific gene therapy. Genetic susceptibility determines certain aspects of the pathophysiology of many cardiac arrhythmias, and it is foreseen that the importance of genetic study will increase as the emphasis in rhythm disorders shifts to prevention.6