The association of sinus node disease and atrial tachyarrhythmias characterizes the bradycardia–tachycardia syndrome, which may result in an increased risk of heart failure, stroke, and death. Ageing and several cardiac and extracardiac diseases, which have the potential to affect both the atrial and the ventricular myocardium, can manifest their influence predominantly on the atria, leading to an atrial cardiomyopathy. In these cases, the same pathological process which leads to sinus node dysfunction can create a favourable substrate also for atrial tachyarrhythmias, which, if not present at the time of the initial diagnosis of the sinus node disease, can occur with an increasing prevalence during follow-up. In younger patients with no evident structural heart disease, a bradycardia–tachycardia syndrome may be the first clinical and unexpected manifestation of a still undiagnosed inherited genetic disease and therefore a specific diagnostic workup is necessary. In bradycardia–tachycardia syndrome, the most frequently encountered atrial tachyarrhythmia is atrial fibrillation, while typical atrial flutter is rarer. In peculiar subgroups of patients, other atrial tachyarrhythmias, such as atypical atrial flutter, macroreentrant or focal atrial tachycardia, may be present. In bradycardia–tachycardia syndrome, the evolution of atrial tachyarrhythmias clearly shows a worsening with an prevalence of associated atrial tachyarrhythmia over time. Pharmacological therapy for arrhythmias is of limited use, due to the concomitant sinus node dysfunction. The modality of pacing used to manage the sinus node disease has to be carefully chosen to minimize the evolution of atrial tachyarrhythmias. In fact, while ventricular pacing increases the incidence of atrial fibrillation and stroke, dual-chamber pacing with a specific algorithm for ventricular pacing minimization and prevention and treatment of atrial tachyarrhythmias reduces a composite endpoint of evolution to permanent atrial fibrillation, hospitalization, and death.
Inhibition of G protein-gated K+ channels by tertiapin-Q rescues sinus node dysfunction and atrioventricular conduction in mouse models of primary bradycardia