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. Author manuscript; available in PMC: 2018 May 9.
Published in final edited form as: J Am Coll Cardiol. 2018 May 8;71(18):2041–2057. doi: 10.1016/j.jacc.2018.03.019

FIGURE 2. Age-Associated Pathological Changes and Their Effect on the Initiation, Manifestation, and Recurrence of Cardiac Arrhythmias.

FIGURE 2

The major culprit mechanisms are related to cellular oxidative damage, cardiomyocyte apoptosis, and increased extracellular matrix volume that can lead to abnormal automaticity, re-entry, and repolarization abnormalities. In addition, ischemic and inflammatory mechanisms are responsible for fluctuating membrane potentials, ectopic pacemakers, and ultimately, myocardial fibrosis. Overall, aging hearts show electrical signal heterogeneity, abnormal electromechanical coupling, atrial and ventricular remodeling, low conduction voltage, and an increased incidence of both atrial and ventricular arrhythmias. Fibrofatty changes of the conduction system lead to bradycardia, AV block, and chronotropic incompetence. AV = atrioventricular; Ca2+ = calcium; EADs = early afterdepolarizations; EM = electromechanical; HR = heart rate; MPs = membrane potentials; VF = ventricular fibrillation; VT = ventricular tachycardia.