Calcified Pipes: You Better Call the Electrician Too.

D espite the high prevalence and morbidity of atrial fibril-lation (AF), the mechanisms of the disease are multi-factorial and remain poorly understood. The initiation of AF requires a trigger, and abnormal atrial substrate is necessary to sustain the arrhythmia. Although there are genetic predispositions to AF, 1 more traditional cardiovascular risk factors such as age, diabetes mellitus, hypertension, obesity, and metabolic syndrome are also associated with AF. 2 Among AF patients, weight loss has been associated with lower AF burden and improved maintenance of sinus rhythm. 3 Reducing weight and blood pressure along with better glycemic and lipid management have been shown to improve arrhythmia-free survival after AF ablation. Nearly two thirds of patients with AF have concomitant coronary heart disease, 5 which can contribute to the initiation and maintenance of AF through myocardial fibrosis, atrial dila-tion, inflammation, and ischemia. 6–9 Animal models of atrial ischemia have shown increased spontaneous atrial ectopic activity and slowing of atrial conduction, leading to initiation and sustained re-entry of AF. Coronary artery calcium (CAC) scores can identify vascular aging and patients at risk for acute coronary events. 10 The CAC score was independently associated with the development of AF in the Multi-Ethnic Study of Atherosclerosis (MESA) study. 11 In the MESA study, patients with higher CAC scores at baseline had a greater incidence of AF in follow-up. Relative to patients with a baseline CAC score of 0, the hazard ratios (HRs) for developing AF were 1.4 In addition, CAC score improved the discrimination of AF risk scores. 11 Questions remained about whether cardiac computed tomography and CAC could identify actionable risk. In this issue of Circulation: Cardiovascular Imaging, O'Neal et al 12 make an important contribution and describe the association between CAC progression and AF in MESA, which recruited patients without diagnosed cardiovascular disease from 6 geographic locations. There were 5612 patients with 2 CAC scores separated by a mean of 2.4±0.8 years. Among the study population, 203 (3.6%) patients developed incident AF over a median follow-up of 5.6 years. Patients with an increase in their CAC score from the first to the second scan were labeled as having CAC progression. The cumulative incidence of AF was >3-fold higher among patients with CAC progression relative to those without CAC progression (10 versus 3 per 1000 patient-years; log-rank, P<0.0001). After multivariable adjustment including baseline CAC score, patients with CAC progression continued to have higher incidence …