A new study provides more evidence of important bidirectional relationships between AF and other cardiovascular comorbidities.
It has long been understood that myocardial infarction (MI) may increase the risk of developing atrial fibrillation (AF), which is often a result of fibrosis or scar tissue in the atria. However, a recent study in JAMA-Internal Medicine by Soliman and colleagues1 found that the opposite relationship may also be true.
The study was a prospective cohort study of 23,928 subjects without coronary heart disease at baseline from the REGARDS (Reasons for Geographic and Racial Differences in Stroke) cohort who were followed for a median of 4.5 years.1 During this period, there were 648 incident MIs. In a comprehensive model that adjusted for socioeconomic differences, comorbidities, inflammatory markers, demographic differences, medication use, and smoking status, the hazard for developing AF was 1.7 times greater in those with a history of MI (95% CI, 1.23-2.30) compared with those without a history of MI. In subgroup analysis, there was some heterogeneity and a positive interaction between risk of incident AF and sex or race. Women had a higher risk than men (HR = 2.16; 95% CI, 1.41-3.31 vs HR = 1.39; 95% CI, 0.91-2.10). The same relationship was true for racial differences: blacks had a higher hazard for AF (HR = 2.52; 95% CI, 1.67-3.86) compared with whites, in whom the risk was not statistically significant (HR = 1.26; 95% CI, 1.83-1.93). Surprisingly, age did not appear to increase the risk for incident AF.
In an accompanying editorial, several strengths of this analysis were pointed out, including the large cohort size and multivariable adjustment as well as the rigorous adjudication of MIs.2 Possible mechanisms raised for this bidirectional relationship included the presence of inflammatory pathways as well as the possibility of coronary embolism from a left atrial appendage thrombus. The authors of the editorial conducted a meta-analysis that shows that the risk of MI is reduced in patients who are treated with warfarin, lending credence to the embolism theory as a possible pathophysiologic mechanism.
Despite its strengths, the lack of an interaction with age continues to remain somewhat questionable in this study, given that aging is known to be one of the strongest factors for the development of incident AF.