Prognosis in Familial Atrial Fibrillation

A trial fibrillation (AF) is a common arrhythmia associated with substantial morbidity and a markedly increased risk of ischemic stroke. It accounts for one third of all strokes in patients above the age of 65 and is also associated with an increased mortality. In recent years, risk models for AF prediction have been developed based on clinical and demographic variables. AF may also present as familial disorder. Several studies have shown an association of genetic variants with AF and indicated that familial AF increases the risk of AF. Considering the high and increasing number of AF patients in daily practice, the clinician is interested in the clinical course of these familial forms of AF and whether familial AF patients would benefit from a different management strategy than other AF patients. Heterogeneity of both genetic background and clinical manifestations in familial AF remains largely uncharacterized. Concomitant rhythm disorders, as well as cardiomyopathies, are common in patients with familial AF. A positive family history for AF in an apparently lone AF patient may be a marker for wider spectrum of cardiac pathology, and one first message is that this should be investigated when the cardiologist identifies a patient with familial AF. Although studies have identified several genetic loci associated with AF, it is still unclear whether genetic profiling can identify AF patients at greatest risk of cardiac events or cardioembolic stroke. One might speculate that a patient with familial AF will have earlier onset of AF and overall longer duration of AF, which might affect the risk of stroke (although this is not clearly demonstrated in other AF patients). An earlier onset and longer duration of AF might also promote a so-called cardiomyopathy in some patients, which may worsen prognosis. In the analysis of a nation-wide cohort study about familial AF in Denmark, Gundlund et al found that age difference was indeed evident with a median age at AF diagnosis of the familial AF patients of 50 years in comparison to the nonfamilial AF patients who had a median age at AF diagnosis of 77 years. However, the researchers found that long-term risks for death and thromboembolic complications were similar in familial and nonfamilial AF patients. The researchers have to be congratulated given that their data set is quite unique. It has the major advantage of being nationwide, thus theoretically avoiding selection biases commonly observed in many works on these issues. Some clinical characteristics are missing and more granular data would be of interest, but the multivariable analyses seem quite robust and they are unlikely to be reproduced easily in many other cohorts. After matching the cases and the controls in a 1:1 match upon age at AF diagnosis, year at AF diagnosis, and sex, there were statistically more prevalent diabetes mellitus, coronary artery disease, and vascular disease in nonfamilial AF, but the absolute differences were relatively minimal. Importantly, matching resulted in very similar CHA2DS2-VASc scores, which was a key determinant for an unbiased analysis of the risk of stroke associated with familial AF per se. The lack of differences in the long-term risk of thromboembolic complications between familial and nonfamilial indicates that the perceived possible different effect of familial pattern against the risk of death and thromboembolic events seems irrelevant in AF patients when using a contemporary risk stratification scheme, the CHA2DS2-VASc score. As a result, this would suggest a similar antithrombotic treatment approach for familial AF patients as for the general AF population. These results are complementary to those recently published by Lubitz et al. Using genome-wide data from an independent large-scale analysis of common variants known to be associated with AF, they found that AF genetic risk was associated with AF and cardioembolic stroke in 18 919 individuals. Nevertheless, given that genetic information improved prediction minimally and afforded small improvements in discrimination of AF risk, the researchers concluded that widespread use of genetic risk profiling does not need to be incorporated into routine clinical decision making. The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Service de Cardiologie, Pôle Coeur Thorax Vasculaire, Centre Hospitalier Universitaire Trousseau et Facult e de M edecine, Universit e Franc ois Rabelais, Tours, France. Correspondence to: Laurent Fauchier, MD, PhD, Service de Cardiologie et Laboratoire d’Electrophysiologie Cardiaque, Centre Hospitalier Universitaire Trousseau, 37044 Tours, France. E-mail: [email protected] J Am Heart Assoc. 2016;5:e004905 doi: 10.1161/JAHA.116.004905. a 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.