No abstract

Introduction Cardiac magnetic resonance (CMR) late gadolinium enhancement (LGE) and T1 mapping techniques enable the quantification of focal and diffuse myocardial LGE, respectively. Studies have shown evidence of fibrosis in middle-age athletes, but not relative to physically active (PA) adults who perform recommended physical activity levels. Therefore, we examined cardiac remodeling and presence of left ventricular (LV) LGE and T1 values in both recreational middle-age endurance athletes (EA) and PA adults. Methods Healthy EA and PA adults (45–65 yr) completed a standardized 3-T CMR protocol with ventricular volumetry, LV LGE, and T1 mapping. Results Seventy-two EA and 20 PA participants (mean age, 53 ± 5 vs 56 ± 4 yr; P < 0.01; V˙O2peak = 50 ± 7 vs 37 ± 9 mL·kg−1·min−1, P < 0.0001) were examined, with CMR data available in 89/92 participants. Focal LV LGE was observed in 30% of participants (n = 27/89): 33% of EA (n = 23/69; 33%) and 20% of PA (n = 4/20; 20%). LGE was present at the right ventricular hinge point (n = 21/89; 23.5%) or identified as ischemic (n = 2/89; 2%) or nonischemic (n = 4/89; 4%). Focal LV LGE was observed similarly in both EA and PA (P = 0.25). EA had larger LV chamber sizes and T1 native values (1169 ± 35 vs 1190 ± 26, P = 0.02) compared with PA, with similar LV ejection fraction. Global extracellular volume (ECV) was similar in both EA and PA (22.6% ± 3.5% vs 21.5% ± 2.6%, P = 0.26), with no relationship between global ECV and LV mass (r = −0.16, P = 0.19). Conclusions Focal LGE at the right ventricular hinge point was detected at the same frequency in both groups, was unrelated to demographic or clinical indices, and was found without evidence of global ECV expansion in EA, suggesting a physiologic remodeling response. The long-term clinical implications of hinge-point LGE require clarification using prospective, long-term follow-up studies.

Until the last decade, vitamin K antagonists (VKAs) were the only agents available for oral anticoagulation. Although effective and accessible, their use was complicated by a narrow therapeutic window, the need for regular monitoring of the international normalized ratio, and an associated susceptibility to interactions with both food and numerous medications. Furthermore, the onset of action was delayed, often requiring bridging with intravenous agents. In more recent years, we have enjoyed the development of nonvitamin-K-dependent, direct oral anticoagulants (DOACs), which either directly inhibit the activity of factor IIa (eg, dabigatran) or factor Xa (eg, rivaroxaban, apixaban, edoxaban). These medications boast a more rapid onset of action, predictable pharmacokinetics, wider therapeutic window, and equal or superior safety profiles. Although these medications appear to have fewer drug-drug interactions than VKAs, their interactions remain of clinical importance, particularly in one of the largest populations requiring anticoagulation: patients with atrial fibrillation. These patients are rarely on single medications, with the majority of them requiring some form of rate or rhythm control due to their arrhythmia. Unfortunately, data on interactions between DOACs and antiarrhythmic medications, despite their common coadministration, remain limited. Here, we summarize the interactions between antiarrhythmics and VKAs and review existing knowledge regarding their interactions with DOACs.