Atrial fibrillation during mavacamten treatment in obstructive hypertrophic cardiomyopathy in the real-world: data from the multicenter MARVEL.HU registry on 133 patients

Background

The direct myosin inhibitor mavacamten, used for the treatment of obstructive hypertrophic cardiomyopathy (oHCM), has been reported to increase the incidence of atrial fibrillation (AF). Based on "real-world" data, the incidence of AF is 11–32%, with a 6–11% incidence rate regarding new-onset AF. In our work we aimed to investigate the occurrence of AF in patients enrolled in the MARVEL.HU (MAvacamten Real-world eVidencE during short- and Long-term follow-up in hypertrophic cardiomyopathy in HUngary) multicentre registry.

Patients and Methods: One-hundred and thirty-three patients with oHCM [71 males (53%), average age: 56±13 years] receiving mavacamten treatment were followed. Titration and follow-up followed the standard instructions for use of mavacamten. The follow-up was an average of 239±158 days [median 226 days (146-302)]; the number of patients completing the week 4 (W4), W12, W24, and W48 visits was 125 (94%), 120 (90%), 105 (79%), and 31 (23%), respectively.

Results

Of the 133 patients, 29 (22%) had documented AF prior to the initiation of mavacamten therapy [paroxysmal: 14/28 (48.3%); persistent: 12/28 (41.4%); permanent: 3/28 (10.3%)]. Patients with AF did not differ from the non-AF oHCM patients in terms of gender (p=0.933) and age distribution (60±13 vs. 56±13 years; p=0.135). Although resting peak left ventricular outflow tract (LVOT) gradient was significantly lower in AF HCM patients [57 (32 to 79) vs. 76 (43 to 114) mmHg; p=0.030], other results were similar regarding their Valsalva-provoked LVOT gradient [84 (61–126) vs. 102 (77 to 142) mmHg; p=0.097], their NT-proBNP levels [1386 (664 to 2969) vs. 1040 (523 to 2883) pg/ml; p=0.659], their LV ejection fraction [63 (60 to 66) vs. 63 (60 to 68) %; p=0.558], and their troponin T levels [14 (10 to 19) vs. 17 (10 to 27) ng/l; p=0.192]. There was also no difference in their NYHA functional class (p=0.439).

During mavacamten treatment AF occurred in 10 patients (7.5%, excluding patients with permanent AF), which was new-onset AF in 3/133 (2.3%) and recurrent AF in 7/133 (5.3%) patients. The median time to AF occurrence from the initiation of mavacamten was 75 days (IQR: 31.8–155.8); and it occurred after 120 days in only 3 patients. Of the 10 AF episodes, 1 were paroxysmal and 9 were persistent. In the latter cases, electrical cardioversion was performed in 5 cases and pharmacological cardioversion in 4 cases. Subsequently, pulmonary vein isolation (PVI) was carried out in 2 cases. At the final follow-up, all patients were in sinus rhythm.

Conclusion

The 2.3% incidence of new-onset AF and 5.3% incidence of recurrent AF observed in our patient cohort are similar or less to data reported in other "real-world" studies and seems less than in oHCM patients before mavacamten treatment. The low rate in AF recurrence beyond 120 days suggests the potential impact of favourable hemodynamic and structural changes occurring as a result of mavacamten therapy.