Aims The treatment with the wearable cardioverter defibrillator (WCD) may protect against sudden cardiac death (SCD) as a bridging therapy until a cardioverter defibrillator may be implanted. Data regarding the impact of WCD on the outcome of patients according gender differences are limited. We analysed a consecutive patient cohort wearing WCD to explore gender differences. Methods and results We analysed 153 consecutive patients of whom were 118 males and 35 females (age, 60±13 vs. 60±16 years old; p=0.88). More males receiving WCD as compared to females suffered from ischemic cardiomyopathy (ICM) (41% vs. 23%; p=0.05), while females were diagnosed with non-ischemic cardiomyopathy (NICM) (60% vs. 42%); p=0.05). The wear time of WCD was equivalent in both groups (21±4 in males vs. 22±3 hours/days in females; p=0.18; and 65±42 in males vs. 65±43 days in females; p=0.96). In both groups, the left ventricular ejection fraction (LVEF) improved in males from 29±10% to 41±12% and in females from 28±12% to 45±13%; p=0.12. At 6-12 month-follow-up, the LVEF increased more in females as compared to males (40% vs. 17%; p=0.003). The rate of rehospitalization due to cardiovascular cause and all-cause-mortality were comparable in both groups at 6-12 month-follow-up (55% in male vs. 54% in female group; p=0.93) (9% in male vs. 11% in female group; p=0.71). Conclusion Compliance for wearing of WCD was excellent regardless of gender. During follow-up, LVEF improved more in females as compared to males. All-cause mortality and the rate of rehospitalization were comparable in both groups.

Aims The treatment with the wearable cardioverter defibrillator (WCD) may protect against sudden cardiac death (SCD) as a bridging therapy until a cardioverter-defibrillator may be implanted. We analyzed in a multicenter setting a consecutive patient cohort wearing WCD to explore gender differences. Methods and results We analyzed 708 consecutive patients, 579 from whom were males and 129 females (age, 60.5±14 vs. 61.6±17 years old; p=0.44). All patients were divided into age quartiles for analysis. While the rate of ischemic cardiomyopathy (ICM) as a cause of prescription of WCD was significantly higher in males as compared to females (42.7% vs. 26.4%; p=0.001), females received it more frequently due to non-ischemic cardiomyopathy (NICM) (55.8% vs. 42.7%); p=0.009). The wear time of WCD was equivalent in both groups (21.1±4.3 hours/days in males vs. 21.5±4.4 hours/days in females; p=0.27; and 62.6±44.3 days in males vs. 56.5±39 days in females; p=0.15). Mortality was comparable in both groups at 2-year-follow-up (6.8% in males vs. 9.7% in females; p=0.55). Appropriate WCD shocks and the incidence of device implantations were similar in both groups (2.4% in males vs. 3.9% in females; p=0.07) (35.1% in males vs. 31.8% in females; p=0.37), respectively. In age quartile analysis, compliance was observed more in older patients as compared to adult patients (87.8% vs. 68.3%; p<0.001). Conclusion Compliance for wearing WCD was excellent regardless of gender. Furthermore, mortality and the incidence of device implantations were comparable in both groups. Appropriate WCD shocks tended to be higher in females as compared to males.

Aims: Gene variants the calcium channels have been associated with Brugada syndrome (BrS). The investigation of the human cellular phenotype and the use of drugs for BrS is still lacking. Methods and results: This study recruited cells from a BrS patient carrying a missense variant (c.425C>T/p.S142F) in CACNB2 with uncertain significance as well as from three healthy persons. Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) generated from skin biopsies of healthy persons and the BrS patient (BrS-hiPSC-CMs) as well as CRISPR/Cas9 corrected cells (isogenic control, site-variant corrected) were used. HiPSC-CMs from the BrS patient showed a significantly reduced L-type calcium channel current (ICa-L). The inactivation curve was shifted to a more positive potential and the recovery from inactivation was accelerated. The protein expression of CACNB2 from the BrS-patient was significantly decreased. Moreover, the correction of the CACNB2 site-variant rescued the changes. In addition, the peak sodium current was significantly reduced as compared with the controls consistent with the reduction of the amplitude and upstroke velocity of action potentials in BrS-hiPSC-CMs. Arrhythmia events were more frequently detected in BrS-hiPSC-CMs. In cells without arrhythmic events, carbachol induced the occurrence of arrhythmias with a higher chance in BrS-hiPSC-CMs than in healthy cells. Whereas ajmaline (sodium channel blocker) did not increase arrhythmic events, bisoprolol (beta-blocker) at low concentration and quinidine decreased arrhythmic events. Conclusions: The CACNB2 variant (c.425C>T/p.S142F) causes a loss-of-function of L-type calcium channels and is pathogenic for this type of BrS. Bisoprolol and quinidine may be effective for treating BrS with this variant.