Abstract
There is a noticeable difference in the incidence of ventricular arrythmias among patients receiving defibrillator devices (ICD or CRT-D) for primary vs. secondary prevention of sudden cardiac death (SCD). The underlying reasons for this difference remain to be fully explained. To assess for differences in myocardial scar characteristics between patients who had defibrillator devices implanted in primary vs. secondary prevention scenarios, and their correlation with arrhythmic events. In this single center retrospective study, patients who underwent late gadolinium enhancement (LGE) cardiac MRI for clinical purposes before the implantation of an ICD or CRT-D were included. Patients with channelopathies (n=2) or inappropriate imaging quality (n=7) were excluded. We used ADAS software to perform myocardial scar characterization in 3D-LGE datasets in all but 16 patients, in which 2D datasets were used. The primary endpoint was a composite of appropriate ICD therapy (appropriate shock or ATP), sustained ventricular tachycardia or SCD. A total of 116 patients (mean age 66±14 years, 81% male) were included, 40 (35%) with devices implanted in secondary prevention. During a median follow-up of 28 months (IQR 16-24), 23 events were identified (18 appropriate ICD therapy, 9 shocks and 9 ATP; 2 SCD; 3 sustained VT), 7 of which (30.4%) in the primary prevention group, and 16 (69.6%) in the secondary prevention group. The event rate was significantly higher in the secondary prevention setting (15.0 events per 100 persons-year [95% CI 7.7 – 22.4] vs. 4.1 events per 100 persons-year [95% CI 1.1 – 7.1]; p < 0.001). Despite a higher LVEF in the secondary prevention group (41 ± 14% vs. 30 ± 13%; p-value < 0.001), no statistically significant differences were found regarding scar tissue characteristics, namely scar and borderzone (BZ) mass, total channel mass, largest channel mass, number of channels and scar heterogeneity (BZ mass / scar mass ratio) – Table. Despite the higher event rate in patients receiving defibrillator devices in secondary vs. prevention, no differences in myocardial scar characteristics were found between both groups. These findings suggest that arrhythmic risk is unlikely to be explained solely by the anatomical substrate, and support a greater role for the interplay between substrate and transient triggers.Tabled 1Primary PreventionSecondary Preventionp-valueScar + BZ mass (g)26.2 (IQR 13.3 - 35.0)23.7 (IQR 11.4 - 33.4)p = 0.322Scar + BZ percentage (%)18.0 (IQR 11.0 – 27.0)17.0 (IQR 9.0 - 26.0)p = 0.545BZ mass (g)17.7 (IQR 11.1 - 24.2)14.8 (IQR 8.8 - 22.0)p = 0.350BZ percentage (%)13.0 (IQR 8.0 - 18.0)11.0 (IQR 6.0 - 17.0)p = 0.677Scar mass (g)6.6 (IQR 3.4 - 11.0)6.9 (IQR 2.0 - 10.3)p = 0.693Scar percentage (%)4.0 (IQR 2.0 - 9.0)5.0 (IQR 1.0 - 8.0)p = 0.695Scar heterogeneity2.4 (IQR 1.7 - 3.9)2.7 (IQR 1.5 - 4.4)p = 0.797Total channels mass (g)3.0 (IQR 0.7 - 4.9)1.8 (IQR 0.0 - 5.0)p = 0.215Biggest channel mass (g)1.4 (IQR 0.5 - 2.5)0.8 (IQR 0.0 - 3.0)p = 0.163Number of channels3.0 (IQR 1.0 - 5.0)3.0 (IQR 0.0 - 5.0)p = 0.520BZ, Borderzone Open table in a new tab
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