P4661Increased levels of sST2 in patients with mitral annulus disjunction and ventricular arrhythmias

Abstract

Abstract Background Mitral annulus disjunction (MAD), a basal displacement of the mitral valve annulus, is described as a possible aetiology of sudden cardiac death. Stretch-induced fibrosis in the sub-valvular apparatus has been suggested as the substrate of arrhythmias. Purpose We hypothesized that the stretch related biomarker soluble Suppression of Tumorigenicity-2 (sST2) is a marker of ventricular arrhythmias in patients with MAD. Methods We included patients with ≥1 mm MAD on cardiac magnetic resonance imaging, and recorded left ventricular ejection fraction (LVEF) and late gadolinium enhancement (LGE) suggesting papillary muscle fibrosis. Circulating levels of sST2 were assessed by blood sampling. The occurrence of ventricular arrhythmias, defined as aborted cardiac arrest, sustained or non-sustained ventricular tachycardia, was assessed retrospectively. Results We included 72 patients with MAD [55 (35–62) years old, 48 (67%) female], of which 22 (31%) had ventricular arrhythmias. Patients with ventricular arrhythmias had lower LVEF (60±6% vs. 63±6%, p=0.04), more prevalent papillary muscle fibrosis [14 (64%) vs. 10 (20%), p<0.001] and higher sST2 levels [31.6±10.1 ng/mL vs. 25.3±9.2 ng/mL, p=0.01] compared to those without. Combining sST2-level, LVEF and papillary muscle fibrosis optimally detected individuals with arrhythmias (area under the curve 0.82, 95% CI 0.73–0.92) and improved the risk model (p<0.05) compared to individual parameters (Figure right panel). Conclusion Circulating sST2 levels were higher in patients with MAD and ventricular arrhythmias compared to patients without arrhythmias. Combining sST2, LVEF and LGE may improve risk stratification in patients with MAD. Acknowledgement/Funding This work was supported by public grant [203489/030] from the Norwegian Research Council, Oslo, Norway. E. Scheirlynck received an ESC research grant