Ventricular activation time as a marker for complex ventricular arrhythmias, sudden cardiac death and ICD implantation in hypertrophic cardiomyopathy

Abstract

Abstract Background Identification of patients with hypertrophic cardiomyopathy (HCM) who are at high risk of sudden cardiac death (SCD) is essential, as life-threatening ventricular arrhythmias (VAs) can be effectively prevented with an implantable cardioverter defibrillator (ICD). Risk stratification using HCM Risk-SCD score is recommended in the 2014 ESC guidelines for the management of patients with HCM. However, the role of electrocardiogram (ECG) in risk stratification is less well established. Purpose We investigated the association between the ventricular activation time (VAT), an ECG marker of the duration of ventricular depolarization, with the HCM Risk-SCD score, the presence of complex VAs, the implantation of an ICD and ICD-therapy for VAs. Methods Patients with a history of HCM, documented by echocardiography, were studied. The 12-lead ECG and echocardiography were performed on the same day. On ECG, we evaluated the VAT in milliseconds, between the onset of the QRS complex to the peak of R wave on V5 or V6 precordial ECG leads. A careful personal and family history for unexplained syncope and SCD was obtained, respectively. The presence of non-sustained ventricular tachycardia (NSVT) and ICD therapy were assessed either with 48h ECG recording or ICD interrogation. HCM Risk-SCD score was calculated by the corresponding ESC online calculator. Statistical analysis was performed using the SPSS software. Results Thirty-three patients with HCM were included (mean age 51±12 years, 78.8% male). According to the HCM Risk-SCD score, HCM patients were divided into three groups: low-risk (<4, 45.5%), intermediate-risk (4 to <6, 24.2%) and high-risk (>6, 30.3%) for SCD. Approximately half of the HCM patients had episodes of NSVT (48.5%) and an ICD (48.5%). Ventricular activation time was significantly prolonged in high-risk group compared either with intermediate-risk (74±24.5 vs 48.7±16.4, p=0.006) or low-risk (74±24.5 vs 44.3±12.6, p<0.001). HCM patients with NSVT had a significantly prolonged VAT compared with those without NSVT (62.19±25.2 vs 47.06±15.3, p=0.022). Moreover, HCM patients with an ICD had a higher VAT than those without an ICD (62.1±25.2 vs 47±15.3, p=0.003). VAT was also significantly prolonged in the group with appropriate ICD therapy for VAs compared with that without ICD therapy (82.8±22.1 vs 52.2±16.4, p=0.007). Finally, there was a significant positive correlation between VAT and NSVT (r=0.352, p=0.044), history of syncope (r=0.604, p<0.001), HCM risk-SCD score (r=0.493, p=0.004), ICD implantation (r=0.508, p=0.003) and ICD therapy (r=0.648, p=0.007) for VAs while there was not a correlation with the family history of SCD. Conclusion Prolongation of VAT is associated with NSVT, HCM risk score for SCD, ICD implantation and ICD therapy for VAs in patients with HCM and it seems to be a novel, easy to measure, ECG marker for risk stratification. Funding Acknowledgement Type of funding sources: None.