ClinicalDevicesCardiac resynchronization therapy and ventricular tachyarrhythmia burden
Graphical abstract
Introduction
Cardiac resynchronization therapy–defibrillator (CRT-D) improves heart failure (HF) symptoms and lowers mortality in patients with a low left ventricular ejection fraction (LVEF) and a wide QRS.1 The benefit of CRT has been proven to be greatest among individuals with complete left bundle branch block (LBBB) morphology on surface electrocardiogram.2 Furthermore, CRT may reduce the rate of cardiac disease progression by establishing biventricular electromechanical synchrony during the early stages of HF.3 Our previous data from MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial–Cardiac Resynchronization Therapy) has suggested that CRT-D also reduces the risk of a first ventricular tachyarrhythmia (VTA) event in patients with HF and LBBB.4 However, data regarding the risk factors for repeated VTA events in this patient population or the effect that CRT-D may have on VTA burden are limited. Importantly, VTA burden may be associated with frequent implantable cardioverter-defibrillator (ICD) shocks, decreased quality of life, and subsequent increase in hospitalizations and death.5, 6, 7 Thus, assessment of VTA burden among patients with HF remains of paramount importance.
In the current study, 1281 patients with LBBB who were enrolled in MADIT-CRT were included. We aimed to (1) evaluate the effect of CRT-D on VTA burden (defined as recurrent VTA events) and death; (2) evaluate the consistency of the CRT-D effect on VTA burden in risk subgroups including patients in New York Heart Association (NYHA) functional classes I and II, those with ischemic cardiomyopathy (ICM), and those with nonischemic cardiomyopathy (NICM); (3) identify risk factors for first and recurrent VTA events; and (4) assess the effect of increasing VTA burden on the risk of subsequent adverse events, including death and HF events.
Section snippets
Study population
The present study cohort comprised 1281 LBBB patients from MADIT-CRT. The rationale and design of MADIT-CRT were previously published.8 Briefly, MADIT-CRT was designed to determine whether CRT-D would reduce the risk of death or HF events in patients with mild HF symptoms, reduced LVEF, and wide QRS complex compared with ICD therapy. Patients were randomly assigned in a 3:2 ratio to receive either a CRT-D or ICD. From December 22, 2004 to April 23, 2008, a total of 1820 patients were enrolled
Study cohort
Baseline clinical characteristics of the study patients categorized by the number of events are given in Table 1. Patients with VTA were younger, more likely to be male, be a current smoker, have previous episodes of NSVT, and have NYHA functional class II symptoms. The percentage of treatment with CRT-D did not differ significantly between patients with 1 episode and those without, yet was significantly lower among those with high VTA burden. The presence of ICM and other comorbidities did not
Discussion
Our findings demonstrate that in HF patients implanted with a defibrillator for primary prevention, (1) treatment with CRT-D was associated with a significant and pronounced reduction in the risk of any VTA recurrence, reduction in the risk of life-threatening VTA, and reduction in the risk of repeated ICD shocks; (2) the association of CRT-D with VTA burden reduction was consistent in all subgroups analyzed but was more pronounced among patients in NYHA functional class I; (3) treatment with
Conclusion
Among patients with HF and LBBB, treatment with CRT-D is associated with a pronounced reduction in VTA burden, frequency of device-delivered shocks, VTA recurrence, and death. These results are consistent regardless of baseline risk factors but are more pronounced among patients with NYHA functional class I symptoms. These data support the need for early intervention with CRT-D in this population.
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Cited by (0)
Funding sources: MADIT-CRT was supported by a research grant from Boston Scientific to the University of Rochester. Drs Aktas, Kutyifa, Zareba, Goldenberg, and Huang have received research grants from Boston Scientific.
Disclosures: All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
ClinicalTrials.gov Identifiers NCT00180271, NCT01294449, and NCT02060110.