Abstract

BackgroundTo differentiate effects of ventricular asynchrony from an underlying hypocontractile cardiomyopathy this study aimed to enhance the understanding of functional impairment and structural remodeling in idiopathic left bundle-branch block (LBBB).We hypothesize, that functional asynchrony with septal flash volume effects alone might not entirely explain the degree of functional impairment. Hence, we suggest the presence of a superimposed contractile cardiomyopathy.MethodsIn this retrospective study, 53 patients with idiopathic LBBB were identified and matched to controls with and without cardiovascular risk factors. Cardiovascular magnetic resonance (CMR) was used to evaluate cardiac function, volumes and myocardial fibrosis using native T1 mapping and late gadolinium enhancement (LGE). Septal flash volume was assessed by CMR volumetric measurements and allowed to stratify patients with systolic dysfunction solely due to isolated ventricular asynchrony or superimposed contractile impairment.ResultsReduced systolic LV-function, increased LV-volumes and septal myocardial fibrosis were found in patients with idiopathic LBBB compared to healthy controls. LV-volumes increased and systolic LV-function declined with prolonged QRS duration. Fibrosis was typically located at the right ventricular insertion points. Subgroups with superimposed contractile impairment appeared with pronounced LV dilation and increased fibrotic remodeling compared to individuals with isolated ventricular asynchrony.ConclusionsThe presence of superimposed contractile impairment in idiopathic LBBB is crucial to identify patients with enhanced structural remodeling. This finding suggests an underlying cardiomyopathy. Future studies are needed to assess a possible prognostic impact of this entity and the development of heart failure.Trial registration: This study was retrospectively registered.

Highlights

  • To differentiate effects of ventricular asynchrony from an underlying hypocontractile cardiomyopathy this study aimed to enhance the understanding of functional impairment and structural remodeling in idiopathic left bundle-branch block (LBBB).We hypothesize, that functional asynchrony with septal flash volume effects alone might not entirely explain the degree of functional impairment

  • There were no significant differences in normal and indexed right ventricle (RV) End-diastolic volume (EDV) (RVEDVI), Right ventricular ejection fraction (RVEF), tricuspid annular plane systolic excursion (TAPSE) and left ventricular (LV) mass between the idiopathic LBBB and control group A

  • There was a negative correlation between RVEF (r = -0.275, ­r2 = 0.076, p < 0.05) and a positive correlation between Right ventricular end-diastolic volume index (RVEDVI) and QRS duration (r = 0.599, ­r2 = 0.359, p < 0.05) (Table 3, Additional file 1: Table S3) indicating functional and structural remodeling at the RV in idiopathic LBBB patients

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Summary

Introduction

To differentiate effects of ventricular asynchrony from an underlying hypocontractile cardiomyopathy this study aimed to enhance the understanding of functional impairment and structural remodeling in idiopathic left bundle-branch block (LBBB).We hypothesize, that functional asynchrony with septal flash volume effects alone might not entirely explain the degree of functional impairment. To differentiate effects of ventricular asynchrony from an underlying hypocontractile cardiomyopathy this study aimed to enhance the understanding of functional impairment and structural remodeling in idiopathic left bundle-branch block (LBBB). Left bundle-branch block (LBBB) is considered to exaggerate or even cause ventricular dysfunction and myocardial remodeling resulting in increased mortality in patients with cardiovascular disease [1,2,3]. Recent imaging studies using echocardiography and cardiovascular magnetic resonance (CMR) in patients with idiopathic LBBB revealed reduced LV ejection fraction (LVEF) and increased LV volumes compared to healthy controls [1, 11]. It remains uncertain if dyssynchrony due to septal flash volume alone explains the degree of functional impairment or if the additional presence of a superimposed hypocontractile cardiomyopathy results in dysfunction and structural remodeling

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