Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.
J Cardiovasc Magn Reson. 2021 Apr 1;23(1):39. doi: 10.1186/s12968-021-00731-6.
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. Hence, we suggest the presence of a superimposed contractile cardiomyopathy.
In 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.
Reduced 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.
The 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.
This study was retrospectively registered.
为了区分心室不同步的影响与潜在的低收缩性心肌病，本研究旨在增强对特发性左束支传导阻滞（LBBB）的功能障碍和结构重塑的理解。我们假设，仅存在间隔 flash 容积效应的功能性不同步可能无法完全解释功能障碍的程度。因此，我们认为存在叠加的收缩性心肌病。
在这项回顾性研究中，确定了 53 例特发性 LBBB 患者，并与存在和不存在心血管危险因素的对照组相匹配。使用心脏磁共振（CMR）评估心脏功能、容积和心肌纤维化，使用原生 T1 映射和晚期钆增强（LGE）。通过 CMR 容积测量评估间隔 flash 容积，并允许将仅因孤立性心室不同步或叠加收缩性损害而导致收缩功能障碍的患者分层。
与健康对照组相比，特发性 LBBB 患者的收缩性 LV 功能降低、LV 容积增加和间隔心肌纤维化增加。LV 容积增加，收缩性 LV 功能随着 QRS 持续时间延长而下降。纤维化通常位于右心室插入点。与仅存在孤立性心室不同步的个体相比，存在叠加收缩性损害的亚组表现为明显的 LV 扩张和增加的纤维化重塑。
在特发性 LBBB 中存在叠加的收缩性损害对于识别具有增强的结构重塑的患者至关重要。这一发现提示存在潜在的心肌病。需要进一步研究来评估这种情况的可能预后影响和心力衰竭的发展。
本研究为回顾性注册。
