Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
JACC Cardiovasc Imaging. 2019 Jun;12(6):967-977. doi: 10.1016/j.jcmg.2017.11.025. Epub 2018 Jan 17.
This study sought to investigate the hypothesis that patients with left bundle branch block (LBBB) are hypersensitive to elevated afterload.
Epidemiological data suggest that LBBB can provoke heart failure in patients with hypertension.
In 11 asymptomatic patients with isolated LBBB and 11 age-matched control subjects, left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) were measured by echocardiography. Systolic arterial pressure was increased by combining pneumatic extremity constrictors and handgrip exercise. To obtain more insight into mechanisms of afterload response, 8 anesthetized dogs with left ventricular (LV) micromanometer and dimension crystals were studied during acutely induced LBBB and aortic constriction. Regional myocardial work was assessed by LV pressure-dimension analysis.
Consistent with normal afterload dependency, elevation of systolic arterial pressure by 38 ± 12 mm Hg moderately reduced LVEF from 60 ± 4% to 54 ± 6% (p < 0.01) in control subjects. In LBBB patients, however, a similar blood pressure increase caused substantially larger reduction in LVEF (p < 0.01), from 56 ± 6% to 42 ± 7% (p < 0.01). There were similar findings for GLS. In the dog model, aortic constriction abolished septal shortening (p < 0.02), and septal work decreased to negative values (p < 0.01). Therefore, during elevated systolic pressure, the septum made no contribution to global LV work, as indicated by net negative work, and instead absorbed energy from work done by the LV lateral wall.
Moderate elevation of arterial pressure caused marked reductions in LVEF and GLS in patients with LBBB. This reflects a cardiodepressive effect of elevated afterload in the dyssynchronous ventricle and was attributed to loss of septal function.
本研究旨在验证左束支传导阻滞(LBBB)患者对后负荷升高敏感的假设。
流行病学数据表明,LBBB 可在高血压患者中引发心力衰竭。
在 11 例无症状孤立性 LBBB 患者和 11 名年龄匹配的对照组患者中,通过超声心动图测量左心室射血分数(LVEF)和整体纵向应变(GLS)。通过组合气动肢体收缩器和手握力运动来增加收缩期动脉压。为了更深入地了解后负荷反应的机制,在 8 只麻醉犬中进行了左心室(LV)微测压和尺寸晶体研究,在急性 LBBB 和主动脉缩窄期间。通过 LV 压力-尺寸分析评估局部心肌做功。
与正常后负荷依赖性一致,收缩期动脉压升高 38 ± 12 mmHg 可使对照组 LVEF 从 60 ± 4%适度降低至 54 ± 6%(p < 0.01)。然而,在 LBBB 患者中,类似的血压升高导致 LVEF 明显降低(p < 0.01),从 56 ± 6%降至 42 ± 7%(p < 0.01)。GLS 也有类似的发现。在犬模型中,主动脉缩窄消除了室间隔缩短(p < 0.02),室间隔做功降低至负值(p < 0.01)。因此,在收缩压升高期间,由于净负功,室间隔对整体 LV 做功没有贡献,而是从 LV 侧壁做功中吸收能量。
动脉压适度升高导致 LBBB 患者的 LVEF 和 GLS 明显降低。这反映了失同步心室中升高的后负荷对心脏的抑制作用,归因于室间隔功能丧失。