Author + information
- Received August 31, 2017
- Revision received November 15, 2017
- Accepted November 16, 2017
- Published online June 3, 2019.
- John Aalen, MDa,b,c,
- Petter Storsten, MDa,b,c,
- Espen W. Remme, Dr.ing., PhDa,b,
- Per A. Sirnes, MD, PhDd,
- Ola Gjesdal, MD, PhDc,
- Camilla K. Larsen, MDa,b,c,
- Erik Kongsgaard, MD, PhDb,c,
- Espen Boe, MDa,b,
- Helge Skulstad, MD, PhDa,b,c,e,
- Jonny Hisdal, PhDe and
- Otto A. Smiseth, MD, PhDa,b,c,e,∗ ()
- aInstitute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway
- bCenter for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway
- cDepartment of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway
- dOstlandske Hjertesenter, Moss, Norway
- eInstitute of Clinical Medicine, University of Oslo, Oslo, Norway
- ↵∗Address for correspondence:
Dr. Otto A. Smiseth, Department of Cardiology, Oslo University Hospital, Rikshospitalet, N-0027 Oslo, Norway.
Objectives This study sought to investigate the hypothesis that patients with left bundle branch block (LBBB) are hypersensitive to elevated afterload.
Background Epidemiological data suggest that LBBB can provoke heart failure in patients with hypertension.
Methods 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.
Results 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.
Conclusions 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.
Dr. Aalen was supported by a grant from the Norwegian Health Association. Drs. Storsten and Kjellstad Larsen were recipients of clinical research fellowships from the South-Eastern Norway Regional Health Authority. Prof. Smiseth is co-inventor but no longer has ownership of the patent “Method for myocardial segment work analysis,” which was used to calculate myocardial work in the clinical study. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received August 31, 2017.
- Revision received November 15, 2017.
- Accepted November 16, 2017.
- 2019 American College of Cardiology Foundation
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