European Heart Journal Advance Access published online on November 29, 2004
European Heart Journal, doi:10.1093/eurheartj/ehi008
Copyright © 2004 by the European Society of Cardiology.
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1 Department of Physiology, Cardiovascular Research Institute Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands; Department of Cardiology, Cardiovascular Research Institute Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands
* To whom correspondence should be addressed. Aims Left ventricular (LV) dilatation, hypertrophy, and septal perfusion defects are frequently observed in patients with left bundle branch block (LBBB). We investigated whether isolated LBBB causes these abnormalities. Methods and results In eight dogs, LBBB was induced by radio frequency ablation. Two-dimensional echocardiography showed that 16 weeks of LBBB decreased LV ejection fraction (by 23 ± 14%) and increased LV cavity volume (by 25 ± 19%) and wall mass (by 17 ± 16%). The LV septal-to-lateral wall mass ratio decreased by 6 ± 9%, indicating asymmetric hypertrophy. After onset of LBBB, myocardial blood flow (MBF, fluorescent microspheres) and systolic circumferential shortening [CSsys, magnetic resonance (MR) tagging] decreased in the septum to 83 ± 16% and -11 ± 20% of baseline, respectively, and increased in LV lateral wall to 118 ± 12% and 180 ± 90% of baseline, respectively. MBF and CSsys values did not change over 16 weeks of LBBB. Changes in external mechanical work paralleled those in CSsys. Glycogen content was not significantly different between septum and LV lateral wall of LBBB hearts (16 weeks) and control samples, indicating absence of hibernation. Conclusions The asynchronous ventricular activation during LBBB leads to redistribution of circumferential shortening and myocardial blood flow and, in the long run, LV remodelling. Septal hypoperfusion during LBBB appears to be primarily determined by reduced septal workload.
Preclinical research
Left bundle branch block induces ventricular remodelling and functional septal hypoperfusion
2 Department of Physiology, Cardiovascular Research Institute Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands
3 Department of Cardiology, Cardiovascular Research Institute Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands
4 Department of Biophysics, Cardiovascular Research Institute Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands
Kevin Vernooy, E-mail: k.vernooy{at}fys.unimaas.nl
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