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European Heart Journal Advance Access published online on March 21, 2007
European Heart Journal, doi:10.1093/eurheartj/ehm030
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Conversion of post-systolic wall thickening into ejectional thickening by selective heart rate reduction during myocardial stunning

Laurence Lucats1,2,3, Bijan Ghaleh1,2,3,4, Xavier Monnet1,2,3, Patrice Colin1,2,3, Alain Bizé1,2,3 and Alain Berdeaux1,2,3,4,*

1 INSERM, Unité 841, Créteil, F-94010, France
2 Laboratoire de Pharmacologie, INSERM U 841, Faculté de Médecine, Faculté de Médecine, IFR 10, Université Paris 12, 8, rue du Général Sarrail, Créteil F-94010, France
3 Ecole Nationale Vétérinaire d'Alfort, INSERM U 841, Maisons-Alfort F-94700, France
4 AP-HP, Groupe Mondor-Chenevier, Fédération de Cardiologie, Créteil F-94000, France

Received 3 October 2006; revised 20 February 2007; accepted 23 February 2007.

* Corresponding author. Tel: +33 1 49 81 36 51; fax: +33 1 49 98 17 77. E-mail address: alain.berdeaux{at}creteil.inserm.fr

Aims: Post-systolic wall thickening (PSWT) occurs after aortic valve closure. This waste of thickening does not participate in ejection. PSWT increases with myocardial ischaemia and stunning but the effects of anti-anginal drugs on PSWT during myocardial dysfunction remain unknown. The effects of two heart rate reducing agents, i.e. the ß-blocker atenolol and the selective If current inhibitor ivabradine, were compared on PSWT.

Methods and results: Coronary stenosis was calibrated in six conscious instrumented dogs to suppress increase in coronary blood flow during a 10 min treadmill exercise to induce myocardial stunning. After exercise completion, stenosis was relieved and saline, atenolol or ivabradine (both at 1 mg/kg iv) were administered. For similar heart rate reduction, ivabradine attenuated stunning, whereas atenolol further depressed systolic wall thickening. PSWT to total wall thickening ratio was significantly decreased by ivabradine vs. saline, whereas total wall thickening was similar. Thus, ivabradine devoted a greater part of thickening to systole by converting PSWT into ejectional thickening. In contrast, atenolol failed to reduce PSWT vs. saline. Atrial pacing abolished the effects of ivabradine but not those of atenolol.

Conclusion: Selective heart rate reduction with ivabradine converts PSWT into ejectional thickening but not with atenolol secondary to its negative inotropism.

Key Words: Myocardial stunning • Post-systolic wall thickening • Heart rate • If- channel • ß-blockade


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