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 beta-blocker atenolol and the selective I(f) 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.
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 beta-blocker atenolol and the selective I(f) 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.