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

Area of Science:

• Cardiology
• Pharmacology
• Myocardial Physiology

Background:

• Post-systolic wall thickening (PSWT) represents myocardial energy expenditure that does not contribute to ejection.
• PSWT exacerbates under conditions of myocardial ischemia and stunning.
• The impact of anti-anginal medications on PSWT during myocardial dysfunction is not well-understood.

Purpose of the Study:

• To investigate the effects of the beta-blocker atenolol and the selective I(f) current inhibitor ivabradine on PSWT.
• To compare the efficacy of heart rate-reducing agents in mitigating myocardial stunning-induced PSWT.

Main Methods:

• Myocardial stunning was induced in six instrumented dogs via calibrated coronary stenosis and treadmill exercise.
• Following exercise, dogs received saline, atenolol, or ivabradine (1 mg/kg IV).
• Post-treatment assessments included heart rate, systolic wall thickening, and PSWT measurements.

Main Results:

• Ivabradine significantly reduced the PSWT to total wall thickening ratio compared to saline, indicating a conversion of PSWT to ejectional thickening.
• Atenolol did not significantly alter PSWT compared to saline and further depressed systolic wall thickening.
• Both drugs reduced heart rate similarly, but ivabradine's effects were abolished by atrial pacing, unlike atenolol's.

Conclusions:

• Selective heart rate reduction with ivabradine effectively converts PSWT into ejectional thickening.
• Atenolol's negative inotropic effects prevent it from reducing PSWT, unlike ivabradine.
• These findings highlight the distinct mechanisms of heart rate-reducing agents in managing myocardial dysfunction.