Acute Heart Rate-Dependent Hemodynamic Function of the Heart in the Post-Myocardial Infarction Rat Model: Change Over...

Optimal heart rate (HR) for acute hemodynamic efficiency in heart failure (HF) is unknown.

Wistar-Kyoto rats were followed-up for 3 and 7 days, 1 or 2 months after myocardial infarction (MI) or sham operation (ShO) and left ventricle (LV) pressure-volume (PV) loops were obtained at various HRs: baseline 400 beats per minute (bpm), reduced by ivabradine to 320 bpm, increased by atrial pacing to 480 bpm, under normal conditions and after preload increase (PI).

In the ShO group, PI augmented cardiac output (CO) by 55%, 67%, 84% at reduced, baseline, and increased HR, respectively. In post-MI rats, PI augmented CO 3 and 7 days, but not 1 and 2 months after MI. At increased HR, in response to PI, CO increased 3 and 7 days, tended to fall 1 and 2 months after MI; this hemodynamic response was salvaged by HR reduction. Further beneficial effects of HR reduction included reduction of LV end-diastolic pressure, increase of ejection fraction, contractility and relaxation velocity 1 and 2 months after MI.

In a rat HF model, optimal HR with regard to acute hemodynamic performance is shifted. Whereas in ShO rats increased HR facilitates CO increase induced by PI, in HF rats, such increase reduces CO, and HR reduction has beneficial effects. Thus, besides reducing progression of HF, HR-reducing interventions also offer immediate hemodynamic benefits.