Canadian Journal of Cardiology

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

Published:August 10, 2018DOI:



      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.



      La fréquence cardiaque optimale pour améliorer l’efficacité hémodynamique à court terme chez les patients atteints d’insuffisance cardiaque est inconnue.


      On a effectué un suivi chez des rats Wistar-Kyoto 3 jours, 7 jours et 1 ou 2 mois après un infarctus du myocarde ou une opération fictive et on a enregistré des boucles pression-volume du ventricule gauche à diverses fréquences cardiaques : fréquence initiale de 400 battements par minute (bpm), fréquence réduite à 320 bpm par l’administration d’ivabradine, fréquence haussée à 480 bpm par stimulation auriculaire dans des conditions normales, et après une augmentation de la précharge.


      Dans le groupe de rats ayant subi une opération fictive, l’augmentation de la précharge a produit un accroissement du débit cardiaque de 55 % à la fréquence cardiaque réduite, de 67 % à la fréquence cardiaque initiale et de 84 % à la fréquence cardiaque haussée. Chez les rats ayant présenté un infarctus du myocarde, l’augmentation de la précharge a produit un accroissement du débit cardiaque 3 et 7 jours après l’infarctus, mais pas 1 et 2 mois après. À la fréquence cardiaque haussée, en réponse à l’augmentation de la précharge, le débit cardiaque avait augmenté à 3 et à 7 jours et tendait à diminuer 1 et 2 mois après l’infarctus; cette réponse hémodynamique a été modifiée par la réduction de la fréquence cardiaque. Parmi les autres bienfaits de la réduction de la fréquence cardiaque, on compte la diminution de la pression ventriculaire gauche en fin de diastole et l’augmentation de la fraction d’éjection, de la contractilité et de la vitesse de relaxation 1 et 2 mois après l’infarctus du myocarde.


      Dans un modèle d’insuffisance cardiaque chez le rat, la fréquence cardiaque optimale pour l’amélioration du rendement hémodynamique à court terme varie. Chez les rats ayant subi une opération fictive, une fréquence cardiaque haussée a favorisé l’accroissement du débit cardiaque induit par une augmentation de la précharge; toutefois, chez les rats atteints d’insuffisance cardiaque, une fréquence cardiaque haussée a réduit le débit cardiaque, tandis qu’une fréquence cardiaque réduite a eu des effets bénéfiques. Ainsi, en plus de ralentir l’évolution de l’insuffisance cardiaque, les interventions visant à réduire la fréquence cardiaque offrent également des bienfaits immédiats sur le plan hémodynamique.
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