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Heart rate reduction improves biventricular function and interactions in experimental pulmonary hypertension
Olga Gomez1, Kenichi Okumura1, Osami Honjo1
1The Labatt Family Heart Center, Division of Cardiology and Cardiovascular Surgery, Hospital for Sick Children and University of Toronto , Toronto, Ontario , Canada.
American Journal of Physiology. Heart and Circulatory Physiology
|November 18, 2017
Summary
Reducing heart rate in experimental pulmonary arterial hypertension (PAH) with carvedilol or ivabradine improves biventricular function. This heart rate reduction enhances cardiac cycle timing and interventricular interactions, improving hemodynamics in PAH.
Area of Science:
- Cardiology
- Physiology
- Pharmacology
Background:
- Pulmonary arterial hypertension (PAH) significantly impairs biventricular function and cardiac cycle timing.
- Interventricular interactions are disrupted in PAH, leading to compromised hemodynamics.
- Mechanisms underlying heart rate reduction benefits in PAH require further elucidation.
Purpose of the Study:
- To investigate the effects of heart rate (HR) reduction on biventricular function and interactions in experimental pulmonary arterial hypertension (PAH).
- To compare the impact of carvedilol and ivabradine on cardiac mechanics and interventricular coordination in PAH.
- To elucidate the mechanisms by which HR reduction improves hemodynamics in PAH.
Main Methods:
- Experimental model of monocrotaline-induced pulmonary arterial hypertension (PAH) in rats.
- Assessment of biventricular function, cardiac cycle timing, and interventricular interactions using echocardiography and conductance catheterization.
- Pharmacological intervention with carvedilol and ivabradine to reduce heart rate in PAH rats.
Main Results:
- PAH rats exhibited delayed cardiac cycle events, impaired right ventricular (RV) and left ventricular (LV) relaxation, and increased LV eccentricity.
- Heart rate reduction with carvedilol and ivabradine (HR 302-303 bpm vs. 359 bpm in PAH) shortened isovolumic contraction times and improved RV relaxation.
- HR reduction enhanced early diastolic LV filling, improved interventricular interactions, and led to better overall hemodynamics, including increased cardiac output and RV contractility.
Conclusions:
- Heart rate reduction, achieved with either carvedilol or ivabradine, significantly improves biventricular filling and hemodynamics in experimental PAH.
- The beneficial effects are attributed to the realignment of right ventricular-left ventricular cardiac cycle events and improved interventricular interactions.
- This study highlights the therapeutic potential of targeting heart rate in managing biventricular dysfunction associated with PAH.
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