Heart rate-induced modifications of concentric left ventricular hypertrophy: exploration of a novel therapeutic concept

Lowering the heart rate is considered to be beneficial in heart failure (HF) with reduced ejection fraction (HFrEF). In a dilated left ventricle (LV), pharmacological heart rate lowering is associated with a reduction in LV chamber size. In patients with HFrEF, this structural change is associated w...

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Published in:American journal of physiology. Heart and circulatory physiology 2016-10, Vol.311 (4), p.H1031-H1039
Main Authors: Klein, Franziska J, Bell, Stephen, Runte, K Elisabeth, Lobel, Robert, Ashikaga, Takamuru, Lerman, Lilach O, LeWinter, Martin M, Meyer, Markus
Format: Article
Language:English
Subjects:
Animals
Cardiac Pacing, Artificial - methods
Elasticity
Evidence-based medicine
Female
Fibrosis
Heart - physiopathology
Heart Failure
Heart rate
Heart Rate - physiology
Hogs
Hypertrophy, Left Ventricular - pathology
Hypertrophy, Left Ventricular - physiopathology
Integrative Cardiovascular Physiology and Pathophysiology
Ligation
Myocardium - pathology
Renal Artery - surgery
Stroke Volume
Swine
Swine, Miniature
Ventricular Remodeling
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Summary:Lowering the heart rate is considered to be beneficial in heart failure (HF) with reduced ejection fraction (HFrEF). In a dilated left ventricle (LV), pharmacological heart rate lowering is associated with a reduction in LV chamber size. In patients with HFrEF, this structural change is associated with better survival. HF with preserved ejection fraction (HFpEF) is increasingly prevalent but, so far, without any evidence-based treatment. HFpEF is typically associated with LV concentric remodeling and hypertrophy. The effects of heart rate on this structural phenotype are not known. Analogous with the benefits of a low heart rate on a dilated heart, we hypothesized that increased heart rates could lead to potentially beneficial remodeling of a concentrically hypertrophied LV. This was explored in an established porcine model of concentric LV hypertrophy and fibrosis. Our results suggest that a moderate increase in heart rate can be used to reduce wall thickness, normalize LV chamber volumes, decrease myocardial fibrosis, and improve LV compliance. Our results also indicate that the effects of heart rate can be titrated, are reversible, and do not induce HF. These findings may provide the rationale for a novel therapeutic approach for HFpEF and its antecedent disease substrate.
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.00301.2016