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Heart-rate reduction by If-channel inhibition with ivabradine restores collateral artery growth in
Stephan H Schirmer1, Achim Degen, Magnus Baumhäkel
1Klinik für Innere Medizin III (Kardiologie, Angiologie und Internistische Intensivmedizin), Universitätsklinikum des Saarlandes, Kirrberger Straße, Homburg/Saar, Germany. stephan.schirmer@uks.eu
European Heart Journal
|August 9, 2011
Summary
Heart rate reduction using ivabradine promotes collateral artery growth in mice with arterial obstructive disease. This improves blood flow by enhancing endothelial function and nitric oxide synthase activity.
Area of Science:
- Cardiovascular Biology
- Vascular Medicine
- Pharmacology
Background:
- Collateral arteries are crucial for tissue survival during ischemia.
- Heart rate is linked to vascular events in patients with arterial obstructive disease.
Purpose of the Study:
- To investigate the effect of heart rate reduction (HRR) on collateral artery growth.
- To determine the mechanisms underlying HRR-induced arteriogenesis.
Main Methods:
- Utilized apolipoprotein E knockout (ApoE-/-) and wild-type mice.
- Administered ivabradine (If-channel inhibitor) for heart rate reduction.
- Assessed hindlimb perfusion via microsphere and angiography; evaluated endothelial function and protein expression (e.g., eNOS).
Main Results:
- Ivabradine reduced heart rate and improved endothelium-dependent relaxation in ApoE-/- mice.
- Ivabradine significantly enhanced hindlimb perfusion in ApoE-/- mice.
- Increased endothelial nitric oxide synthase (eNOS) activity and reduced pro-arteriogenic cytokines were observed with ivabradine treatment.
Conclusions:
- Heart rate reduction with ivabradine stimulates adaptive collateral artery growth.
- Improved endothelial function and eNOS activity are key mechanisms.
- Modulation of inflammatory gene expression contributes to ivabradine's effects on arteriogenesis.
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