Ivabradine in chronic stable angina: Effects by and beyond heart rate reduction. (15th July 2016)
- Record Type:
- Journal Article
- Title:
- Ivabradine in chronic stable angina: Effects by and beyond heart rate reduction. (15th July 2016)
- Main Title:
- Ivabradine in chronic stable angina: Effects by and beyond heart rate reduction
- Authors:
- Camici, Paolo G.
Gloekler, Steffen
Levy, Bernard I.
Skalidis, Emmanouil
Tagliamonte, Ercole
Vardas, Panos
Heusch, Gerd - Abstract:
- Abstract: Heart rate plays a major role in myocardial ischemia. A high heart rate increases myocardial performance and oxygen demand and reduces diastolic time. Ivabradine reduces heart rate by inhibiting the I f current of sinoatrial-node cells. In contrast to beta-blockers, ivabradine has no negative inotropic and lusitropic effect for a comparable heart rate reduction. Consequently, diastolic duration is increased with ivabradine compared to beta-blockers. This has potential consequences on coronary blood flow since compression of the vasculature by the surrounding myocardium during systole impedes flow and coronary blood flow is mainly diastolic. Moreover, ivabradine does not unmask alpha-adrenergic vasoconstriction and, unlike beta-blockers, maintains coronary dilation during exercise. In comparison with beta-blockers, ivabradine increases coronary flow reserve and collateral perfusion promoting the development of coronary collaterals. Ivabradine attenuates myocardial ischemia and its consequences even in the absence of heart rate reduction, possibly through reduced formation of reactive oxygen species. In conclusion, ivabradine differs from other anti-anginal agents by improving coronary blood flow and by additional pleiotropic effects. These properties make ivabradine an effective anti-anginal and anti-ischemic agent for the treatment of patients with coronary artery disease. Highlights: Ivabradine is an anti-anginal agent with an original pharmacodynamic profileAbstract: Heart rate plays a major role in myocardial ischemia. A high heart rate increases myocardial performance and oxygen demand and reduces diastolic time. Ivabradine reduces heart rate by inhibiting the I f current of sinoatrial-node cells. In contrast to beta-blockers, ivabradine has no negative inotropic and lusitropic effect for a comparable heart rate reduction. Consequently, diastolic duration is increased with ivabradine compared to beta-blockers. This has potential consequences on coronary blood flow since compression of the vasculature by the surrounding myocardium during systole impedes flow and coronary blood flow is mainly diastolic. Moreover, ivabradine does not unmask alpha-adrenergic vasoconstriction and, unlike beta-blockers, maintains coronary dilation during exercise. In comparison with beta-blockers, ivabradine increases coronary flow reserve and collateral perfusion promoting the development of coronary collaterals. Ivabradine attenuates myocardial ischemia and its consequences even in the absence of heart rate reduction, possibly through reduced formation of reactive oxygen species. In conclusion, ivabradine differs from other anti-anginal agents by improving coronary blood flow and by additional pleiotropic effects. These properties make ivabradine an effective anti-anginal and anti-ischemic agent for the treatment of patients with coronary artery disease. Highlights: Ivabradine is an anti-anginal agent with an original pharmacodynamic profile since it decreases HR without a negative inotropic effect and without a coronary vasoconstrictor effect. Ivabradine increases diastolic duration and coronary blood flow and preserves coronary dilation during exercise. Ivabradine differs from other anti-anginal agents by improving coronary blood flow and by additional pleiotropic effects. These properties make ivabradine an effective anti-anginal and anti-ischemic treatment in patients with CAD. … (more)
- Is Part Of:
- International journal of cardiology. Volume 215(2016)
- Journal:
- International journal of cardiology
- Issue:
- Volume 215(2016)
- Issue Display:
- Volume 215, Issue 2016 (2016)
- Year:
- 2016
- Volume:
- 215
- Issue:
- 2016
- Issue Sort Value:
- 2016-0215-2016-0000
- Page Start:
- 1
- Page End:
- 6
- Publication Date:
- 2016-07-15
- Subjects:
- Angina pectoris -- Anti-anginal drug -- Beta-blocker -- Coronary artery disease -- Coronary blood flow -- Coronary collateral circulation
Cardiology -- Periodicals
Electronic journals
616.12 - Journal URLs:
- http://www.clinicalkey.com/dura/browse/journalIssue/01675273 ↗
http://www.sciencedirect.com/science/journal/01675273 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.ijcard.2016.04.001 ↗
- Languages:
- English
- ISSNs:
- 0167-5273
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4542.158000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 2283.xml