Ivabradine: Cardiovascular Effects

Rognoni, Andrea; Bertolazzi, Marzia; Macciò, Sergio; Rognoni, G

doi:10.2174/157489009787260016

Cited by 6 publications

(4 citation statements)

References 36 publications

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“…Already used for other cardiovascular disorders, ivabradine promises better oxygenation of the heart when it is subjected to a stress inducing a rapid, sustained and dose-dependent reduction of HR at rest and during exercise without a significant effect on atrio-ventricular conduction, left ventricular contraction/relaxation or vascular tissues [36]. These properties associated with an improvement in left ventricular loading related to bradycardia result in an increase in stroke volume and preservation in cardiac output even during exercise [37].…”

Section: Introductionmentioning

confidence: 99%

The Biological Effects of Ivabradine in Cardiovascular Disease

Speranza

Franceschelli

Riccioni³

2012

Molecules

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A large number of studies in healthy and asymptomatic subjects, as well as patients with already established cardiovascular disease (CAD) have demonstrated that heart rate (HR) is a very important and major independent cardiovascular risk factor for prognosis. Lowering heart rate reduces cardiac work, thereby diminishing myocardial oxygen demand. Several experimental studies in animals, including dogs and pigs, have clarified the beneficial effects of ivabradine associated with HR lowering. Ivabradine is a selective inhibitor of the hyperpolarisation activated cyclic-nucleotide-gated funny current (If) involved in pacemaker generation and responsiveness of the sino-atrial node (SAN), which result in HR reduction with no other apparent direct cardiovascular effects. Several studies show that ivabradine substantially and significantly reduces major risks associated with heart failure when added to guideline-based and evidence-based treatment. However the biological effect of ivabradine have yet to be studied. This effects can appear directly on myocardium or on a systemic level improving endothelial function and modulating immune cell migration. Indeed ivabradine is an 'open-channel' blocker of human hyperpolarization-activated cyclic nucleotide gated channels of type-4 (hHCN4), and a 'closed-channel' blocker of mouse HCN1 channels in a dose-dependent manner. At endothelial level ivabradine decreased monocyte chemotactin protein-1 mRNA expression and exerted a potent anti-oxidative effect through reduction of vascular NADPH oxidase activity. Finally, on an immune level, ivabradine inhibits the chemokine-induced migration of CD4-positive lymphocytes. In this review, we discuss the biological effects of ivabradine and highlight its effects on CAD.

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Section: Introductionmentioning

confidence: 99%

The Biological Effects of Ivabradine in Cardiovascular Disease

Speranza

Franceschelli

Riccioni³

2012

Molecules

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“…It could reduce the RV preload, eventually affecting the left ventricular stroke volume. The International Society for Heart and Lung Transplantation (ISHLT) consensus statement recommends against routine use of beta blockers to prevent ST in RV failure [ 12 ]. Rate-lowering drugs such as beta blockers lengthen the diastolic period, which increases the SV and CO in systolic left ventricular failure, but they are not effective and can even be detrimental in heart failure with preserved ejection fraction [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

Novel Use of Ivabradine for Persistent Sinus Tachycardia in a Patient on Extracorporeal Life Support With Right Ventricular Dysfunction

Akopyan,

Shah,

Rackauskas

et al. 2024

Cureus

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“…Ivabradine is a HR-lowering drug considered to be devoid of a direct effect on cardiac contractility/relaxation, AV conduction, or systemic vascular resistance [23,24]. It thus enables to investigate the selective role of pharmacological HR reduction on hemodynamics.…”

Section: Discussionmentioning

confidence: 99%

Atenolol’s Inferior Ability to Reduce Central vs Peripheral Blood Pressure Can Be Explained by the Combination of Its Heart Rate-Dependent and Heart Rate-Independent Effects

Teeäär

Serg

Paapstel

et al. 2020

International Journal of Hypertension

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Objective. Whether the inferior ability of atenolol to reduce central (aortic) compared to peripheral (brachial) blood pressure (BP) is related to its heart rate (HR)-dependent or -independent effects, or their combination, remains unclear. To provide further mechanistic insight into this topic, we studied the acute effects of atenolol versus nebivolol and ivabradine on systolic blood pressure amplification (SBPA; peripheral systolic BP minus central systolic BP) in a model of sick sinus syndrome patients with a permanent dual-chamber cardiac pacemaker in a nonrandomized single-blind single-group clinical trial. Methods. We determined hemodynamic indices noninvasively (Sphygmocor XCEL) before and at least 3 h after administration of oral atenolol 50 or 100 mg, nebivolol 5 mg, or ivabradine 5 or 7.5 mg during atrial pacing at a low (40 bpm), middle (60 bpm), and high (90 bpm) HR level in 25 participants (mean age 65.5 years, 12 men). Results. At the low HR level, i.e., when the drugs could exert their HR-dependent and HR-independent effects on central BP, only atenolol produced a significant decrease in SBPA (mean change 0.74 ± 1.58 mmHg (95% CI, 0.09–1.40; P=0.028)), indicating inferior central vs peripheral systolic BP change. However, we observed no significant change in SBPA with atenolol at the middle and high HR levels, i.e., when HR-dependent mechanisms had been eliminated by pacing. Conclusion. The findings of our trial with a mechanistic approach to the topic imply that the inferior ability of atenolol to reduce central vs peripheral BP can be explained by the combination of its heart rate-dependent and -independent effects. This trial is registered with NCT03245996.

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Ivabradine: Cardiovascular Effects

Cited by 6 publications

References 36 publications

The Biological Effects of Ivabradine in Cardiovascular Disease

The Biological Effects of Ivabradine in Cardiovascular Disease

Novel Use of Ivabradine for Persistent Sinus Tachycardia in a Patient on Extracorporeal Life Support With Right Ventricular Dysfunction

Atenolol’s Inferior Ability to Reduce Central vs Peripheral Blood Pressure Can Be Explained by the Combination of Its Heart Rate-Dependent and Heart Rate-Independent Effects

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