Key result
Ivabradine selectively inhibits the If channel to lower heart rate without negative inotropic effects, providing similar antianginal properties to atenolol and amlodipine for chronic stable angina.
Why the study?
Does ivabradine improve myocardial ischaemia and angina in patients with chronic stable angina?
Does ivabradine improve myocardial ischaemia and angina in patients with chronic stable angina?
Ivabradine represents a promising novel approach for heart rate reduction and antianginal therapy in patients with chronic stable angina in sinus rhythm.
May offer an alternative for stable angina in sinus rhythm; leaves open confirmation in prospective RCTs.
Heart rate lowering is important in the treatment of symptomatic coronary artery disease (angina). A lower heart rate results in improved myocardial perfusion, reduced myocardial oxygen demand and therefore less myocardial ischaemia. This has traditionally been achieved with beta-blockers, or rate limiting calcium-channel antagonists. However, both these drugs are associated with significant side-effects in a proportion of patients. Ivabradine is a new drug which selectively and specifically inhibits the If channel in the sinoatrial node. It offers great promise in achieving heart rate reduction in patients in sinus rhythm without major side effects. Ivabradine has no negative inoptropic effects and does not appear to have any major side-effects. It has similar antianginal properties to both atenolol and amlodipine. Ivabradine represents a new approach to lowering heart rate in patients with chronic stable angina and potentially in unstable angina and chronic heart failure.
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Nixon et al. (2008) conducted a review in Chronic stable angina. Ivabradine vs. Atenolol and amlodipine was evaluated. Ivabradine selectively inhibits the If channel to lower heart rate without negative inotropic effects, providing similar antianginal properties to atenolol and amlodipine for chronic stable angina.
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