The BEAUTIFUL study: randomized trial of ivabradine in patients with stable coronary artery disease and left ventricular systolic dysfunction – baseline. failure.9 A trial of ivabradine involving patients well as for the fidelity of this report to the trial tricular systolic dysfunction (BEAUTIFUL). The BEAUTIFUL Study: Effects of Ivabradine in Patients With Stable Coronary Artery Disease and Left Ventricular Systolic Dysfunction.
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Its predominant effect is to reduce heart rate without affecting contractility.
With the BEAUTIFUL Results, Procoralan* (ivabradine) is the First Antianginal Tr
Heart rate reduction with beta blockers has been identified in clinical literature and trials as a contributor to better prognosis in patients with heart failure. However, beta blockers have undesirable adverse effects i. In patients in normal sinus rhythm who cannot tolerate target doses of beta blockers or who experience high heart rates despite optimal beta blocker therapy, ivabradine may be a useful addition to standard heart failure therapy.
The efficacy of ivabradine in heart failure patients is demonstrated via a randomized, multi-center, double-blind, placebo-controlled, parallel-group trial – SHIFT – which was published in Over 6, patients were randomized and followed for about The primary composite endpoint was cardiovascular death or hospital admission for worsening heart failure.
The secondary endpoints were all-cause hospital admission, hospital admission for worsening heart failure, any cardiovascular hospital admission, or composite cardiovascular death, or hospital admission for worsening heart failure, or hospital admission for non-fatal myocardial infarction MI. Patients assigned to ivabradine were started on 5 mg twice daily and the dose was modified according to the heart rate, which was assessed in 2 weeks.
The dose of beta blockers was maintained during the trial; no reduction in dosage was observed while titrating ivabradine. The primary outcome was time to first cardiovascular death, admission to the hospital for acute MI, and admission to the hospital for new onset or worsening heart failure. There were no statistically significant differences between the two groups for the primary endpoint.
The primary composite endpoint was death from cardiovascular causes or non-fatal MI.
No significant difference was seen beautifkl regards to the primary outcome. However, it is noted that the study allowed patients to be titrated to a higher dose of ivabradine i. Ivabradine is the only selective I f channel inhibitor to date. There are no other medications within this class. The recommended starting dose of ivabradine is 5 mg by mouth twice daily with meals. Assess the patient after 2 weeks and adjust the dose to achieve a resting heart rate between beats per minute Table I.
Adjust the dose as needed based on resting heart rate and tolerability.
The maximum recommended dose is 7. In patients with a history of conduction defects, or other patients in whom bradycardia could lead to beauriful compromise, initiate therapy at 2. Ivabradine blocks the hyperpolarization-activated cyclic nucleotide-gated channel responsible for the cardiac pacemaker I f current, which regulates heart rate. Ivabradine crosses frial cell membrane and interacts within the pore loop from the intracellular side.
The inhibition slows down depolarization and reduces heart rate. Binding and un-binding of ivabradine at the channel site only occurs when the channel is in an “open” state.
BEAUTIFUL TRIAL –
Given that the number of open channels directly correlates with heart rate, the actions of ivabradine are considered “rate-dependent” and the pharmacological reduction of heart rate is a function of heart rate at baseline.
Ivabradine is approved in Europe for the symptomatic treatment of chronic stable angina in coronary artery disease CAD patients who are in normal sinus rhythm and have a resting heart rate of 70 bpm or greater. Patients may take ivabradine in combination with standard therapy, including beta blockers, or when beta blocker therapy is contraindicated or not tolerated.
Additional warnings and precautions include: To date, there are no well-established, head-to-head studies comparing ivabradine with other rate-lowering medications used in heart failure, such as digoxin. Digoxin may also be used in concomitant atrial fibrillation, whereas ivabradine cannot.
However, there was no statistically significant difference in the primary outcome of all-cause or cardiovascular mortality. Due to having a narrow therapeutic index window in heart failure, in contrast to ivabradine, digoxin requires close monitoring with regards to serum drug levels, renal function, and electrolytes. No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC.
Differences between drugs within the class Ivabradine is the only selective I f channel inhibitor to date. Administration The beautigul starting dose of ivabradine is 5 mg by mouth twice daily with meals.
Recommended dose adjustment according to heart rate In patients with a history of conduction defects, or other patients in whom ivabrwdine could lead to hemodynamic compromise, initiate therapy at 2.
Pharmacologic action Ivabradine blocks the hyperpolarization-activated cyclic nucleotide-gated channel responsible for the cardiac pacemaker I f current, which regulates heart rate. Alternative approaches To date, there are no well-established, head-to-head studies comparing ivabradine with other rate-lowering medications used in heart failure, such as digoxin.
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