Abstract
The heart rate represents a marker of cardiac workload and oxygen demand. It is an expression of increased sympathetic tone und thus an important prognostic parameter. The heart rate is modulated at the sinus node by the slew rate of the slow diastolic depolarization. This is determined by the activation of the I(f)-channel. A new approach is the specific inhibition of this channel by ivabradine. Clinically, this drug leads to a decrease of heart rate and ischemic phases, more pronounced as by atenolol. For the future ivabradine represents a new possibility for the therapy of coronary heart disease, maybe also of heart failure or specific arrhythmias involving the sinus node.
MeSH terms
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Angina Pectoris / drug therapy
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Anti-Arrhythmia Agents / therapeutic use*
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Benzazepines / therapeutic use*
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Cause of Death
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Cyclic Nucleotide-Gated Cation Channels
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Electrocardiography / drug effects
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Exercise Test / drug effects
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Heart Rate / drug effects*
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Humans
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Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
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Ion Channels / antagonists & inhibitors
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Ion Channels / drug effects*
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Ivabradine
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Muscle Proteins / antagonists & inhibitors*
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Myocardial Infarction / complications
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Myocardial Infarction / mortality
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Potassium Channels
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Prognosis
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Randomized Controlled Trials as Topic
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Sinoatrial Node / drug effects
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Stereoisomerism
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Tachycardia / drug therapy*
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Tachycardia / mortality
Substances
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Anti-Arrhythmia Agents
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Benzazepines
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Cyclic Nucleotide-Gated Cation Channels
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HCN4 protein, human
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Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
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Ion Channels
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Muscle Proteins
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Potassium Channels
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Ivabradine