Title:Cardioprotective Effects of the If Current Inhibition by Ivabradine During Cardiac Dysfunction
Volume: 14
Issue: 14
Author(s): Jin B. Su
Affiliation:
Keywords:
Beta-blockers, calcium channel blockers, cardiac function, f-channel inhibitor, heart rate, heart failure, myocardial
ischemia, pacemaker currents.
Abstract: Heart rate is a fundamental determinant of cardiac function. Normally, the increase in heart rate is accompanied
by increased cardiac function. But under pathological conditions such as myocardial infarction and heart failure, accelerated
heart rate may become detrimental as it decreases the diastolic time for left ventricular filling and myocardial perfusion
but increases left ventricular myocardial oxygen demand. Therefore, heart rate reduction is an appropriate strategy to
protect cardiac function. Heart rate reduction can be achieved by different bradycardic drugs, including beta-blockers, calcium
channel blockers and selective f-channel inhibitors. By competing with norepinephrine and epinephrine for binding
sites, beta-blockers block beta-adrenoceptor-mediated responses to sympathetic stimulation. This induces heart rate reduction
and negative inotropy. Calcium channel blockers block calcium influx via specific calcium channels, causing vasodilation
and decreases in heart rate, conduction velocity within the heart and myocardial force generation. The selective fchannel
inhibitor, ivabradine, inhibits If currents that play an exclusive role in pacemaking and thereby slows heart rate
without altering myocardial inotropy. Since these drugs differ in their mechanisms of action, they may cause different
beneficial and side effects and thus different outcome according to pathological states. After briefly describing the mechanisms
involved in beta-blockers and calcium channel blockers, this review focuses on the bradycardic property of ivabradine
and its pleiotropic actions.
