Hi Ugur,

since ivabradine acts on If channels that selectively regulate action potential of sinoatrial node cardiomyocytes, I would quote that ivabradine does not work in atrial fibrillation patients.

On the other hand, how do you think atrial fibrillation should be induced by potent reduction of heart rate associated with ivabradine administration?

Ivabradine  use is limited  to  sinus tachycardia and when you  don't  wish to have a hemodynamic compromise with HR reduction 

I think Dr. Sachdeva has given a complete answer and patient need to be observed periodically.

I am not aware of any reported association of ivabradine use resulting in Afib. Though, as Mr. Curcio noted above, the cardiac effects of ivabradine are most pronounced in the SA node, therefore it is not given to Afib patients who are in need of rate control. Ivabradine is used to control excessive catecholamine response resulting in sinus tachycardia, the latter of which places a higher metabolic/oxygen demand on the myocardium which over time is detrimental to heart function. Reducing this affect results in less workload and fatigue on the heart, and hence the reason they are indicated with heart failure when a patient is maximized on beta blocker therapy or is intolerant to such.

With regard to your initial question, since tachycardia by default has a higher metabolic demand and one would expect over time for heart function to be weakened secondary to this, periodic monitoring alone is insufficient. One needs to address the underlying driver of this chronotropic hyperactivity whether it be weight, stress, hyperthyroidism, pulmonary disease, etc.

It might be helpful to consider exploring the research available on factors that contribute to endothelial dysfunction which in turn affect nitric oxide and calcium signaling -- both of which are necessary for smooth muscle relaxation. Without such, the heart is prevented from fully relaxing and provokes a compensatory tachycardic response, often resulting in Afib or other arrhythmias.