Abstract
Cardiac conduction disorders are common diseases which cause slow heart rate and syncope. The best way to treat these diseases by now is to implant electronic pacemakers, which, yet, have many disadvantages, such as the limited battery life and infection. Biopacemaker has been expected to replace the electronic devices. Automatic ventricular myocytes (VMs) could show pacemaker activity, which was induced by depressing inward-rectifier K+ current (I K1). In this study, a 2D model of human biopacemaker was created from the ventricular endocardial myocytes. We examined the stability of the created biopacemaker and investigated its driving capability by finding the suitable size and spatial distribution of the pacemaker for robust pacing and driving the surrounding quiescent cardiomyocytes. Our results suggest that the rhythm of the pacemaker is similar to that of the single cell at final stable state. The driving force of the biopacemaker is closely related to the pattern of spatial distribution of the pacemaker.
Highlights
In the heart, the sinoatrial node (SAN) cells are the source of the normal excitation, initiating the heartbeat and control the rhythm [1]
After 500,000 ms, the single automatic cell (AC), that is, the pacemaker cell used in the present paper, kept in stable state with a cycle length of 852 ms
We studied the relationship between driving capability and the quantity of ACs, finding that autorhythmic pacemaker activity of the ACs was depressed by the surrounding Ventricular myocyte action potential (AP) (VM) even under the condition that there were plenty of ACs, which might already lose the biological meaning
Summary
The sinoatrial node (SAN) cells are the source of the normal excitation, initiating the heartbeat and control the rhythm [1]. The failure of the SAN cells causes heart rhythm disorders, leading to syncope, easy fatigability, or circulatory collapse. The best way to treat these diseases is to implant electronic pacemakers, which have been used clinically for more than half a century with continuous refinement and reduced mortality associated with complete heart block and SAN dysfunction [3]. There are still many disadvantages: (a) the limited battery life requires replacement at periodic intervals; (b) infection may require removal of the pacemaker; (c) the setting rate is not able to respond to emotion; (d) the device must be tailored to the growth of pediatric patients [4].
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