Dynamic changes of cardiac conduction during rapid pacing.

Area of Science:

• Cardiac Electrophysiology
• Computational Biology

Background:

• Reentry is a major cause of cardiac arrhythmias, driven by slow and unidirectional conduction block.
• Abrupt heart rate changes can dynamically alter conduction properties, impacting arrhythmogenesis.

Purpose of the Study:

• Investigate the dynamic changes in conduction velocity (CV) and unidirectional conduction block (UCB) in cardiac tissue following abrupt decreases in pacing cycle length (CL).
• Elucidate the underlying ionic mechanisms governing these rate-dependent conduction changes using computational modeling.

Main Methods:

• Utilized patterned neonatal rat ventricular myocyte cultures on microelectrode arrays to study CV and UCB dynamics.
• Employed the Pandit-Clark-Giles-Demir model to simulate ionic mechanisms of rate-dependent conduction changes.

Main Results:

• In linear strands, CV initially slowed then recovered at very short CLs (110-220 ms), attributed to action potential duration (APD) changes and Na(+) current (I(Na)) recovery.
• In tissue expansions, UCB initially increased then decreased at shorter CLs (180-240 ms).
• Simulations indicated that ion accumulation and Na(+)/K(+) pump activity critically influenced both CV and UCB dynamics.

Conclusions:

• Cardiac conduction velocity and unidirectional conduction block exhibit complex, dynamic behaviors in response to abrupt heart rate changes.
• These dynamics are governed by a interplay of factors including I(Na) recovery, postrepolarization refractoriness, APD, ion accumulation, and Na(+)/K(+) pump function.