Introduction Cellular Coupling, Cardiac Activation Patterns and Arrhythmia

What were the consequences Prophylactic antiarrhythmic drug treatment has changed to a therapy which is carried out with great caution and care. The surprising finding that antiarrhythmic drugs can provoke arrhythmia made it evident that arrhythmia is not only a phenomenon of a single cell but involves the whole tissue and that more determinants are involved than only the transmembrane currents. 

The term, arrhythmogenic substrate, became a matter of interest to many researchers. The arrhythmogenic substrate means the pathologic and anatomic preconditions for the initiation of tachyarrhythmias such as myocardial fibrosis, aneurysm, the border zone between normal and ischemic or infarcted tissue, scars, diffuse myocardial injury in cardiomyopathy or the chronic alterations induced by myocarditis, and furthermore, accessory pathways or variations in the specific cardiac conduction system. These anatomic or pathologic altera- 

In the course of this development focusing on the arrhythmogenic substrate on the basis of tissue alterations the question how myocardial cells interact with each other became the center of attention. The intercellular communication via intercellular low-resistance pathways (gap junctions), other forms of coupling and the cardiac networking became an important subject of research. 

How are cardiac cells coupled How do cardiac cells interact electrically These are important questions to be addressed and they lead to the topic of cardiac networking. Sperelakis [1979] distinguished three forms of transfer of excitation (1) mechanical transmission (2) chemical transmission, and 

In summary, from the present point of view the most important mechanism for transmission of excitation is coupling via the gap junction channels. 

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Introduction Cellular Coupling, Cardiac Activation Patterns and Arrhythmia... 

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