This review outlines the fundamental biophysical mechanisms of radiofrequency catheter ablation, emphasizing the importance of temperature control and electrode-tissue contact for effective lesion formation.
Radiofrequency (RF) catheter ablation has become the treatment of choice for many symptomatic cardiac arrhythmias. It is presumed that the primary cause of tissue injury by RF ablation is thermally mediated, resulting in a relatively discrete homogeneous lesion. The mechanism by which RF current heats tissue is resistive heating of a narrow rim (< 1 mm) of tissue that is in direct contact with the ablation electrode. Deeper tissue heating occurs as a result of passive heat conduction from this small region of volume heating. Lesion size is proportional to the temperature at the electrode-tissue interface and the size of the ablation electrode. Temperatures above 50 degrees C are required for irreversible myocardial injury, but temperatures above 100 degrees C result in coagulum formation on the ablation electrode, a rapid rise in electrical impedance, and loss of effective tissue heating. Lesion formation is also dependent on optimal electrode-tissue contact and duration of RF delivery. Newer developments in RF ablation include temperature monitoring, longer ablation electrodes coupled to high-powered RF generators, and novel ablation electrode designs.
Nath et al. (Sat,) studied this question.