Hyperthermia causes significant changes in myocardial cellular electrophysiological properties that include membrane depolarization, reversible and irreversible loss of excitability, and abnormal automaticity. There appear to be specific temperature ranges for reversible and irreversible electrophysiological changes. These observations may have important implications for tissue temperature monitoring during radiofrequency catheter ablation.
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.
Microwave ablation has the potential to directly heat a greater volume of tissue than RF ablation but only with efficient MW antennas. The primary mechanism of tissue injury for both MW and RF ablation appears to be thermal.
RF catheter ablation not only results in a marked reduction in blood flow within the acute pathological lesion but also causes reduced flow beyond the borders of the acute lesion because of microvascular endothelial cell injury. The progression or resolution of tissue injury within the region beyond the border of the pathological lesion may explain the late electrophysiological effects of RF ablation.
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