Purpose: Late lesion extension may be involved in the genesis of delayed radiofrequency (RF) effects. Because RF lesion is thermally mediated, we hypothesized that induction of heat shock response (thermotolerance) would modulate lesion healing. We evaluated the effects of thermotolerance on the dimensions and remodeling of RF lesions in a rat model of heart failure.
Methods: Wistar rats (weight 300 g) subjected to heat stress (n = 22, internal temperature of 42 °C for 10 min) were compared to controls (n = 22, internal temperature of 37 °C for 10 min). After 48 h (peak of HSP70 myocardial concentration), a modified unipolar RF lesion (customized catheter, tip 4.5 mm in diameter; 12 W; 10 s) was created on the left ventricular free wall. Animals were sacrificed 2 h (n = 10 per group) and 4 weeks (n = 12 per group) after ablation for lesion analysis. An echocardiogram was obtained at 4 weeks.
Results: There was no difference between groups regarding the size of acute (controls 27 ± 2 vs. treated 27 ± 3 mm(2)) and chronic lesions (controls 17 ± 1 vs. treated 19 ± 1 mm(2)). Histology of lesions did not differ between groups. The echocardiogram revealed dilation of the cavities and moderate systolic dysfunction without difference between groups. Acute lesion dimensions were similar between control and treated animals over time (ablation undertaken 3, 12, 24, 48, and 72 h after hyperthermia) and also using a conventional ablation catheter (50 °C; 15 W; 10 s).
Conclusion: Thermotolerance does not reduce the size or remodeling of RF lesions in the rat myocardium.