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This study aims to compare radiofrequency (RF) heat lesion size across electrodes and generator settings available for interventional pain management.Monopolar lesions are generated ex vivo in animal tissue using sharp cannulae with tip diameters 23, 22, 20, 18, 16 gauge; tip lengths 5, 6, 10, 15 mm; set temperatures 60, 70, 80, 90°C; set times 1, 1.5, 2, 3, 5, 10 minutes. Lesions are generated using the RRE electrode, cooled RF, and parallel-tip bipolar RF for comparison. Lesion sizes are assessed by automated photographic temperature inference from over 400 lesions, using multiple lesions per configuration.Monopolar lesion width and length increase with each factor (P 0.001). Increasing cannula diameter from 22 to 16 gauge increases average lesion width 58-65% (3-4 mm) at 80°C and 2 minutes. Increasing temperature from 60°C to 90°C increases lesion width 108-152% at 2 minutes. Although dimensions grow most rapidly over the first minute, average lesion width is 11-20% larger at 2 minutes, and 23-32% larger at 3 minutes, compared with 1 minute. Lesion length extends distal and proximal to the tip, and exceeds tip length by 1-5 mm at 80°C and 2 minutes. Conventional 16 gauge cannulae at 80-90°C for 2-3 minutes generate lesions of average width similar to that produced by the cooled RF configuration proposed for sacroiliac joint denervation. Bipolar RF between parallel cannulae produces a rounded brick-shaped lesion of comparable shape to three sequential monopolar lesions generated using the same cannulae and generator settings.Tip gauge, tip length, temperature, and time substantially affect RF lesion size.

Pulmonary arterial hypertension (PAH) results in increased right ventricle (RV) afterload leading to RV remodeling, tricuspid regurgitation (TR), and RV failure. Though characterizing the mechanisms of TR in PAH may suggest new treatment strategies, the mechanisms leading to TR in PAH have not been characterized. In the present study, eleven porcine tricuspid valves were studied in an in vitro right heart simulator. Annular dilatations of 1.2 and 1.4 times normal area, papillary muscle (PM) displacement simulating concentric RV dilatation and eccentric RV dilatation due to concomitant left ventricle dysfunction, and two levels of PAH hemodynamics were simulated independently and in combination. Relative TR, tenting area (TA) along each coaptation line, and coaptation area (CA) of each leaflet were quantified. Results showed a significant increase (p ≤ 0.05) in TR with both increased mean pulmonary artery pressure (mPAP) and annular dilatation of 1.4 times normal. Increased mPAP significantly decreased TA but tended to increase CA, while PM displacement significantly increased TA but did not affect CA, suggesting competing effects of transvalvular pressure and leaflet tethering. Annular dilatation significantly decreased anterior and posterior CA but did not affect TA. These results may inform future TV repairs in PAH to reduce TR and improve RV hemodynamics.

Tricuspid regurgitation (TR) is associated with increased mortality in patients undergoing mitral valve repair. In recent decades, TR has been addressed using annuloplasty concomitantly with mitral valve repair by some surgeons. However, repair efficacy and durability are often suboptimal. Increased understanding of tricuspid valve coaptation and the effects of pathological and repair conditions may be useful to inform future repair design. In the present study, we propose a two-dimensional in vitro technique, available coaptation area (ACA), to quantify the area of each tricuspid leaflet available for coaptation. Preliminary results showed that annular dilatation caused a significant (p

Pulmonary hypertension (PHTN) is a pathological condition defined as a mean pulmonary artery pressure (mPAP) greater than 25 mmHg. PHTN can result from a number of lung and heart pathologies, including abnormalities of the pulmonary vasculature, left heart disease, chronic lung disease, and chronic thrombotic disease [1]. Regardless of the cause, the increased afterload on the right heart results in right ventricle (RV) hypertrophy and dilatation and tricuspid regurgitation (TR) [2]. RV dilatation is thought to result in the displacement of the tricuspid valve (TV) papillary muscles (PM) and dilatation of the TV annulus, negatively impacting TV function.Copyright © 2012 by ASME