Cuenca-Dacal Luis, Mercado-Montoya Marcela, Gómez-Bustamante Tatiana, Berjano Enrique, Izquierdo Maite, Lozano José M, Pérez Juan J, González-Suárez Ana
BioMIT, Department of Electronic Engineering, Universitat Politècnica de València, Building 7F, Camino de Vera, 46022 Valencia, Spain.
Silico STEM S.A.S., Medellín 050035, Colombia.
J Cardiovasc Dev Dis. 2025 Jul 24;12(8):283. doi: 10.3390/jcdd12080283.
Epicardial RFA is often required when ventricular tachyarrhythmias originate from epicardial or subepicardial substrates that cannot be effectively ablated endocardially. Our objective was to evaluate the impact of intrapericardial fluid accumulation on the lesion size in the myocardium and the extent of thermal damage to adjacent structures, particularly the lung.
An in silico model of epicardial RFA was developed, featuring an irrigated-tip catheter placed horizontally on the epicardium. A 50 W-30 s RF pulse was simulated. Temperature distributions and resultant thermal lesions in both the myocardium and lung were computed.
An increase in pericardial space from 2.5 mm to 4.5 mm resulted in a reduction of myocardial lesion depth by up to 1 mm, while the volume of lung damage decreased from 200 to 300 mm to nearly zero, irrespective of myocardial or epicardial fat thickness. Myocardial lesion size was markedly influenced by the thickness of the epicardial fat layer. In the absence of fat and with a narrow pericardial space, lesions reached up to 262 mm in volume and 6.1 mm in depth. With 1 mm of fat, lesion volume decreased to below 100 mm and depth to 3 mm; with 2 mm, to under 40 mm and 2 mm; and with 3 mm, to less than 16 mm and 1.2 mm. Lung damage increased moderately with greater fat thickness. Cooling the irrigation fluid from 37 °C to 5 °C reduced lung damage by up to 51%, while myocardial lesion size decreased by only 15%.
Intrapericardial fluid accumulation can limit myocardial lesion formation while protecting adjacent structures. Cooling the irrigation fluid may reduce collateral damage without compromising myocardial lesion depth.
当室性心律失常起源于心外膜或心外膜下基质而无法通过心内膜有效消融时,通常需要进行心外膜射频消融术(RFA)。我们的目的是评估心包内积液对心肌损伤大小以及对相邻结构(尤其是肺)热损伤程度的影响。
建立了一个心外膜RFA的计算机模拟模型,其特点是将灌注导管水平放置在心外膜上。模拟了50W - 30s的射频脉冲。计算了心肌和肺中的温度分布以及由此产生的热损伤。
心包间隙从2.5mm增加到4.5mm会导致心肌损伤深度减少多达1mm,而肺损伤体积从200至300立方毫米降至几乎为零,与心肌或心外膜脂肪厚度无关。心肌损伤大小受心外膜脂肪层厚度的显著影响。在没有脂肪且心包间隙狭窄的情况下,损伤体积可达262立方毫米,深度为6.1mm。有1mm脂肪时,损伤体积降至100立方毫米以下,深度降至3mm;有2mm脂肪时,降至40立方毫米以下和2mm;有3mm脂肪时,降至16立方毫米以下和1.2mm。肺损伤随脂肪厚度增加而适度增加。将灌注液温度从37°C降至5°C可使肺损伤减少多达51%,而心肌损伤大小仅减少15%。
心包内积液可限制心肌损伤形成,同时保护相邻结构。冷却灌注液可减少附带损伤,而不影响心肌损伤深度。