The impact of atherosclerosis and vascular collagen on energy-based vessel sealing

Abstract Background Bipolar energy ligation of vessels in surgery is common. Although rare, serious failures occur. Atherosclerosis may contribute to seal failures by altering vascular compressibility and collagen content; however, no data exist. Materials and methods Femoral and iliac arteries of six Yucatan swine with an identified genetic locus predisposing them to atherosclerosis were denuded with a Fogarty catheter. Animals were fed a high-fat diet for 28 wk. A Yorkshire pig was used as a normal control and fed a standard diet. At 28 wk, arteries were measured for their diameters, sealed, and divided in vivo with LigaSure. The sealed artery sections were excised and subjected to burst pressure testing. Half of the seal distal to the aorta was kept intact for histology and collagen and elastin quantification. A multiple linear regression model was used to assess variables contributing to burst pressure. Covariates included were vessel diameter, degree of atherosclerosis, and collagen content. Results Experimental animals were hypercholesterolemic. Atherosclerosis occurred in 90% of seals in induced animals, with severe atherosclerosis in 62% of seals. There was site-selective deposition of atherosclerotic plaques in larger diameter iliac vessels. A model including collagen and size best predicted burst pressure. Every 10-U increase in collagen resulted in 15% increase in burst pressure (95% confidence interval = 0.2%–32%, P = 0.047, R 2 = 0.36). Atherosclerosis was unrelated to burst pressure controlling for collagen and size. Conclusions Collagen and size provide the best model fit for predicting burst pressure. Quantitative research in human vasculature is warranted to better understand the influence of atherosclerosis and collagen content on seal failures.