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The effect of tear depth on the propagation of aortic dissections in isolated porcine thoracic aorta

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Abstract

An in vitro model was used to determine the influence of tear depth on the propagation pressure of aortic dissections. Saline was injected into the media of segments of 20 porcine thoracic aortas to create blebs. A circumferential slit was made on the intimal side of each bleb, connecting the true lumen to the false lumen. Each aorta was then pressurized under no-flow conditions until propagation in either the anterograde or retrograde direction occurred. Histological sections of each principal propagating edge were used to determine depth of tear, measured as the ratio of elastin layers in the intimal flap to the elastin layers in the intact wall. Propagation occurred for tear depths ranging from 0.44 to 0.89, with dissections closest to the adventitia (with tear depths near 1) requiring the lowest pressures. Propagation pressure (P) depends on the number of elastin layers (L) in the outer wall of a dissection,P=0.44L+25(kPa),r2=0.465,p=0.003and also on tear depth (d):P=−58d+81(kPa),r2=0.547,p<0.001.Various in vivo factors are discussed which may affect these experimentally determined relationships.

Introduction

Dissection is an often fatal condition because it leads to aortic rupture. Dissections are initiated by a tearing of the intima and a portion of the subjacent media. Due to the laminated structure of the aortic media, the tear then spreads parallel to the true lumen, both circumferentially and longitudinally, creating a false lumen. Tearing, propagation and secondary tear formation have previously been distinguished because of the differences in forces required for each of the stages (Carson and Roach, 1990; van Baardwijk and Roach, 1987). While treatment varies depending on the location of the dissection, both medical and surgical approaches are aimed at preventing propagation and new tears through the lowering of systolic pressure and pulse pressure, and through attempts at surgically reinforcing the damaged aortic wall (Fann and Millar, 1995).

Although it has been reported from necropsy studies that fatal dissection almost exclusively involves the outer half of the aortic media (Roberts, 1981), the likelihood of propagation or rupture has yet to be quantified. In vitro studies have implicated tear depth as an important factor in propagation (Mitsui et al., 1994; van Baardwijk and Roach, 1987). This study was aimed at determining the relationship between the depth of tear and propagation pressure of a bleb using an in vitro porcine model.

Section snippets

Methods

Twenty porcine thoracic aortas, removed just distal to the arch, were obtained from a local abattoir in accordance with Canadian regulations. All were cut to approximately 17–19 cm in length to fit the pressurization apparatus, ensuring that the vessels would not become tortuous. Specimens of this size always had a minimum of four pairs of intercostal arteries. Excess connective tissue and fat were removed from the exterior of each vessel and any branches were tied off. The aortas were then

Results

A total of 16 specimens propagated, 1 ruptured, and 3 neither propagated nor ruptured. Blebs with tear depths between 0.44 and 0.89 were observed to propagate between pressures of 26.3 and 60.0 kPa. The artery that ruptured tore at the dissected wall, directly across from the location of the intimal tear at 46.7 kPa; this aorta is included in the data for dissections that did propagate. Its tear depth was 0.56±0.03. A summary of the maximum pressures reached for arteries that did not propagate or

Discussion

The dependence of propagation pressure on tear depth was expected since the thickness of the outer wall should determine the stress distribution in a dissection. An interesting result was the relationship between , . van Baardwijk and Roach (1983)showed that the number of medial elastin layers decreases linearly along the thoracic aorta in sheep, therefore L and d are not necessarily related. The total number of elastin layers in the intact wall at the propagating edges of these aortas ranged

Acknowledgements

We would like to thank Joy Dunmore-Buyze and Dr Ian MacDonald for collecting tissue specimens. This research was funded by the Medical Research Council of Canada.

References (13)

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