Prominent Role of Tensile Stress in Propagation of a Dissection After Coronary Stenting
Computational Fluid Dynamic Analysis on True 3D-Reconstructed Segment
A 61-year-old man underwent direct stenting in the mid right coronary artery with a 3.5×18-mm stent deployed at a pressure of 14 atm. Without further balloon inflation, the control angiogram showed a stepdown-like pattern at the distal edge of the stent (Figure 1A). At that site, intravascular ultrasound (IVUS) imaging (see Movie, available at http://www.circulationaha.org) showed a ruptured plaque and a minor dissection. Shortly after IVUS, the dissection extended distally and became subocclusive (Figure 1, B and C). Deployment of 2 additional stents arrested propagation of the dissection. The final angiogram showed a satisfactory result, with TIMI 3 flow. Despite the importance of edge dissection, the mechanism of propagation in coronary arteries has not been described. It seems reasonable that the pressure force induced by flow on a dissected flap would stimulate propagation. To study this flow-induced force, the coronary artery lumen and wall were reconstructed in true 3D (Figure 2A) by fusion of angiographic and IVUS data. Application of computational fluid dynamics to the reconstruction visualized the pressure development in the axial direction (Figure 2B) as well as that over the cross sections surrounding the protruding flap (Figure 2C). The pressure difference found between the intimal and luminal sides of the flap is ≈1 mm Hg. In contrast, with this low value, greater local changes in pressure and associated force can be deduced from the Laplace equation applied to the changing morphology of the dissected vessel wall. Normally, the tensile force exerted by the fibrous cap and thickened intima creates a significant pressure drop from the lumen to the subintimal space. This pressure drop is proportional to the ratio of intima thickness to wall thickness, eg, for respective thicknesses of 0.2 mm and 1 mm, this amounts to one fifth of luminal pressure. In case of an intimal rupture, blood enters the subintimal space. This eliminates the lumen-to-subintima pressure drop and results in retraction of the inner vessel wall layers. Moreover, the outer wall layers then become exposed to the full blood pressure and expand (Figure 2A). Both effects lead to propagation of the dissection. A similar mechanism has been described for aortic dissection. Indeed, this also explains retrograde expansion of a dissection, as is frequently observed after balloon dilatation. Nevertheless, a major flow-related difference between retrogradely or distally propagating dissections occurs when the dissection spreads circumferentially over >180°. Then, only for distally propagating dissections, the flow-induced pressure difference becomes important, because this forces the flap to flip over, thus causing a total vessel occlusion.
Movie is available as a Data Supplement at http://www.circulationaha.org
The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St.Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
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