(Circulation. 2000;102:e22.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
From the Interventional Cardiology (G.V.L., J.N.H., P.W.S.) and Hemodynamics (J.J.W., R.K., C.J.S.) Departments, Thoraxcenter, University Hospital Dijkzigt, Rotterdam, Netherlands, and Interuniversity Cardiology Institute of The Netherlands.
| Introduction |
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The lesion was crossed with a hydrophilic guidewire and was predilated. A 4.0x13-mm self-expandable Wallstent (Schneider Co) was implanted for optimization of the angioplasty result (as verified with intracoronary ultrasound [IVUS]). Because the stent was insufficiently appositioned, poststenting balloon inflations were applied to further optimize the angiographic and ultrasonic results. After this successful intervention, no rise in creatinine phosphokinase was seen. The day after the procedure, the patient was dismissed from the hospital.
Six months later, a control angiogram was performed. Since the
original procedure, the patient had remained free of angina.
Coronary anatomy was assessed through both biplane
angiography and IVUS. No angiographic restenosis at the
stented site was seen; IVUS revealed only mild neointimal
hyperplasia (Figure 1
).
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Recently, we reported a novel technique combining IVUS and
angiography (ANGUS) for 3D reconstruction of coronary
arteries.1 Through a combination of this technique with
computational fluid dynamics, fluid particle behavior can be calculated
at any site of interest and compared with the local wall
thickness.2 In the present patient, we applied this
technique to the stented RCA. Figure 1
shows the angiographic
left anterior oblique view of the RCA (A) with respective IVUS images,
computed fluid particle dynamics of 3 hypothetical red blood cells
entering the vessel (B), and a 3D reconstruction of the wall thickness
color-coded on the lumen surface (C). The impression of
neointimal hyperplasia seen on the angiogram was only
partly confirmed by IVUS, which revealed a 1-mm neointimal
thickness; this discrepancy may be caused by flow impairment induced by
the IVUS catheter still present in the lumen. Furthermore, this
picture shows that at the stented site, a small helical excursion of
the particles can be observed, possibly influenced by the angulated
vessel segment immediately preceding the stent location.
Figure 2
shows a detailed view of the
proximal RCA (center). Panel A shows the IVUS image with a
fibrocalcific plaque between the 9 and 12 oclock positions; panel B
highlights wall thickness, panel C the local wall shear stress
(WSS) values, and panel D the velocity patterns of 3
hypothetical cells entering the vessel. From this image, it becomes
clear that the eccentric plaque area shown on IVUS corresponds with a
high-wall-thickness spot ("hot" red spot in B) and with a zone of
low focal shear stress accompanied by flow abnormalities.
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Disturbed flow patterns have been associated with oscillatory WSS, which has been implicated in plaque formation in the carotid artery.3 Although investigation is ongoing as to whether oscillatory WSS, gradients in WSS, or low WSS is deleterious to the vascular wall, this frictional force exerted by the flowing blood at the endothelium of the artery has repeatedly been implicated in the pathogenesis of atherosclerosis2 and vascular remodeling.4 In human coronary arteries in vivo, the existence of helical flow has not yet been demonstrated. This case shows, for the first time, the presence of helical particle movement in a coronary artery and its relation to wall thickness and WSS. Because this patient is still symptom- and event-free 2.5 years after the initial stent implantation, it may be hypothesized that the absence of severe flow disturbances at the stented surface of the RCA (with possibly the presence of high shear stress) is an effective measure in the prevention of restenosis. Conversely, intensely disturbed flow patterns can sustain focal atherogenesis in other parts of the vessel.
| Footnotes |
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The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Lukes Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
Circulation encourages readers to submit cardiovascular images to the Circulation Editorial Office, St Lukes Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.
| References |
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2.
Krams R, Wentzel JJ, Oomen JA, et al. Evaluation of
endothelial shear stress and 3D geometry as factors
determining the development of atherosclerosis and
remodeling in human coronary arteries in vivo: combining 3D
reconstruction from angiography and IVUS (ANGUS) with computational
fluid dynamics. Arterioscler Thromb Vasc Biol. 1997;17:20612065.
3.
Ku DN, Giddens DP, Zarins CK, et al. Pulsatile flow
and atherosclerosis in the human carotid bifurcation:
positive correlation between plaque location and low oscillating shear
stress. Arteriosclerosis. 1985;5:293302.
4. Zarins CK, Zatina MA, Giddens DP, et al. Shear stress regulation of artery lumen diameter in experimental atherogenesis. J Vasc Surg. 1987;5:413420.[Medline] [Order article via Infotrieve]
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