CORRESPONDENCE: RESEARCH CORRESPONDENCE
Plaque Composition and its Relationship With Acknowledged Shear Stress Patterns in Coronary Arteries
Gastón A. Rodriguez-Granillo, MD,
Héctor M. García-García, MD,
Jolanda Wentzel, PhD,
Marco Valgimigli, MD,
Keiichi Tsuchida, MD,
Wim van der Giessen, MD, PhD,
Peter de Jaegere, MD, PhD,
Evelyn Regar, MD, PhD,
Pim J. de Feyter, MD, PhD and
Patrick W. Serruys, MD, PhD, FACC*
* Thoraxcenter, Bd406, Dr. Molewaterplein 40, 3015-GD Rotterdam, the Netherlands (Email: p.w.j.c.serruys{at}erasmusmc.nl).
To the Editor: Several studies in coronary and peripheral arteries have demonstrated that atherosclerosis has a tendency to arise more frequently in low-oscillatory shear stress (LOSS) regions such as in inner curvature of nonbranching segments and opposite to the flow divider (FD) at bifurcations (1–3). In particular, atherosclerotic disease has certain predilection for the outer wall of the left main coronary artery bifurcation, sparing the FD (2). Intravascular ultrasound (IVUS) has been used to describe the extent, distribution, and profile of plaques in the proximal left anterior descending coronary artery (LAD) (2). Nevertheless, in vivo data regarding tissue composition of this region remain unknown. Furthermore, to date, no study has explored the characteristics of plaques located in the proximal LAD compared to the left main coronary artery (LMCA). In the present study, we sought to explore the morphologic and compositional characteristics of plaque located at an acknowledged LOSS area (outer wall of the ostial LAD [OLAD]) and compare them to the characteristics of plaque located at an average shear stress region (distal LMCA [DLMCA]).
This prospective investigators-driven study included patients where the LAD was interrogated before any intervention using IVUS radiofrequency data (RFD) analysis (IVUS-VH; Volcano Therapeutics, Rancho Cordova, California). The IVUS-VH uses spectral analysis of IVUS RFD to construct tissue maps that were correlated with a specific spectrum of the RFD and assigned color codes (Fig. 1) (4). The IVUS-VH was performed with 30-MHz (Ultracross; Boston Scientific, Santa Clara, California) and 20-MHz (Eagle Eye; Volcano Therapeutics) catheters, and contour detection was determined using previously reported methodology (5). Informed consent was obtained from all patients. Plaque eccentricity was defined as the ratio of maximal to minimal plaque thickness (1). Plaque burden was defined as ([EEMarea – lumenarea]/EEMarea) x 100. The carina of the bifurcation was identified as the frame immediately distal to the take-off of the circumflex.
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Figure 1 Intravascular ultrasound cross-section images from the carina of the left anterior descending coronary artery and of the left main coronary artery. The left side shows the reconstructed grayscale, and the right side shows the color-coded data (green = fibrous; yellow-green = fibrolipidic; red = necrotic core; white = calcium) provided by the IVUS-VH unit (Volcano Therapeutics, Rancho Cordova, California). LCx = left circumflex artery; MPT = maximal plaque thickness.
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The maximal plaque thickness (MPT) was calculated at this level and spatially located according to a circumference ranging from 0° to 360°, being the inner and opposite part of the carina at 0° and 180°, respectively. Lesions were therefore prospectively divided into two groups, according to their localization in the outer (from 91° to 271°) or inner (from 270° to 90°) hemisphere of the carina.
Two regions were prospectively identified and their morphology and composition compared. The OLAD was defined as the carina and the immediate 3-mm distal segment, because the flow in this area is still influenced by the bifurcation (6). Similarly, the DLMCA was identified as the 3-mm segment immediately proximal to the bifurcation. Compositional and geometrical data were expressed as mean percentages.
Discrete variables are presented as counts and percentages. Continuous variables are presented as mean ± SD. Differences in means among groups were analyzed by two-sample t test. A p value of <0.05 (two-sided) was considered to indicate statistical significance.
Forty-four patients were finally included in the analysis. The clinical presentation was stable angina in 23 patients (52.3%), unstable angina in 10 patients (22.7%) and acute myocardial infarction in 11 patients (5%); the mean age of the patients was 58.8 ± 11.5 years, and 33 patients (75%) were male. Geometric and compositional comparative results between the OLAD and the DLMCA are depicted in Table 1. Plaque burden was larger in the OLAD than in the DLMCA (45.5 ± 10.2% vs. 36.4 ± 10.8%; p < 0.0001). OLAD plaques presented more calcified (4.13 ± 5.1% vs. 1.28 ± 2.0%; p < 0.0001) and necrotic (12.36 ± 9.2% vs. 7.90 ± 8.6%, p < 0.0001) core content.
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Table 1. Volumetrical and Compositional Comparative Results Between the Ostial Left Anterior Descending Coronary Artery (OLAD) and the Distal Left Main Coronary Artery (DLMCA)
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The MPT was located in the outer hemisphere of the carina in 77.3% (n = 34) of the cases and the mean angle was 170.7 ± 60.6°. Only one case presented the MPT at 0 degrees. Necrotic core content was larger in outer than in inner lesions (14.4 ± 10.0% vs. 6.3 ± 6.9%; p = 0.02).
The current investigation extends earlier findings on atheroma distribution in the LAD by comparing in vivo plaque burden and composition in acknowledged areas of low and average shear stress. It has been previously established that an inverse relationship exists between LOSS and thickness of the vessel wall (3). The pathophysiology of such phenomena can briefly be explained by the fact that LOSS induces a loss of the physiologic flow-oriented alignment of the endothelial cells, thus causing an enhancement of the expression of adhesion molecules and a weakening of cell junctions, ultimately leading to an increase in permeability to lipids and macrophages (3,7–9). The results of the present study are in line with histopathologic data, showing higher concentrations of necrotic core and calcium in an acknowledged area subject to LOSS. Such difference may be driven by the lipid leakage present in these areas (8). The high lipid load in addition to the eccentric characteristics of the atheroma would potentially render these plaques more susceptible to rupture (10). Conversely, the more stable phenotype observed in DLMCA lesions supports the low incidence of atherothrombotic events at this level (11). Finally, these results may provide another potential explanation for the higher risk of restenosis after percutaneous coronary intervention of bifurcation lesions.
In summary, we found that OLAD atherosclerotic plaques present larger plaque burden, eccentricity, and MPT than DLMCA plaques. In addition, a larger calcified and necrotic core content was found distal to the circumflex take-off. Lesions were predominantly located in the outer wall of the carina, and such location was associated with larger necrotic core content.
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References
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1. Jeremias A, Huegel H, Lee DP, et al. Spatial orientation of atherosclerotic plaque in nonbranching coronary artery segments Atherosclerosis 2000;152:209-215.[CrossRef][Web of Science][Medline]2. Kimura BJ, Russo RJ, Bhargava V, McDaniel MB, Peterson KL, DeMaria AN. Atheroma morphology and distribution in proximal left anterior descending coronary arteryin vivo observations. J Am Coll Cardiol 1996;27:825-831.[Abstract] 3. Kornet L, Hoeks AP, Lambregts J, Reneman RS. In the femoral artery bifurcation, differences in mean wall shear stress within subjects are associated with different intima-media thicknesses Arterioscler Thromb Vasc Biol 1999;19:2933-2939.[Abstract/Free Full Text] 4. Nair A, Kuban BD, Tuzcu EM, Schoenhagen P, Nissen SE, Vince DG. Coronary plaque classification with intravascular ultrasound radiofrequency data analysis Circulation 2002;106:2200-2206.[Abstract/Free Full Text] 5. Rodriguez-Granillo GA, Serruys PW, Garcia-Garcia HM, et al. Coronary artery remodelling is related to plaque composition. Heart 2005 Jun 17; [Epub ahead of print].. 6. Gijsen F, Thury A, Lamers B, Wentzel JJ, Schuurbiers JCH, Serruys PW, Slager CJ. 3D plaque distribution and its relationship to shear stress in a human coronary artery bifurcation in vivo. Presented at: Summer Bioengineering Conference, June 22–26, 2005 Vail, Colorado.. 7. Berceli SA, Warty VS, Sheppeck RA, Mandarino WA, Tanksale SK, Borovetz HS. Hemodynamics and low density lipoprotein metabolism. Rates of low density lipoprotein incorporation and degradation along medial and lateral walls of the rabbit aorto-iliac bifurcation Arteriosclerosis 1990;10:686-694.[Abstract] 8. Kaazempur-Mofrad MR, Isasi AG, Younis HF, et al. Characterization of the atherosclerotic carotid bifurcation using MRI, finite element modeling, and histology Ann Biomed Eng 2004;32:932-946.[CrossRef][Web of Science][Medline] 9. Slager CJ, Wentzel J, Gijsen FJH, Schuurbiers JCH, van der Wal AC, van der Steen AFW, Serruys PW. The role of shear stress in the generation of rupture-prone vulnerable plaques Nat Clin Pract 2005;2:401-407.[CrossRef] 10. Falk E, Shah PK, Fuster V. Coronary plaque disruption Circulation 1995;92:657-671.[Free Full Text] 11. Wang JC, Normand SL, Mauri L, Kuntz RE. Coronary artery spatial distribution of acute myocardial infarction occlusions Circulation 2004;110:278-284.[Abstract/Free Full Text]
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