Author + information
- Received February 21, 2013
- Accepted March 4, 2013
- Published online November 1, 2013.
- Lucas H. Timmins, PhD∗,†,
- Benjamin D. Mackie, MD∗,
- John N. Oshinski, PhD†,‡,
- Don P. Giddens, PhD† and
- Habib Samady, MD∗∗ ()
- ∗Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia
- †Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, Georgia
- ‡Department of Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, Georgia
- ↵∗Reprint requests and correspondence:
Dr. Habib Samady, Division of Cardiology–Interventional Cardiology, Department of Medicine, Emory University School of Medicine, 1364 Clifton Road NE, Suite F622, Atlanta, Georgia 30322.
Low and oscillatory wall shear stress (WSS) have been implicated in the pathogenesis of atherosclerosis (1,2). Furthermore, cardiac allograft vasculopathy (CAV) has the highest rate of progression opposite flow dividers, suggesting a role of regional fluid dynamics (3). However, to our knowledge, the association between regional WSS and clinically manifest CAV has not previously been described.
We present images from a 45-year-old man, 15 years post-heart transplant (HTx), who has undergone annual surveillance coronary angiography. His angiogram 7 years post-HTx demonstrated no significant CAV (Fig. 1A). In subsequent years, he developed significant CAV, underwent percutaneous coronary intervention (PCI) in the 1st diagonal and 1st obtuse marginal arteries, and was treated with standard immunosuppressive therapy, statins, and aspirin. He recently presented with a large anterior non–ST-segment elevated myocardial infarction (NSTEMI), and emergent angiography revealed a 99% stenosis in the mid-left anterior descending coronary artery (LAD) with Thrombolysis In Myocardial Infarction flow grade 2 (Fig. 1B, Online Video 1).
In order to calculate WSS, 3-dimensional geometric reconstruction and computational fluid dynamics (CFD) simulation were performed from the patient’s 7-year post-HTx angiogram (when he had no significant CAV). CFD utilizes computational methods to quantify velocity and pressure data throughout the domain of interest (e.g., vessel). Post-processing of these data allows for quantification of various fluid dynamics parameters (e.g., WSS ).
Results revealed low velocity (Online Video 2) and low WSS, defined as the frictional force exerted on the luminal surface by flowing blood, magnitudes (Fig. 2A, Online Video 3) opposite the flow divider at the site of the subsequent culprit lesion that persisted throughout the cardiac cycle. Furthermore, oscillatory WSS was observed at the site of subsequent culprit lesion formation as demonstrated by the WSS angle deviation (Fig 2B) and reversal of WSS vectors during the cardiac cycle (Fig. 3, Online Video 4).
These images introduce a hypothesis-generating association between low and oscillatory WSS and subsequent development of a focal, clinically manifest CAV, that warrants future investigation.
For accompanying videos, please see the online version of this paper.
This research was funded by an American Heart Association Postdoctoral Fellowship (to Dr. Timmins). Dr. Oshinski is a consultant for Neostem. Dr. Samady has received research funding from Toshiba, Volcano, and St. Jude Medical. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received February 21, 2013.
- Accepted March 4, 2013.
- American College of Cardiology Foundation
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