Author + information
- Andreas A. Giannopoulos, MD, PhD∗ ( and )
- Yiannis S. Chatzizisis, MD, PhD
- ↵∗Cardiac Imaging, Department of Nuclear Medicine, University Hospital Zurich, Ramistrasse 100, CH-8091 Zurich, Switzerland
We read with interest the paper by Lee et al. (1) on the added value of noninvasive computational hemodynamic assessment of coronary arteries in the relentless pursuit of predicting plaques that are culprits for acute coronary syndromes. The EMERALD (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary CT Angiography and Computational Fluid Dynamic) study (1) comes into a compelling background of clinical studies that have investigated the reasonable hypothesis that integration of computational hemodynamics with anatomical information would enhance our ability to localize high-risk plaques and to predict those plaques that could lead to an acute coronary syndrome. Here the investigators similarly demonstrated the added value of a composite of 4 computationally estimated hemodynamic factors, further suggesting that lesion-specific hemorheology might have a more significant impact on plaque-specific events than global, vessel-specific hemodynamics do (such as computed tomography–derived fractional flow reserve).
When focusing on 1 of the hemodynamic parameters that were investigated, the assessment and implementation of wall shear stress (WSS) in the prognostic model warrants a commentary. The investigators estimated WSS by simulating blood flow in resting state and in stress conditions, approximating maximum hyperemia. High WSS, presumably derived from simulation of stress conditions and by using a binary variable for adverse WSS at a single cutoff value of 154.7 dynes/cm2, was regarded as an adverse hemodynamic parameter. Our knowledge on the relationship between WSS and coronary atherosclerosis comes from animal and clinical studies that have studied the effects of resting state WSS. Values of WSS at both extremes are present throughout the natural history of a coronary plaque. Low resting WSS holds a key role in the initiation and progression of coronary plaques and is closely associated with pathobiological markers of nonstenotic high-risk plaques (2). On the other end, high resting WSS is also present at certain time points in the life course of coronary plaques favoring a longitudinal transformation to high risk.
When compared with studies that have also computationally assessed WSS in the human coronary arteries, the EMERALD study reports strikingly higher absolute WSS values (ranging from 145.5 ± 87.6 dynes/cm2 for nonculprit lesions to 221.8 ± 113.2 dynes/cm2 for culprit lesions). Although there is not a definite agreement of the normal range of WSS values, these absolute numbers far exceed those reported from the invasive assessment of WSS in human coronaries assuming Poiseuille flow and from the typically used low WSS cutoff value of <10 dynes/cm2. Such particularly high absolute WSS range values have been previously reported also by a computed tomography–based computational fluid dynamic study (3) that, similarly to the work by Lee et al. (1), mentions as a computational methodological step the estimation of microvasculature response to adenosine.
The actual prognostic value of computationally simulated hemodynamic parameters, particularly that of WSS, remains vague. That is unless there is a consensus on how coronary blood flow for WSS research should be simulated. When looking into plaque progression, is it perhaps more appropriate to simulate coronary flow and WSS in the physiological resting conditions that flow exhibits its effects in the coronaries? On the other hand, investigating the potential relationship of WSS with coronary plaque-specific acute cardiovascular events is it perhaps more appropriate to simulate flow in hyperemia? These assumptions are just a needle in a haystack within the physiological assumptions in the ever-growing field of coronary flow simulations. Although it is rather exciting and, in a way, expected in the fast-paced preventive cardiology field to develop prognostic models combining several parameters, one must be certain of the validity and the accuracy of each one of these parameters. Until then we should interpret the favorable or not results of simulation studies with caution.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation
- Lee J.M.,
- Choi G.,
- Koo B.K.,
- et al.
- Chatzizisis Y.S.,
- Coskun A.U.,
- Jonas M.,
- Edelman E.R.,
- Feldman C.L.,
- Stone P.H.
- Han D.,
- Starikov A.,
- Ó Hartaigh B.,
- et al.