OJMI  Vol.1 No.1 , September 2011
Examination of Possible Flow Turbulence during Flow-Mediated Dilation Testing
ABSTRACT
The validity of the flow-mediated dilation (FMD) test has been doubted due to the lack of normalization to the primary stimulus, shear stress. Shear stress can be calculated using a simplified mathematical model based on Poiseuille’s law. Poiseuille’s law assumes that the blood velocity profile is parabolic. The presence of turbulence will violate this assumption. The Reynolds number (RE) is used to define critical values for the transition from laminar to turbulent flow. Between RE values of 2000 and 4000, flow enters a transitional phase where turbulence is possible. Purpose: To determine whether brachial artery blood flow becomes turbulent during reactive hyperemia following forearm ischemia. Methods: Eleven healthy male subjects (25 ± 5 years) were tested. Brachial artery diameters and blood velocities were measured continuously following 2, 4, 6 and 10 minutes ischemia. The peak post-ischemic RE (REpeak) and RE integrated over 40 seconds (RE40) post-ischemia were calculated. Results: There was a significant change in REpeak (F4,7 = 98.573, p = ≤ 0.001) and RE40) (F4,7) = 50.613, p = ≤ 0.001) in response to ischemia. Within-subjects contrasts revealed a significant increase in REpeak and RE40 for each duration of ischemia versus baseline (p = ≤ 0.001). Following 4 minutes of ischemia there was approximately 12 seconds of potentially turbulent flow. Conclusion: Blood flow transitions between laminar and turbulent flow during ischemia-induced reactive hyperemia. This may limit the efficacy of estimating shear stress when using the standard FMD test protocol.

Cite this paper
nullL. Stoner, M. Sabatier and J. Young, "Examination of Possible Flow Turbulence during Flow-Mediated Dilation Testing," Open Journal of Medical Imaging, Vol. 1 No. 1, 2011, pp. 1-8. doi: 10.4236/ojmi.2011.11001.
References
[1]   R. Ross, “The Pathogenesis of Atherosclerosis: A Perspective for the 1990s,” Nature, Vol. 362, No. 6423, 1993, pp. 801-809. doi:10.1038/362801a0

[2]   D. S. Celermajer, et al., “Non-Invasive Detection of Endothelial Dysfunction in Children and Adults at Risk of Atherosclerosis,” Lancet, Vol. 340, No. 8828, 1992, pp. 1111-1115. doi:10.1016/0140-6736(92)93147-F

[3]   T. Yoshida, et al., “Prognostic Value of Flow-Mediated Dilation of the Brachial Artery in Patients with Cardiovascular Disease,” Internal Medicine, Vol. 45, No. 9, 2006, pp. 575-579. doi:10.2169/internalmedicine.45.1534

[4]   J. Grewal, et al., “Assessment of Novel Risk Factors in Patients at Low Risk for Cardiovascular Events Based on Framingham Risk Stratification,” Clinical & Investigative Medicine, Vol. 26, No. 4, 2003, pp. 158-165.

[5]   M. C. Corretti, et al., “Guidelines for the Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery: A Report of the International Brachial Artery Reactivity Task Force,” Journal of the American College of Cardiology, Vol. 39, No., 2002, pp. 257-265. doi:10.1016/S0735-1097(01)01746-6

[6]   M. J. Sabatier, et al., “Doppler Ultrasound Assessment of Posterior Tibial Artery Size in Humans,” Journal of Clinical Ultrasound, Vol. 34, No. 5, 2006, pp. 223-230. doi:10.1002/jcu.20229

[7]   L. Stoner, et al., “Relationship between Blood Velocity and Conduit Artery Diameter and the Effects of Smoking on Vascular Responsiveness,” Journal of Applied Physiology, Vol. 96, No. 6, 2004, pp. 2139-2145. doi:10.1152/japplphysiol.01107.2003

[8]   C. D. Black, B. Vickerson and K. K. McCully, “Noninvasive Assessment of Vascular Function in the Posterior Tibial Artery of Healthy Humans,” Dynamic Medicine, Vol. 2, No. 1, 2003, p. 1. doi:10.1186/1476-5918-2-1

[9]   K. E. Pyke and M. E. Tschakovsky, “The Relationship between Shear Stress and Flow-Mediated Dilatation: Implications for the Assessment of Endothelial Function,” The Journal of Physiology, Vol. 568, No. 2, 2005, pp. 357-369. doi:10.1113/jphysiol.2005.089755

[10]   G. F. Mitchell, et al., “Local Shear Stress and Brachial Artery Flow-Mediated Dilation: The Framingham Heart Study,” Hypertension, Vol. 44, No. 2, 2004, pp. 134-139. doi:10.1161/01.HYP.0000137305.77635.68

[11]   B. A. Parker, T. L. Trehearn and J. R. Meendering, “Pick Your Poiseuille: Normalizing the Shear Stimulus in Studies of Flow-Mediated Dilation,” Journal of Applied Physiology, Vol. 107, No. 4, 2009, pp. 1357-9. doi:10.1152/japplphysiol.91302.2009

[12]   L. Stoner and K. McCully, “Blood Velocity Parameters that Contibute to Flow-Mediated Dilation,” LAP LAMBERT Academic Publishing, Saarbrücken, 2011.

[13]   A. Koller, D. Sun and G. Kaley, “Role of Shear Stress and Endothelial Prostaglandins in Flow- and Viscosity-Induced Dilation of Arterioles in vitro,” Circulation Research, Vol. 72, No. 6, 1993, pp. 1276-1284.

[14]   S. Chien, et al., “Effects of Hematocrit and Plasma Proteins on Human Blood Rheology at Low Shear Rates,” Journal of Applied Physiology, Vol. 21, No. 1, 1966, pp. 81-87.

[15]   D. D. Duncan, et al., “The Effect of Compliance on Wall Shear in Casts of a Human Aortic Bifurcation,” Journal of Biomechanical Engineering, Vol. 112, No. 2, 1990, pp. 183-8. doi:10.1161/01.HYP.0000137305.77635.68

[16]   A. Gnasso, et al., “Association between intima-Media Thickness and Wall Shear Stress in Common Carotid Arteries in Healthy Male Subjects,” Circulation, Vol. 94, No. 12, 1996, pp. 3257-3262.

[17]   R. Dammers, et al., “Shear Stress Depends on Vascular Territory: Comparison between Common Carotid and Brachial Artery,” Journal of Applied Physiology, Vol. 94, No. 2, 2003, pp. 485-489.

[18]   O. Reynolds, “An Experimental Investigation of the Circumstances Which Determine Whether the Motion of Water Shall be Direct or Sinuous, and of the Law of Resistance in Parallel Channels,” Philosophical Transactions of the Royal Society B: Biological Sciences, Vol. 174, 1883, pp. 935-982.

[19]   N. Westerhof, N. Stergiopulos and M. I. M. Noble, “Snapshots of Hemodynamics,” Springer, New York, 2005.

[20]   L. Stoner, et al., “Occasional Cigarette Smoking Chronically Affects Arterial Function,” Ultrasound in Medicine & Biology, Vol. 34, No. 12, 2008, pp. 1885-1892. doi:10.1161/01.HYP.0000137305.77635.68

[21]   K. E. Pyke and F. Jazuli, “Impact of Repeated Increases in Shear Stress via Reactive Hyperemia and Handgrip Exercise: No Evidence of Systematic Changes in Brachial Artery FMD,” American Journal of Physiology - Heart and Circulatory Physiology, Vol. 300, No. 3, 2011, pp. H1078-1089. doi:10.1152/ajpheart.00736.2010

[22]   K. E. Pyke, E. M. Dwyer and M. E. Tschakovsky, “Impact of Controlling Shear Rate on Flow-Mediated Dilation Responses in the Brachial Artery of Humans,” Journal of Applied Physiology , Vol. 97, No. 2, 2004, pp. 499-508. doi:10.1152/japplphysiol.01245.2003

[23]   R. A. Harris, et al., “Variability of Flow-Mediated Dilation Measurements with Repetitive Reactive Hyperemia,” Vascular Medicine, Vol. 11, No. 1, 2006, pp. 1-6. doi:10.1191/1358863x06vm641oa

[24]   N. J. Hangiandreou, et al., “The Effects of Irreversible JPEG Compression on an Automated Algorithm for Measuring Carotid Artery Intima-Media Thickness from Ultrasound Images,” Journal of Digital Imaging, Vol. 15, No. S1, 2002, pp. 258-260.

[25]   L. Stoner, et al., “Upper versus Lower Extremity Arterial Function after Spinal Cord Injury,” Journal of Spinal Cord Medicine, Vol. 29, No. 2, 2006, pp. 138-146.

[26]   T. J. Kizhakekuttu, et al., “Measuring FMD in the brachial artery: how important is QRS gating?” Journal of Applied Physiology, Vol. 109, No. 4, 2010, pp. 959-65. doi:10.1152/japplphysiol.00532.2010

[27]   L. Stoner, et al., “The Relationship between Blood Velocity and Conduit Artery Diameter, and the Effects of Smoking on Vascular Responsiveness,” Journal of Applied Physiology, Vol. 96, No. 9, 2004, pp. 2139-2145.

[28]   J. L. Olive, et al., “Blood Flow and Muscle Fatigue in SCI Individuals during Electrical Stimulation,” Journal of Applied Physiology, Vol. 94, No. 2, 2003, pp. 701-8.

[29]   L. Stoner and K. McCully, “Peak- and Time-Integrated Shear Rates Independently Predict Flow-Mediated Dilation,” Journal of Clinical Ultrasound, 2011, In Press.

[30]   R. Joannides, et al., “Evaluation of the Determinants of Flow-Mediated Radial Artery Vasodilatation in Humans,” Clinical and Experimental Hypertension, Vol. 19, No. 5-6, 1997, pp. 813-826.

[31]   A. C. Betik, V. B. Luckham and R. L. Hughson, “Flow-mediated Dilation in Human Brachial Artery after Different Circulatory Occlusion Conditions,” American Journal of Physiology - Heart and Circulatory Physiol-ogy, Vol. 286, No. 1, 2004, pp. H442-H448. doi:10.1152/ajpheart.00314.2003

[32]   J. Padilla, et al., “Normalization of Flow-Mediated Dilation to Shear Stress Area under the Curve Eliminates the Impact of Variable Hyperemic Stimulus,” Cardiovascular Ultrasound, Vol. 6, 2008, p. 44. doi:10.1186/1476-7120-6-44

[33]   B. Silke and D. McAuley, “Accuracy and Precision of Blood Pressure Determination with the Finapres: An Overview Using Re-sampling Statistics,” Journal of Human Hypertension, Vol. 12, No. 6, 1998, pp. 403-9. doi:10.1038/sj.jhh.1000600

[34]   M. J. Mullen, et al., “Heterogenous Nature of Flow Mediated Dilatation in Human Conduit Arteries in vivo: Relevance to Endothelial Dysfunction in Hypercholes-terolemia,” Circulation Research, Vol. 88, No. 2, 2001, pp. 145-151.

[35]   R. Joannides, et al., “Influence of Vascular Dimension on Gender Difference in Flow-Dependent Dilatation of Peripheral Conduit Arteries,” American Journal of Physiology - Heart and Circulatory Physiology, Vol. 282, No. 4, 2002, pp. H1262-H1269. doi:10.1152/ajpheart.00209.2001

[36]   J. A. Frangos, et al., “Flow Effects on Prostacyclin Production by Cultured Human Endothelial Cells,” Science, Vol. 227, No. 4693, 1985, pp. 1477-1479. 10.1126/science.3883488

[37]   M. J. Kuchan, H. Jo and J. A. Frangos, “Role of G Proteins in Shear Stress-Mediated Nitric Oxide Production by Endothelial Cells,” American Journal of Physiology, Vol. 267, No. 3, 1994, pp. C753-C758.

[38]   J. A. Frangos, T. Y. Huang and C. B. Clark, “Steady Shear and Step Changes in Shear Stimulate Endothelium via Independent Mechanisms--Superposition of Transient and Sustained Nitric Oxide Production,” Biochemical and Biophysical Research Communications, Vol. 224, No. 3, 1996, pp. 660-665. doi:10.1006/bbrc.1996.1081

[39]   H. Macarthur, et al., “Selective Inhibition of Agonist-Induced but Not Shear Stress-Dependent Release of Endothelial Autacoids by Thapsigargin,” British Journal of Pharmacology, Vol. 108, No. 1, 1993, pp. 100-105.

[40]   S. N. Doshi, et al., “Flow-Mediated Dilatation Following Wrist and upper Arm Occlusion in Humans: The Contribution of Nitric Oxide,” Clinical Science, Vol. 101, No. 6, 2001, pp. 629-635. doi:10.1042/CS20010033

[41]   M. Lie, O. M. Sejersted and F. Kiil, “Local Regulation of Vascular cross Section during Changes in Femoral Arterial Blood Flow in Dogs,” Circulation Research, Vol. 27, No. 5, 1970, pp. 727-737.

[42]   S. M. Hilton, “A Peripheral Arterial Conducting Mechanism Underlying Dilatation of the Femoral Artery and Concerned in Functional Vasodilatation in Skeletal Muscle,” The Journal of Physiology, Vol. 149, 1959, pp. 93-111.

[43]   Y. Inaba, J. A. Chen and S. R. Bergmann, “Prediction of Future Cardiovascular Outcomes by Flow-Mediated Vasodilatation of Brachial Artery: A Meta-Analysis,” International Journal of Cardiovascular Imaging, Vol. 26,No. 6, 2010, pp. 631-640. doi:10.1007/s10554-010-9616-1

[44]   D. J. Green, et al., “Flow-Mediated Dilation and Cardiovascular Event Prediction: Does Nitric Oxide Matter?” Hypertension, Vol. 57, No. 3, 2011, pp. 363-9. doi:10.1161/HYPERTENSIONAHA.110.167015

 
 
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