doi: 10.1161/CIRCULATIONAHA.106.652222
(Circulation. 2006;114:e614.)
© 2006 American Heart Association, Inc.
Correspondence |
Letter by Jankowski Regarding Article, "Atherosclerotic Lesion Size and Vulnerability Are Determined by Patterns of Fluid Shear Stress"
I Department of Cardiology, Collegium Medicum Jagiellonian University, Krakow, Poland
I read with great interest the article by Cheng et al1 demonstrating the relationship between atherosclerotic plaque formation and shear stress. The authors conclude that lowered shear stress induces atherosclerotic plaque, whereas increased shear stress protects against atherosclerosis. However, I would like to draw the authors’ attention to the elegant study of Tropea et al,2 who proved that reduced arterial wall tensile stress is related to a decreased rate of atherosclerosis progression. Importantly, Tropea et al2 developed a model that reduced tensile stress of the arterial wall but that did not influence shear stress.2 On the other hand, Cheng et al1 used a perivascular shear-stress modifier (referred to as a cast) that modified shear stress but also influenced tensile stress of the arterial wall.1 Indeed, although shear stress was increased, the tensile stress of the vessel wall must have been reduced inside the cast. Importantly, both the cast (in the study of Cheng et al1) and wrap (in the study of Tropea et al2) protected against atherosclerosis progression; however, only the cast increased shear stress. This suggests that reduced tensile stress is a major determinant of the protection against atherosclerosis progression. On the other hand, significant atherosclerosis progression was noted proximal to both the cast and the wrap (it is in the region with low shear stress but increased tensile stress). Thus, Cheng et al1 could not demonstrate the independent tensile-stress influence of shear stress on the arterial wall. Moreover, they have shown that infusion of angiotensin II is related to the intraplaque hemorrhages only in the region proximal to the cast—that is, in the region with increased tensile and lowered shear stress of the arterial wall.1 It seems reasonable to suspect that angiotensin II infusion increases pulse pressure and subsequently increases the tensile stress of the arterial wall.3 It should be also noted that the study of Tropea et al2 is in agreement with a number of studies indicating that the pulsatile component of blood pressure is a major determinant of a patient’s prognosis.4,5
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Acknowledgments |
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Disclosures
None.
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References |
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 Top References |
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1. Cheng C, Tempel D, van Haperen R, van der Baan A, Grosveld F, Daemen MJ, Krams R, de Crom R. Atherosclerotic lesion size and vulnerability are determined by patterns of fluid shear stress. Circulation. 2006; 113: 2744–2753.
2. Tropea BI, Schwarzacher SP, Chang A, Asvar C, Huie P, Sibley RK, Zarins CK. Reduction of aortic wall motion inhibits hypertension-mediated experimental atherosclerosis. Arterioscler Thromb Vasc Biol. 2000; 20: 2127–2133.
3. Wilkinson IB, MacCallum H, Hupperetz PC, van Thoor CJ, Cockcroft JR, Webb DJ. Changes in the derived central pressure waveform and pulse pressure in response to angiotensin II and noradrenaline in man. J Physiol. 2001; 530: 541–550.
4. Roman MJ, Kizer JR, Ali T, Lee ET, Galloway JM, Fabitz RR, Henderson JA, Howard BV. Central blood pressure better predicts cardiovascular events than does peripheral blood pressure: the Strong Heart Study. Circulation. 2005; 112 (suppl II): II-778. Abstract.
5. Jankowski P, Czarnecka D, Loster M, Cury
o A, Brzozowska-Kiszka M, Styczkiewicz K, Kloch M, Kopacz E, Wili
ski J, Kawecka-Jaszcz K. Intraaortic pulsatility is a better predictor of event-free survival when compared with systolic, diastolic, mean and pulse pressures: the Aortic Blood Pressure and Survival Study. J Hypertens. 2006; 24 (suppl 4): S71. Abstract.
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