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Br Heart J. 1995 December; 74(6): 641–644.
PMCID: PMC484121

Decreased platelet function in aortic valve stenosis: high shear platelet activation then inactivation.


OBJECTIVE--To elucidate the mechanism of the bleeding tendency observed in patients with aortic valve stenosis. DESIGN--A prospective study of high and low shear platelet function tests in vitro in normal controls compared with that in patients with severe aortic valve stenosis with a mean (SD) systolic gradient by Doppler of 75 (18) mm Hg before and at least 4 months after aortic valve replacement. SETTING--District general hospital. RESULTS--The patients showed reduced retention in the high shear platelet function tests. (a) Platelet retention in the filter test was 53.6 (12.6)% in patients with aortic valve stenosis and 84.8 (9.6)% in the controls (P < 0.001). (b) Retention in the glass bead column test was 49.8 (19.2) in the patients and 87.4 (8.7) in the controls (P < 0.001). (c) The standard bleeding time was longer in the patients (P < 0.06). Results of the high shear tests (a, b, and c) after aortic valve replacement were within the normal range. The platelet count was low but within the normal range before surgery and increased postoperatively (P < 0.01). There were no differences in the results of standard clotting tests, plasma and intraplatelet von Willebrand's factor, or in 15 platelet aggregation tests using five agonists between patients with aortic valve stenosis and controls. CONCLUSIONS--The high shear haemodynamics of aortic valve stenosis modify platelet function in vivo predisposing to a bleeding tendency. This abnormality of platelet function is detectable only in vitro using high shear tests. The abnormal function is reversed by aortic valve replacement. High shear forces in vitro activate and then inactivate platelets. By the same mechanisms aortic valve stenosis seems to lead to high shear damage in vivo, resulting in a clinically important bleeding tendency in some patients.

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Selected References

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  • Warkentin TE, Moore JC, Morgan DG. Aortic stenosis and bleeding gastrointestinal angiodysplasia: is acquired von Willebrand's disease the link? Lancet. 1992 Jul 4;340(8810):35–37. [PubMed]
  • Butler J, Rocker GM, O'Brien JR, Etherington M, Pillai R, Westaby S. Platelet responses to cardiopulmonary bypass. Assessment by a shear stress activation technique. J Cardiovasc Surg (Torino) 1992 Jan-Feb;33(1):33–37. [PubMed]
  • O'Brien JR, Etherington MD. Heart valve stenosis and von Willebrand's factor multimers. Lancet. 1992 Sep 5;340(8819):616–616. [PubMed]
  • Ikeda Y, Handa M, Kawano K, Kamata T, Murata M, Araki Y, Anbo H, Kawai Y, Watanabe K, Itagaki I, et al. The role of von Willebrand factor and fibrinogen in platelet aggregation under varying shear stress. J Clin Invest. 1991 Apr;87(4):1234–1240. [PMC free article] [PubMed]
  • O'Brien JR, Salmon GP. Shear stress activation of platelet glycoprotein IIb/IIIa plus von Willebrand factor causes aggregation: filter blockage and the long bleeding time in von Willebrand's disease. Blood. 1987 Nov;70(5):1354–1361. [PubMed]
  • Peterson DM, Stathopoulos NA, Giorgio TD, Hellums JD, Moake JL. Shear-induced platelet aggregation requires von Willebrand factor and platelet membrane glycoproteins Ib and IIb-IIIa. Blood. 1987 Feb;69(2):625–628. [PubMed]
  • O'Brien JR. High shearing forces in blood: haemostasis, thrombosis and atherogenesis. Thromb Res. 1994 Oct 1;76(1):103–108. [PubMed]
  • O'Brien JR, Heywood JB. Some interactions between human platelets and glass: von Willebrand's disease compared with normal. J Clin Pathol. 1967 Jan;20(1):56–64. [PMC free article] [PubMed]
  • Folts JD, Crowell EB, Jr, Rowe GG. Platelet aggregation in partially obstructed vessels and its elimination with aspirin. Circulation. 1976 Sep;54(3):365–370. [PubMed]
  • Ikeda H, Koga Y, Kuwano K, Nakayama H, Ueno T, Yoshida N, Adachi K, Park IS, Toshima H. Cyclic flow variations in a conscious dog model of coronary artery stenosis and endothelial injury correlate with acute ischemic heart disease syndromes in humans. J Am Coll Cardiol. 1993 Mar 15;21(4):1008–1017. [PubMed]
  • Rifkin PL, Friedberg NM, Zucker MB. The effect of apyrase on platelet retention in normal subjects and in patients with abnormal cardiac valves or with von Willebrand's disease. Thromb Diath Haemorrh. 1973 Sep 15;30(1):215–220. [PubMed]
  • O'Brien JR, Salmon GP. An independent haemostatic mechanism: shear induced platelet aggregation. Adv Exp Med Biol. 1990;281:287–296. [PubMed]
  • Moake JL, Turner NA, Stathopoulos NA, Nolasco L, Hellums JD. Shear-induced platelet aggregation can be mediated by vWF released from platelets, as well as by exogenous large or unusually large vWF multimers, requires adenosine diphosphate, and is resistant to aspirin. Blood. 1988 May;71(5):1366–1374. [PubMed]
  • Chow TW, Hellums JD, Moake JL, Kroll MH. Shear stress-induced von Willebrand factor binding to platelet glycoprotein Ib initiates calcium influx associated with aggregation. Blood. 1992 Jul 1;80(1):113–120. [PubMed]
  • Badimon L, Badimon JJ, Galvez A, Chesebro JH, Fuster V. Influence of arterial damage and wall shear rate on platelet deposition. Ex vivo study in a swine model. Arteriosclerosis. 1986 May-Jun;6(3):312–320. [PubMed]
  • O'Brien JR, Etherington MD. "Rebleeding" the reversal of shear stress activation of platelets--a possible clue to thrombogenesis. Thromb Res. 1992 Mar 15;65(6):821–822. [PubMed]
  • Lyon RT, Runyon-Hass A, Davis HR, Glagov S, Zarins CK. Protection from atherosclerotic lesion formation by reduction of artery wall motion. J Vasc Surg. 1987 Jan;5(1):59–67. [PubMed]
  • Cozzi PJ, Lyon RT, Davis HR, Sylora J, Glagov S, Zarins CK. Aortic wall metabolism in relation to susceptibility and resistance to experimental atherosclerosis. J Vasc Surg. 1988 May;7(5):706–714. [PubMed]
  • Bomberger RA, Zarins CK, Taylor KE, Glagov S. Effect of hypotension on atherogenesis and aortic wall composition. J Surg Res. 1980 May;28(5):402–409. [PubMed]
  • Harris CN, Kaplan MA, Parker DP, Dunne EF, Cowell HS, Ellestad MH. Aortic stenosis, angina, and coronary artery disease. Interrelations. Br Heart J. 1975 Jun;37(6):656–661. [PMC free article] [PubMed]

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