nach oben

Current Atherosclerosis Reports

Erschienen in:

01.04.2014 | Vascular Biology (RS Rosenson, Section Editor)

Endothelial Shear Stress and Blood Viscosity in Peripheral Arterial Disease

verfasst von: Young I. Cho, Daniel J. Cho, Robert S. Rosenson

Erschienen in: Current Atherosclerosis Reports | Ausgabe 4/2014

Einloggen, um Zugang zu erhalten

Abstract

This review examines the emerging role of endothelial shear stress (ESS) and blood viscosity on the initiation and progression of atherosclerosis in peripheral arterial disease. Among the variables determining ESS, blood viscosity has to date been the most overlooked by clinical researchers. Blood viscosity is a laboratory assessment that is minimally invasive and modifiable using pharmacologic therapy as well as by hemodilution. Monitoring and controlling blood viscosity not only modulates ESS, but also reduces peripheral vascular resistance and increases blood flow to the lower extremities.

Selvin E, Erlinger TP. Prevalence of and risk factors for peripheral arterial disease in the United States results from the National Health and Nutrition Examination Survey, 1999–2000. Circulation. 2004;110(6):738–43.PubMedCrossRef

Ouriel K. Peripheral arterial disease. Lancet. 2001;358(9289):1257–64.PubMedCrossRef

Golomb BA, Dang TT, Criqui MH. Peripheral arterial disease morbidity and mortality implications. Circulation. 2006;114(7):688–99.PubMedCrossRef

Pasqualini L, Schillaci G, Vaudo G, Innocente S, Ciuffetti G, Mannarino E. Predictors of overall and cardiovascular mortality in peripheral arterial disease. Am J Cardiol. 2001;88(9):1057–60.PubMedCrossRef

Criqui MH, Langer RD, Fronek A, Feigelson HS, Klauber MR, McCann TJ, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med. 1992;326(6):381–6.PubMedCrossRef

6.•

Joosten MM, Pai JK, Bertoia ML, Rimm EB, Spiegelman D, Mittleman MA, et al. Associations between conventional cardiovascular risk factors and risk of peripheral artery disease in men. JAMA. 2012;308(16):1660–7. The study reported that in male PAD patients, smoking, hypertension, hypercholesterolemia, and type 2 diabetes account for the majority of risk associated with development of clinically significant PAD.PubMedCentralPubMedCrossRef

7.•

Moyer VA. Screening for peripheral artery disease and cardiovascular disease risk assessment with the ankle–brachial index in adults: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2013;159(5):342–8. This study reviewed the evidence on the use of resting ankle-brachial index (ABI) as a screening test for PAD or as a risk predictor for cardiovascular disease (CVD) and concluded that the current evidence is insufficient to assess the balance of benefits and harms of screening for PAD and CVD risk assessment with the ABI in adults.PubMedCrossRef

8.••

Malek AM, Alper SL, Izumo S. Hemodynamic shear stress and its role in atherosclerosis. JAMA. 1999;282(21):2035–42. This classic study identified hemodynamic shear stress as an important determinant of endothelial function and phenotype. Arterial-level shear stress (>15 dyne/cm2) induces endothelial quiescence and an atheroprotective gene expression profile, while low shear stress (<4 dyne/cm2), which is prevalent at atherosclerosis-prone sites, stimulates an atherogenic phenotype.PubMedCrossRef

Zarins CK, Giddens DP, Bharadvaj B, Sottiurai VS, Mabon RF, Glagov S. Carotid bifurcation atherosclerosis. Quantitative correlation of plaque localization with flow velocity profiles and wall shear stress. Circ Res. 1983;53(4):502–14.PubMedCrossRef

10.

Davies PF. Hemodynamic shear stress and the endothelium in cardiovascular pathophysiology. Nat Clin Pract Cardiovasc Med. 2009;6(1):16–26.PubMedCentralPubMedCrossRef

11.

Langille BL, O'Donnell F. Reductions in arterial diameter produced by chronic decreases in blood flow are endothelium-dependent. Science. 1986;231(4736):405–7.PubMedCrossRef

12.

Fukumoto Y, Hiro T, Fujii T, Hashimoto G, Fujimura T, Yamada J, et al. Localized elevation of shear stress is related to coronary plaque rupture: a 3-dimensional intravascular ultrasound study with in-vivo color mapping of shear stress distribution. J Am Coll Cardiol. 2008;51(6):645–50.PubMedCrossRef

13.

Tricot O, Mallat Z, Heymes C, Belmin J, Leseche G, Tedgui A. Relation between endothelial cell apoptosis and blood flow direction in human atherosclerotic plaques. Circulation. 2000;101(21):2450–3.PubMedCrossRef

14.

DePaola N, Gimbrone M, Davies PF, Dewey C. Vascular endothelium responds to fluid shear stress gradients. Arterioscler Thromb Vasc Biol. 1992;12(11):1254–7.CrossRef

15.

Schirmer CM, Malek AM. Estimation of wall shear stress dynamic fluctuations in intracranial atherosclerotic lesions using computational fluid dynamics. Neurosurgery. 2008;63(2):326–34.PubMedCrossRef

16.

White CR, Frangos JA. The shear stress of it all: the cell membrane and mechanochemical transduction. Philos Trans R Soc Lond B Biol Sci. 2007;362(1484):1459–67.PubMedCentralPubMedCrossRef

17.

Chachisvilis M, Zhang YL, Frangos JA. G protein-coupled receptors sense fluid shear stress in endothelial cells. Proc Natl Acad Sci. 2006;103(42):15463–8.PubMedCentralPubMedCrossRef

18.

Eng E, Ballermann BJ. Diminished NF-kappaB activation and PDGF-B expression in glomerular endothelial cells subjected to chronic shear stress. Microvasc Res. 2003;65(3):137–44.PubMedCrossRef

19.

Li YS, Haga JH, Chien S. Molecular basis of the effects of shear stress on vascular endothelial cells. J Biomech. 2005;38(10):1949–71.PubMedCrossRef

20.

Malek AM, Jiang L, Lee I, Sessa WC, Izumo S, Alper SL. Induction of nitric oxide synthase mRNA by shear stress requires intracellular calcium and G-protein signals and is modulated by PI 3 kinase. Biochem Biophys Res Commun. 1999;254(1):231–42.PubMedCrossRef

21.

Dardik A, Chen L, Frattini J, Asada H, Aziz F, Kudo FA, et al. Differential effects of orbital and laminar shear stress on endothelial cells. J Vasc Surg. 2005;41(5):869–80.PubMedCrossRef

22.

Dardik A, Yamashita A, Aziz F, Asada H, Sumpio BE. Shear stress-stimulated endothelial cells induce smooth muscle cell chemotaxis via platelet-derived growth factor-BB and interleukin-1 [alpha]. J Vasc Surg. 2005;41(2):321–31.PubMedCrossRef

23.

Glagov S, Zarins C, Giddens DP, Ku DN. Hemodynamics and atherosclerosis. Insights and perspectives gained from studies of human arteries. Arch Pathol Lab Med. 1988;112(10):1018–31.PubMed

24.

Chatzizisis YS, Jonas M, Coskun AU, Beigel R, Stone BV, Maynard C, et al. Prediction of the localization of high-risk coronary atherosclerotic plaques on the basis of low endothelial shear stress: an intravascular ultrasound and histopathology natural history study. Circulation. 2008;117(8):993–1002.PubMedCrossRef

25.

Groen HC, Gijsen FJ, van der Lugt A, Ferguson MS, Hatsukami TS, van der Steen AF, et al. Plaque rupture in the carotid artery is localized at the high shear stress region: a case report. Stroke. 2007;38(8):2379–81.PubMedCrossRef

26.••

Stone PH, Saito S, Takahashi S, Makita Y, Nakamura S, Kawasaki T, et al. Prediction of progression of coronary artery disease and clinical outcomes using vascular profiling of endothelial shear stress and arterial plaque characteristics the PREDICTION study. Circulation. 2012;126(2):172–81. Although the PREDICTION study focused on endothelial shear stress in the coronary arteries and not peripheral, it demonstrated clear correlation between plaque progressions and low endothelial shear stress. Like many other shear stress studies, blood viscosity was assumed to be a constant Newtownian value. However, the relationship between plaque growth and shear stress is noteworthy.PubMedCrossRef

27.

Friedman MH, Bargeron CB, Deters OJ, Hutchins GM, Mark FF. Correlation between wall shear and intimal thickness at a coronary artery branch. Atherosclerosis. 1987;68(1–2):27–33.PubMedCrossRef

28.

Stone PH, Coskun AU, Kinlay S, Clark ME, Sonka M, Wahle A, et al. Effect of endothelial shear stress on the progression of coronary artery disease, vascular remodeling, and in-stent restenosis in humans in vivo 6-month follow-up study. Circulation. 2003;108(4):438–44.PubMedCrossRef

29.•

Hayase H, Tokunaga K, Nakayama T, Sugiu K, Nishida A, Arimitsu S, et al. Computational fluid dynamics of carotid arteries after carotid endarterectomy or carotid artery stenting based on postoperative patient-specific computed tomography angiography and ultrasound flow data. Neurosurgery. 2011;68(4):1096–101; discussion 1101. The study compared the postoperative rheological conditions after CAS with those after CEA with patch angioplasty (patch CEA) through the use of computational fluid dynamics (CFD) based on patient-specific data. Rotational slow flow was observed in the internal carotid artery bulb after patch CEA. ESS analysis found regional low ESS near the outer wall of the bulb.

30.

Groen HC, Simons L, van den Bouwhuijsen QJ, Bosboom EM, Gijsen FJ, van der Giessen AG, et al. MRI-based quantification of outflow boundary conditions for computational fluid dynamics of stenosed human carotid arteries. J Biomech. 2010;43(12):2332–8.PubMedCrossRef

31.

Papathanasopoulou P, Zhao S, Kohler U, Robertson MB, Long Q, Hoskins P, et al. MRI measurement of time-resolved wall shear stress vectors in a carotid bifurcation model, and comparison with CFD predictions. J Magn Reson Imaging. 2003;17(2):153–62.PubMedCrossRef

32.

Schirmer CM, Malek AM. Wall shear stress gradient analysis within an idealized stenosis using non-Newtonian flow. Neurosurgery. 2007;61(4):853–63.PubMedCrossRef

33.

Schirmer CM, Malek AM. Prediction of complex flow patterns in intracranial atherosclerotic disease using computational fluid dynamics. Neurosurgery. 2007;61(4):842–51, discussion 852.PubMedCrossRef

34.

Takeuchi S, Karino T. Flow patterns and distributions of fluid velocity and wall shear stress in the human internal carotid and middle cerebral arteries. World Neurosurg. 2010;73(3):174–85, discussion e127.PubMedCrossRef

35.

Younis HF, Kaazempur-Mofrad MR, Chan RC, Isasi AG, Hinton DP, Chau AH, et al. Hemodynamics and wall mechanics in human carotid bifurcation and its consequences for atherogenesis: investigation of inter-individual variation. Biomech Model Mechanobiol. 2004;3(1):17–32.PubMedCrossRef

36.•

Galizia MS, Barker A, Liao Y, Collins J, Carr J, McDermott MM, et al. Wall morphology, blood flow and wall shear stress: MR findings in patients with peripheral artery disease. Eur Radiol. 2013:(In press). The clinical study demonstrated the feasibility of combining multi-contrast morphological imaging of the peripheral arterial wall with PC-MRI with three-directional velocity encoding. Velocities, oscillatory shear stress and total flow were similar between patients with normal arteries and wall thickening/plaque. Patients with plaques demonstrated regionally increased peak systolic WSS and enhanced WSS eccentricity.

37.

Smedby O, Nilsson S, Bergstrand L. Development of femoral atherosclerosis in relation to flow disturbances. J Biomech. 1996;29(4):543–7.PubMedCrossRef

38.

Smedby O, Johansson J, Molgaard J, Olsson AG, Walldius G, Erikson U. Predilection of atherosclerosis for the inner curvature in the femoral artery. A digitized angiography study. Arterioscler Thromb Vasc Biol. 1995;15(7):912–7.PubMedCrossRef

39.

Smedby O, Bergstrand L. Tortuosity and atherosclerosis in the femoral artery: what is cause and what is effect? Ann Biomed Eng. 1996;24(4):474–80.PubMedCrossRef

40.

Wood NB, Zhao SZ, Zambanini A, Jackson M, Gedroyc W, Thom SA, et al. Curvature and tortuosity of the superficial femoral artery: a possible risk factor for peripheral arterial disease. J Appl Physiol (1985). 2006;101(5):1412–8.CrossRef

41.

Ku DN, Giddens DP, Zarins CK, Glagov S. Pulsatile flow and atherosclerosis in the human carotid bifurcation. Positive correlation between plaque location and low oscillating shear stress. Arterioscler Thromb Vasc Biol. 1985;5(3):293–302.CrossRef

42.

Wensing PJ, Meiss L, Mali WP, Hillen B. Early atherosclerotic lesions spiraling through the femoral artery. Arterioscler Thromb Vasc Biol. 1998;18(10):1554–8.PubMedCrossRef

43.

Tarbell JM. Mass transport in arteries and the localization of atherosclerosis. Annu Rev Biomed Eng. 2003;5(1):79–118.PubMedCrossRef

44.

Scholten FG, Warnars GA, Mali WPTM, van Leeuwen MS. Femoropopliteal occlusions and the adductor canal hiatus, Duplex study. Eur J Vasc Surg. 1993;7(6):680–3.PubMedCrossRef

45.

Magid R, Murphy TJ, Galis ZS. Expression of matrix metalloproteinase-9 in endothelial cells is differentially regulated by shear stress. Role of c-Myc. J Biol Chem. 2003;278(35):32994–9.PubMedCrossRef

46.

Rosenson R. Viscosity and ischemic heart disease. J Vasc Med Biol. 1993;4:206.

47.

Cocklet GR, Meiselman HJ. Macro- and micro-rheological properties of blood. In: Baskurt OK HM, Rampling MW, Meiselman HJ, editors. Handbook of hemorheology and hemodynamics. Amsterdam: IOS Press; 2007. p. 45–71.

48.

Stoltz JF, Singh M, Riha P. Hemorheology in practice. Wahington DC: IOS Press; 1999.

49.

Chien S. Determinants of blood viscosity and red cell deformability. Scand J Clin Lab Investig. 1981;41(S156):7–12.CrossRef

50.•

Baskurt OK, Meiselman HJ. Erythrocyte aggregation: Basic aspects and clinical importance. Clin Hemorheol Microcirc. 2013;53(1):23–37. The study by two leading rheology researchers articulates that the extent of aggregation of erythrocytes is the main determinant of low shear blood viscosity. A detailed understanding of aggregation effects is important from a clinical point of view because red blood cell aggregation is increased during a variety of pathophysiological processes, including infections, circulatory and metabolic disorders, hematological pathologies and several other disease states.PubMed

51.

Kwaan HC. Role of plasma proteins in whole blood viscosity: a brief clinical review. Clin Hemorheol Microcirc. 2010;44(3):167–76.PubMed

52.

Guyton AC, Hall JE. Textbook of medical physiology (Guyton physiology). 10th ed. Philadelphia: Saunders; 2000.

53.

Ernst E, Matrai A, Kollar L. Placebo-controlled, double-blind study of haemodilution in peripheral arterial disease. Lancet. 1987;1(8548):1449–51.PubMedCrossRef

54.

Pulanic D, Rudan I. The past decade: fibrinogen. Coll Antropol. 2005;29(1):341–9.PubMed

55.

Baskurt OK, Meiselman HJ. Blood rheology and hemodynamics. Semin Thromb Hemost. 2003;29(5):435–50.PubMedCrossRef

56.

Fantl P, Ward HA. Molecular weight of human fibrinogen derived from phosphorus determinations. Biochem J. 1965;96(3):886–9.PubMedCentralPubMed

57.

Fung YC. Biomechanics. New York: Spriner-Verlag; 1981.CrossRef

58.

Sloop GD, Mercante DE. Opposite effects of low-density and high-density lipoprotein on blood viscosity in fasting subjects. Clin Hemorheol Microcirc. 1998;19(3):197–203.PubMed

59.

Stamos TD, Rosenson RS. Low high density lipoprotein levels are associated with an elevated blood viscosity. Atherosclerosis. 1999;146(1):161–5.PubMedCrossRef

60.

Slyper A, Le A, Jurva J, Gutterman D. The influence of lipoproteins on whole-blood viscosity at multiple shear rates. Metabolism. 2005;54(6):764–8.PubMedCrossRef

61.

Lowe GD, Rumley A, Norrie J, Ford I, Shepherd J, Cobbe S, et al. Blood rheology, cardiovascular risk factors, and cardiovascular disease: the West of Scotland Coronary Prevention Study. Thromb Haemost. 2000;84(4):553–8.PubMed

62.

Rosenson RS, McCormick A, Uretz EF. Distribution of blood viscosity values and biochemical correlates in healthy adults. Clin Chem. 1996;42(8 Pt 1):1189–95.PubMed

63.

Rosenson RS, Shott S, Tangney CC. Hypertriglyceridemia is associated with an elevated blood viscosity: triglycerides and blood viscosity. Atherosclerosis. 2002;161(2):433–9.PubMedCrossRef

64.

Seplowitz AH, Chien S, Smith FR. Effects of lipoproteins on plasma viscosity. Atherosclerosis. 1981;38(1):89–95.PubMedCrossRef

65.

Leonhardt H, Arntz HR, Klemens UH. Studies of plasma viscosity in primary hyperlipoproteinemia. Atherosclerosis. 1977;28:29–40.PubMedCrossRef

66.

Dormandy JA, Gutteridge JM, Hoare E, Dormandy TL. Effect of clofibrate on blood viscosity in intermittent claudication. Br Med J. 1974;4(5939):259–62.PubMedCentralPubMedCrossRef

67.

Weiss N. Lipid apheresis and rheopheresis for treatment of peripheral arterial disease. Atheroscler Suppl. 2009;10(5):62–9.PubMedCrossRef

68.

Dormandy J, Hoare E, Khattab A, Arrowsmith D, Dormandy T. Prognostic significance of rheological and biochemical findings in patients with intermittent claudication. Br Med J. 1973;4(5892):581–3.PubMedCentralPubMedCrossRef

69.

Dormandy JA, Hoare E, Colley J, Arrowsmith DE, Dormandy TL. Clinical, haemodynamic, rheological, and biochemical findings in 126 patients with intermittent claudication. Br Med J. 1973;4(5892):576–81.PubMedCentralPubMedCrossRef

70.

Dormandy JA, Hoare E, Postlethwaite J. Importance of blood viscosity. Rheological claudication. Proc R Soc Med. 1974;67(6 Pt 1):446–7.PubMedCentralPubMed

71.

Angelkort B, Spurk P, Habbaba A, Mahder M. Blood flow properties and walking performance in chronic arterial occlusive disease. Angiology. 1985;36(5):285–92.PubMedCrossRef

72.

Lowe GD, Fowkes FG, Dawes J, Donnan PT, Lennie SE, Housley E. Blood viscosity, fibrinogen, and activation of coagulation and leukocytes in peripheral arterial disease and the normal population in the Edinburgh Artery Study. Circulation. 1993;87(6):1915–20.PubMedCrossRef

73.

Tzoulaki I, Murray GD, Lee AJ, Rumley A, Lowe GD, Fowkes FG. Inflammatory, haemostatic, and rheological markers for incident peripheral arterial disease: Edinburgh Artery Study. Eur Heart J. 2007;28(3):354–62.PubMedCrossRef

74.••

Ricci I, Sofi F, Liotta AA, Fedi S, Macchi C, Pratesi G, et al. Alterations of haemorheological parameters in patients with peripheral arterial disease. Clin Hemorheol Microcirc. 2013;55(2):271–6. This recent clinical study of 90 PAD patients and 180 control subjects showed a significant association between the highest tertiles of plasma viscosity and PAD.PubMed

75.•

Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, Findeiss L, et al. Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(14):1555–70. The most recent practice guidelines for the management of patients with peripheral artery disease highlighted cilostazol and antiplatelet drug therapy as the only pharmacologic treatments clearly shown to be effective for PAD patients with claudication.PubMedCrossRef

76.

Thompson PD, Zimet R, Forbes WP, Zhang P. Meta-analysis of results from eight randomized, placebo-controlled trials on the effect of cilostazol on patients with intermittent claudication. Am J Cardiol. 2002;90(12):1314–9.PubMedCrossRef

77.

Elam M, Heckman J, Crouse J, Hunninghake D, Herd J, Davidson M, et al. Effect of the novel antiplatelet agent cilostazol on plasma lipoproteins in patients with intermittent claudication. Arterioscler Thromb Vasc Biol. 1998;18(12):1942–7.PubMedCrossRef

78.

Money SR, Herd JA, Isaacsohn JL, Davidson M, Cutler B, Heckman J, et al. Effect of cilostazol on walking distances in patients with intermittent claudication caused by peripheral vascular disease. J Vasc Surg. 1998;27(2):267–75.PubMedCrossRef

79.

Beebe HG, Dawson DL, Cutler BS, Herd JA, Strandness Jr DE, Bortey EB, et al. A new pharmacological treatment for intermittent claudication: results of a randomized, multicenter trial. Arch Intern Med. 1999;159(17):2041–50.PubMedCrossRef

80.

Dawson DL, Cutler BS, Meissner MH, Strandness DE. Cilostazol has beneficial effects in treatment of intermittent claudication results from a multicenter, randomized, prospective, double-blind trial. Circulation. 1998;98(7):678–86.PubMedCrossRef

81.

Dawson DL, Cutler BS, Hiatt WR, Hobson II RW, Martin JD, Bortey EB, et al. A comparison of cilostazol and pentoxifylline for treating intermittent claudication. Am J Med. 2000;109(7):523–30.PubMedCrossRef

82.

Regensteiner JG, Ware JE, McCarthy WJ, Zhang P, Forbes WP, Heckman J, et al. Effect of cilostazol on treadmill walking, community‐based walking ability, and health‐related quality of life in patients with intermittent claudication due to peripheral arterial disease: meta‐analysis of six randomized controlled trials. J Am Geriatr Soc. 2002;50(12):1939–46.PubMedCrossRef

83.

Dawson DL, Zheng Q, Worthy SA, Charles B, Bradley Jr DV. Failure of pentoxifylline or cilostazol to improve blood and plasma viscosity, fibrinogen, and erythrocyte deformability in claudication. Angiology. 2002;53(5):509–20.PubMedCrossRef

84.

Accetto B. Beneficial hemorheologic therapy of chronic peripheral arterial disorders with pentoxifylline: results of double-blind study versus vasodilator-nylidrin. Am Heart J. 1982;103(5):864–9.PubMedCrossRef

85.

Berman W, Berman N, Pathak D, Wood S. Effects of pentoxifylline (Trental) on blood flow, viscosity, and oxygen transport in young adults with inoperable cyanotic congenital heart disease. Pediatr Cardiol. 1994;15(2):66–70.PubMed

86.

Di Perri T, Carandente O, Vittoria A, Guerrini M, Messa GL. Studies of the clinical pharmacology and therapeutic efficacy of pentoxifylline in peripheral obstructive arterial disease. Angiology. 1984;35(7):427–35.PubMedCrossRef

87.

Perego M, Sergio G, Artale F, Giunti P, Danese C. Haemorrheological improvement by pentoxifylline in patients with peripheral arterial occlusive disease. Curr Med Res Opin. 1986;10(2):135–8.PubMedCrossRef

88.

Solerte SB, Fioravanti M, Cerutti N, Severgnini S, Locatelli M, Pezza N, et al. Retrospective analysis of long-term hemorheologic effects of pentoxifylline in diabetic patients with angiopathic complications. Acta Diabetol. 1997;34(2):67–74.PubMedCrossRef

89.

Sonkin P, Sinclair S, Hatchell D. The effect of pentoxifylline on retinal capillary blood flow velocity and whole blood viscosity. Am J Ophthalmol. 1993;115(6):775–80.PubMed

90.

Billett H, Kaul D, Connel M, Fabry M, Nagel R. Pentoxifylline (Trental) has no significant effect on laboratory parameters in sickle cell disease. Nouv Rev Fr Hématol. 1989;31(6):403–7.PubMed

91.

Karandashov V, Petukhov E, Zrodnikov V. Effects of pentoxifylline drugs and UV photohemotherapy on blood viscosity. Bull Exp Biol Med. 1998;126(5):1155–6.CrossRef

92.

Perhoniemi V, Salmenkivi K, Sundberg S, Johnsson R, Gordin A. Effects of flunarizine and pentoxifylline on walking distance and blood rheology in claudication. Angiology. 1984;35(6):366–72.PubMedCrossRef

93.

Reilly D, Quinton D, Barrie W. A controlled trial of pentoxifylline (Trental 400) in intermittent claudication: clinical, haemostatic and rheological effects. N Z Med J. 1987;100(828):445–7.PubMed

94.

Mohler ER, Hiatt WR, Creager MA. Cholesterol reduction with atorvastatin improves walking distance in patients with peripheral arterial disease. Circulation. 2003;108(12):1481–6.PubMedCrossRef

95.

Banyai S, Banyai M, Falger J, Jansen M, Alt E, Derfler K, et al. Atorvastatin improves blood rheology in patients with familial hypercholesterolemia (FH) on long-term LDL apheresis treatment. Atherosclerosis. 2001;159(2):513–9.PubMedCrossRef

96.

Empen K, Geiss HC, Lehrke M, Otto C, Schwandt P, Parhofer KG. Effect of atorvastatin on lipid parameters, LDL subtype distribution, hemorrheological parameters and adhesion molecule concentrations in patients with hypertriglyceridemia. Nutr Metab Cardiovasc Dis. 2003;13(2):87–92.PubMedCrossRef

97.

Plutzky J. Effect of lipid-lowering therapy on vasomotion and endothelial function. Curr Cardiol Rep. 1999;1(3):238–43.PubMedCrossRef

98.

Palareti G, Poggi M, Torricelli P, Balestra V, Coccheri S. Long-term effects of ticlopidine on fibrinogen and haemorheology in patients with peripheral arterial disease. Thromb Res. 1988;52(6):621–9.PubMedCrossRef

99.

Fagher B, Persson S, Persson G, Larsson H. Blood viscosity during long-term treatment with ticlopidine in patients with intermittent claudication. A double-blind study. Angiology. 1993;44(4):300–6.PubMedCrossRef

100.••

Kim D, Cho DJ, Kim YB, Cho YI. Reduced amputation rate with hemorheological therapy in critical limb ischemia patients. Clin Hemorheol Microcirc. 2014;(In press). This observational clinical study demonstrated that weekly isovolemic hemodilution performed over four consecutive weeks reduced mean hematocrit and low shear blood viscosity levels, resulting in an overall improvement of perfusion. The average rate of major lower extremity amputations with standard of care was 93 % (14 of 15), as compared with 31 % of patients undergoing lower extremity amputation after hemodilution (4 of 13) (p = 0.001).

Titel: Endothelial Shear Stress and Blood Viscosity in Peripheral Arterial Disease
verfasst von: Young I. Cho
Daniel J. Cho
Robert S. Rosenson
Publikationsdatum: 01.04.2014
Verlag: Springer US
Erschienen in: Current Atherosclerosis Reports / Ausgabe 4/2014
Print ISSN: 1523-3804
Elektronische ISSN: 1534-6242
DOI: https://doi.org/10.1007/s11883-014-0404-6

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

^{Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag}

Kostenlos registrieren

Neu im Fachgebiet Innere Medizin

Echinokokkose medikamentös behandeln oder operieren?

06.05.2024 DCK 2024 Kongressbericht

Die Therapie von Echinokokkosen sollte immer in spezialisierten Zentren erfolgen. Eine symptomlose Echinokokkose kann – egal ob von Hunde- oder Fuchsbandwurm ausgelöst – konservativ erfolgen. Wenn eine Op. nötig ist, kann es sinnvoll sein, vorher Zysten zu leeren und zu desinfizieren.

Aquatherapie bei Fibromyalgie wirksamer als Trockenübungen

03.05.2024 Fibromyalgiesyndrom Nachrichten

Bewegungs-, Dehnungs- und Entspannungsübungen im Wasser lindern die Beschwerden von Patientinnen mit Fibromyalgie besser als das Üben auf trockenem Land. Das geht aus einer spanisch-brasilianischen Vergleichsstudie hervor.

Wo hapert es noch bei der Umsetzung der POMGAT-Leitlinie?

03.05.2024 DCK 2024 Kongressbericht

Seit November 2023 gibt es evidenzbasierte Empfehlungen zum perioperativen Management bei gastrointestinalen Tumoren (POMGAT) auf S3-Niveau. Vieles wird schon entsprechend der Empfehlungen durchgeführt. Wo es im Alltag noch hapert, zeigt eine Umfrage in einem Klinikverbund.

Das Risiko für Vorhofflimmern in der Bevölkerung steigt

02.05.2024 Vorhofflimmern Nachrichten

Das Risiko, im Lauf des Lebens an Vorhofflimmern zu erkranken, ist in den vergangenen 20 Jahren gestiegen: Laut dänischen Zahlen wird es drei von zehn Personen treffen. Das hat Folgen weit über die Schlaganfallgefährdung hinaus.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Live-Webinar "Chronische Unterbauch- und Viszeralschmerzen in der Praxis managen"

Springer Medizin

Abstract

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 4/2014

Vascular Imaging in Diabetes

Screening Low-Risk Individuals for Coronary Artery Disease

A Latin American Perspective on the New ACC/AHA Clinical Guidelines for Managing Atherosclerotic Cardiovascular Disease

HDL Hypothesis: Where Do We Stand Now?

Modulation of the Renin-Angiotensin-Aldosterone System in Heart Failure