Recent epidemiological evidences indicates a complex association of hypertension with vascular endothelial dysfunction which causes the development and progression of atherosclerosis leading to adverse cardiovascular and cerebrovascular events due to reduction in nitric oxide (NO) bioavailability. The aim of the study was to investigate the value on reactive hyperemia peripheral arterial tonometry (RH-PAT) as a noninvasive tool to assess and compare endothelial function in between hypertensive and normotensives. Although they do not measure vascular function in the coronary circulation directly, they have been shown to correlate reasonably with its more invasive counterparts. A total of 73 hypertensive patients and 48 normotensive patients were consecutively recruited from Cardiology outpatient department of first affiliated hospital of Fujian medical university. Peripheral endothelial function was measured by using EndoPAT device to assess reactive hyperemia induced vasodilation and expressed by the reactive hyperemia index (RHI) with age, sex, BMI, height with the control subjects and further the relationship between RHI and clinical characteristics laboratory cardiovascular risk factors were also investigated. Statistical analysis were performed using SPSS software version 19.0. The normality of the distribution of variables were performed by the Kolmogorov-Smirnov test and homogeneity test of variance. Continuous variables were expressed as mean ± SD and categorical variables were expressed as percentages. Comparison between two normal groups were made by t-test, for abnormal distributed variables Mann-Whitney U test was used and χ2 test was performed for comparison of categorical variables. Pearson’s correlation analysis was used to assess associations between measured parameters and a p-value < 0.05 was considered to be statistically significant. RHI was significantly lower in hypertensive subjects compared to normotensive subjects (1.69 ± 0.46 vs 2.27 ± 0.60, p < 0.001) and when both groups were divided into different subgroups according to (sex, age < or ≥ 55, smoking, high cholesterol, physical activity, BMI, alcohol habit), significantly low RHI was noted in the hypertensive subgroups, p < 0.05. In the both groups there was no significant difference in normal cholesterol category where as in hypertensive group, subjects with regular physical activity had significantly high RHI as compared to those with no physical activity at all. In a univariate analysis age (r = -0.482, P = 0.001), Systolic BP (r = -0.312, P = 0.001), GFR (r = 0.196, P = 0.031), physical activity (r = 0.536, P = 0.001) were found to significantly correlate with RHI. In a multivariate analysis, only age (β = 0.004, P = 0.001) and SBP (β = 0.003, P = 0.010) significantly and independently correlated with RHI. RHI was significantly attenuated in hypertensive subjects and showed significant correlation between age, SBP, GFR, and physical activity indicating endothelial dysfunction, suggesting RH-PAT may be used as a non-invasive test to identify hypertensive patients with an early endothelial dysfunction.
| Published in | Cardiology and Cardiovascular Research (Volume 1, Issue 3) |
| DOI | 10.11648/j.ccr.20170103.11 |
| Page(s) | 67-75 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2017. Published by Science Publishing Group |
Endothelial Dysfunction, Hypertension, Atherosclerosis, Cardiovascular Risk, Nitric Oxide, Oxidative Stress
| [1] | Hall JE, Granger JP, do Carmo JM, da silva AA, Dubinion J, George E, et al. Hypertension: physiology and pathophysiology. Compr Physiol 2012; 2: 2393-442. |
| [2] | Behrens G, Leitzmann MF. The association between physical activity and renal cancer: systemic review and meta-analysis. Br j Cancer 2013; 108: 798-811. |
| [3] | Lackland, DT; Weber, MA (May 2015). "Global burden of cardiovascular disease and stroke: hypertension at the core". The Canadian journal of cardiology. 31 (5): 569–71. |
| [4] | Egan BM, Zhao Y, Axon RN. US trends in prevalence, awareness, treatment, and control of hypertension, 1988–2008. JAMA. 2010; 303: 2043–2050. |
| [5] | E. L. Schiffrin, “Reactivity of small blood vessels in hypertension: relation with structural changes: state of the art lecture,” Hypertension, vol. 19, no. 2, supplement, pp. II1–II9, 1992. |
| [6] | E. L. Schiffrin, “Resistance arteries as endpoints in hypertension,” Blood Pressure, Supplement, vol. 6, no. 2, supplement, pp. S24–S30, 1997. |
| [7] | Tsutsui M, Shimokawa H, Otsuji Y, Yanagihara N. Pathophysiological relevance of NO signaling in the cardiovascular system: novel insight from mice lacking all NO synthases. Pharmacol Ther 2010; 128: 499–508. | A. |
| [8] | Widlansky ME, Gokce N, Keaney JF, Jr, Vita JA. The clinical implications of endothelial dysfunction. J Am Coll Cardiol. 2003; 42: 1149–1160. |
| [9] | T. Heitzer, T. Schlinzig, K. Krohn, T. Meinertz, and T. Munzel, “Endothelial dysfunction, oxidative stress, and risk of ¨cardiovascular events in patients with coronary artery disease,”Circulation, vol. 104, no. 22, pp. 2673–2678, 2001. |
| [10] | V. Schachinger, M. B. Britten, and A. M. Zeiher, “Prognostic ¨impact of coronary vasodilator dysfunction on adverse longterm outcome of coronary heart disease,” Circulation, vol. 101, no. 16, pp. 1899–1906, 2000. |
| [11] | Davignon J, Ganz P. Role of endothelial dysfunction in atherosclerosis. Circulation. 2004; 109: III27–3. |
| [12] | G. Brevetti, A. Silvestro, V. Schiano, and M. Chiariello, “Endothelial dysfunction and cardiovascular risk prediction in peripheral arterial disease: additive value of flow-mediated dilationto ankle-brachial pressure index,” Circulation, vol. 108, no. 17, pp. 2093–2098, 2003. |
| [13] | P. J. Halcox, W. H. Schenke, G. Zalos et al., “Prognostic valueof coronary vascular endothelial dysfunction,” Circulation, vol.106, no. 6, pp. 653–658, 2002. |
| [14] | Panza JA, Quyyumi AA, Brush JE, Epstein SE. Abnormal endothelium-dependent vascular relaxation in patients with essential hypertension. N Engl J Med 1990; 323: 22–27. |
| [15] | Linder L, Kiowski W, Buhler FR, Lüscher TF. Indirect evidence for release of endothelium-derived relaxing factor in human forearm circulation in vivo: blunted response in essential hypertension. Circulation 1990; 81: 1762–1767. |
| [16] | Egashira K, Suzuki S, Hirooka Y, Kai H, Sugimachi M, Imaizumi T, Takeshita A. Impaired endothelium-dependent vasodilation in large epicardial and resistance coronary arteries in patients with essential hypertension: different responses to acetylcholine and substance P. Hypertension 1995; 25: 201–206. |
| [17] | Perticone F, Ceravolo R, Pujia A, Ventura G, Iacopino S, Scozzafava A, Ferraro A, Chello M, Mastroroberto P, Verdecchia P, Schillaci G. Prognostic significance of endothelial dysfunction in hypertensive patients. Circulation 2001; 104: 191–196. |
| [18] | W. F. Penny, O. Ben-Yehuda, K. Kuroe et al., “Improvementof coronary artery endothelial dysfunction with lipid-lowering therapy: heterogeneity of segmental response and correlationwith plasma-oxidized low density lipoprotein,” Journal of the American College of Cardiology, vol. 37, no. 3, pp. 766–774, 2001. |
| [19] | Celermajer, D. S., Sorensen, K. E., Gooch, V. M., Spiegelhalter, D. J., Miller, O. I., Sullivan, I. D., Lloyd, J. K., Deanfield, J. E. Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Lancet. 340 (8828): 1111-5 (1992). |
| [20] | Schächinger, V., Britten, M. B., Zeiher, A. M. Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease. Circulation. 101 (6): 1899-1906 (2000). |
| [21] | Cooke, J. P. The diversity of vascular disease: a clinician's perspective. In, Endothelial Cells in Health a nd Disease. Ed. Aird, W. C. (Publ. Taylor and Francis Group, 2005). |
| [22] | Higashi Y, Sasaki S, Nakagawa K, Matsuura H, Kajiyama G, Oshima T. A noninvasive measurement of reactive hyperemia that can be used to assess resistance artery endothelial function in humans. Am JCardiol 2001; 87: 121–5. |
| [23] | Bonetti PO, Lerman LO, Lerman A. Endothelial dysfunction: a marker of atherosclerotic risk. Arterioscler Thromb Vasc Biol 2003; 23: 169–75. |
| [24] | E. Donald, J. P. Halcox, M. Charakida et al., “Methodological approaches to optimize reproducibility and power in clinical studies of flow-mediated dilation,” Journal of the American College of Cardiology, vol. 51, no. 20, pp. 1959–1964, 2008. |
| [25] | Widlansky ME, Gokce N, Keaney JF Jr., Vita JA. The clinicalimplications of endothelial dysfunction. J Am Coll Cardiol 2003; 42: 1149–60. |
| [26] | Hijmering ML, Stroes ES, Pasterkamp G, Sierevogel M, Banga JD, Rabelink TJ. Variability of flow mediated dilation: consequences for clinical application. Atherosclerosis 2001; 157: 369–73. |
| [27] | Monnink SH, Tio RA, van Boven AJ, van Gilst WH, van Veldhuisen DJ (Aug 2004). "The role of coronary endothelial function testing in patients suspected for angina pectoris". Int J Cardiol. 96 (2): 123–9. |
| [28] | Bonetti PO, Barsness GW, Keelan PC, et al. Enhanced external counterpulsation improves endothelial function in patients with symptomatic coronary artery disease. J Am Coll Cardiol 2003; 41: 1761–8. |
| [29] | Gerhard-Herman M, Creager MA, Hurley S, et al. Assessment of endothelial function (nitric oxide) at the tip of a finger. Circulation 2002; 102 Suppl II: 851. |
| [30] | J. T. Kuvin, A. R. Patel, K. A. Sliney et al., “Assessment of peripheral vascular endothelial function with fnger arterial pulse wave amplitude,” American Heart Journal, vol. 146, no. 1, pp. 168–174, 2003. |
| [31] | S. C. Millasseau, J. M. Ritter, K. Takazawa, and P. J. Chowienczyk, “Contour analysis of the photoplethysmographic pulse measured at the fnger,” Journal of Hypertension, vol. 24, no. 8, pp. 1449–1456, 2006. |
| [32] | Nohira, A., Gerhard-Herman, M., Creager, M. A., Hurley, S., Mitra, D., Ganz, P. Role of Nitric Oxide in Regulation of Digital pulse Volume Amplitude in Humans. J Appl Physiology. 101 (2): 545-8 (2006). |
| [33] | Bonetti, P. O., Pumper, G. M., Higano, S. T., Holmes, D. R., Kuvin, J. T., Lerman, A. Noninvasive Identification of Patients with Early Coronary Atherosclerosis by Assessment of Digital Reactive Hyperemia. J Am Coll Cardiol. 44 (11), 2137-2141 (2004). |
| [34] | Bonetti, P. O. Attenuation of Digital Reactive Hyperemia in Patients with Early and Advanced Coronary Artery Disease. J Am Coll Cardiol. 45 (3) (Suppl): 407A (2005). |
| [35] | Hamburg, N. M., Keyes, M. J., Larson, M. G., Vasan, R. S., Schnabel, R., Pryde, M. M., Mitchell, G. F., Sheffy, J., Vita, J. A., Benjamin, E. J. Cross-Sectional Relations of Digital Vascular Function to Cardiovascular Risk Factors in the Framingham Heart Study. Circulation. 117 (19): 2467-2474 (2008). |
| [36] | Mahmud, F. H., Earing, M. G., Lee, R. A., Lteif, A. N., Driscoll, D. J., Lerman, A. Altered Endothelial Function in Asymptomatic Male Adolescents with Type I Diabetes. Congenit Heart Dis. 1 (3): 98-103 (2006). |
| [37] | Yamaoka-Tojo, M., Tojo, T., Kosugi, R., Hatakeyama, Y., Yoshida, Y., Machida, Y., Aoyama, N., Masuda, T., Izumi, T. Effects of ezetimibe add-on therapy for high-risk patients with dyslipidemia. Lipids Health Dis. 8 (1): 41 (2009). |
| [38] | Writing Group of 2010 Chinese Guidelines for the Management of Hypertension. 2010 Chinese Guidelines for the Management of Hypertension. Chin J Hypertens. 2011; 19: 701-708. |
| [39] | de Jongh S, Lilien MR, Bakker HD, Hutten BA, Kastelein JJ, Stroes ES. Family history of cardiovascular events and endothelial dysfunction in children with familial hypercholesterolemia. Atherosclerosis 2002; 163: 193–197. |
| [40] | Wilson PW, D’Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. Prediction of coronary heart disease using risk factor categories. Circulation 1998; 97: 1837–1847. |
| [41] | Kuvin JT, Patel AR, Sliney KA, Pandian NG, Sheffy J, Schnall RP, Karas RH, Udelson JE. Assessment of peripheral vascular endothelial function with finger arterial pulse wave amplitude. Am Heart J 2003; 146: 168–174. |
| [42] | Bonetti PO, Pumper GM, Higano ST, Holmes DR Jr, Kuvin JT, Lerman A. Noninvasive identification of patients with early coronary atherosclerosis by assessment of digital reactive hyperemia. J Am Coll Cardiol 2004; 44: 2137–2141. |
| [43] | Whitworth JA. 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) a statement on management of hypertension. J Hypertens 2003; 21: 1983–1992. |
| [44] | Widlansky ME, Gokce N, Keaney JF Jr, Vita JA. The clinical implications of endothelial dysfunction. J Am Coll Cardiol 2003; 42: 1149–1160. |
| [45] | Tsutsui M, Shimokawa H, Otsuji Y, Yanagihara N. Pathophysiological relevance of NO signaling in the cardiovascular system: novel insight from mice lacking all NO synthases. Pharmacol Ther 2010; 128: 499–508. |
| [46] | Lekakis J, Papamichael C, Vemmos C, Nanas J, Kontoyannis D, Stamatelopoulos S, Moulopoulos S. Effect of acute cigarette smoking on endothelium-dependent brachial artery dilatation in healthy individuals. Am J Cardiol 1997; 79: 529–531? |
| [47] | Celermajer DS, Sorensen KE, Georgakopoulos D, Bull C, Thomas O, Robinson J, Deanfield JE. Cigarette smoking is associated with doserelated and potentially reversible impairment of endothelium-dependent dilation in healthy young adults. Circulation 1993; 88: 2149–2155. |
| [48] | Yanbaeva DG, Dentener MA, Creutzberg EC, Wesseling G, Wouters EF. Systemic effects of smoking. Chest. 2007; 131: 1557–66. |
| [49] | Hallden S, Sjogren M, Hedblad B, Engstrom G, Narkiewicz K, Hoffmann M, et al. Smoking and obesity associated BDNF gene variance predicts total and cardiovascular mortality in smokers. Heart. 2013; 99: 949–53. |
| [50] | Ijzerman RG, Serne EH, van Weissenbruch MM, de Jongh RT, Stehouwer CD. Cigarette smoking is associated with an acute impairment of microvascular function in humans. Clin Sci (Lond). 2003; 104: 247–52. |
| [51] | Williams SB, Cusco JA, Roddy MA, Johnstone MT, Creager MA. Impaired nitric oxide-mediated vasodilation in patients with non-insulin-dependent diabetes mellitus. J Am Coll Cardiol 1996; 27: 567–574. |
| [52] | Haller MJ, Stein J, Shuster J et al (2007) Peripheral artery tonometry demonstrates altered endothelial function in children with type 1 diabetes. Pediatr Diabetes 8: 193–198. |
| [53] | Harrington J, Peña AS, Gent R, Hirte C, Couper J (2010) Aortic intima media thickness is an early marker of atherosclerosis in children with type 1 diabetes mellitus. J Pediatr 156: 237–241. |
| [54] | Järvisalo MJ, Raitakari M, Toikka JO et al (2004) endothelial dysfunction and increased arterial intima-media thickness in children with type 1 diabetes. Circulation 109: 1750–1755. |
| [55] | Dupuis J, Tardif JC, Rouleau JL, Ricci J, Arnold M, Lonn E, Roux R, Title LM, Amyot R, Bonafede N, Woo A, Cannon CP. Intensity of lipid lowering with statins and brachial artery vascular endothelium reactivity after acute coronary syndromes (from the BRAVER trial). Am J Cardiol 2005; 96: 1207–1213. |
| [56] | de Jongh S, Lilien MR, Bakker HD, Hutten BA, Kastelein JJ, Stroes ES. Family history of cardiovascular events and endothelial dysfunction in children with familial hypercholesterolemia. Atherosclerosis 2002; 163: 193–197. |
| [57] | Hickson SS, Butlin M, Graves M, Taviani V, Avolio AP, McEniery CM, et al. The relationship of age with regional aortic stiffness and diameter. JACC Cardiovasc Imaging. 2010; 3: 1247–55. |
| [58] | Zeiher AM, Drexler H, Saurbier B, Just H. Endothelium-mediated coronary blood flow modulation in humans. Effects of age, atherosclerosis, hypercholesterolemia, and hypertension. J Clin Invest 1993; 92: 652–662. |
| [59] | Jonk AM, Houben AJ, de Jongh RT, Serne EH, Schaper NC, Stehouwer CD. Microvascular dysfunction in obesity: a potential mechanism in the pathogenesis of obesity-associated insulin resistance and hypertension. Physiology. 2007; 22: 252–260. |
| [60] | Clarkson P, Montgomery HE, Mullen MJ, Donald AE, Powe AJ, Bull T, Jubb M, World M, Deanfield JE. Exercise training enhances endothelial function in young men. J Am Coll Cardiol 1999; 33: 13791385. |
| [61] | Dsouza CA, Shapiro LF, Clevenger CM, Dinenno FA, Monahan KD, Tanaka H, Seals DR. Regular aerobic exercise prevents and restores age-related declines in endothelium-dependent vasodilation in healthy men. Circulation 2000; 102: 1351–1357. |
| [62] | Roque FR, Briones AM, Garcia-Redondo AB, Galan M, Martinez-Revelles S, Avendano MS, et al. Aerobic exercise reduces oxidative stress and improves vascular changes of small mesenteric and coronary arteries in hypertension. Br J Pharmacol 2013; 168: 686-703. |
| [63] | Mehta JL, Lopez LM, Chen L & Cox OE. Alterations in nitric oxide synthase activity, superoxide anion generation, and platelet aggregation in systemic hypertension, and effects of celiprolol. Am J Cardiol 1994; 74: 901−990. |
| [64] | Sagar S et al. Oxygen free radicals in essential hypertension. Mol Cell Biochem 1992; 111: 103−108. |
| [65] | Harrison DG, Gongora MC. Oxidative stress and hypertension. Med Clin North Am 2009; 93: 621–635. |
| [66] | Kizhakekuttu TJ, Widlansky ME. Natural antioxidants and hypertension: promise and challenges. Cardiovasc Ther 2010; 28: e20–e32. |
| [67] | Drexler H, Horning B. Endothelial dysfunction in human disease. J Mol Cell Cardiol 1999; 31: 51–60. |
| [68] | Cai H, Harrison DG. Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress. Circ Res 2000; 87: 840–844. |
| [69] | Taddei S, Virdis A, Mattei P, Ghiadoni L, Sudano I, Salvetti A. Defective L-arginine-nitric oxide pathway in offspring of essential hypertensive patients. Circulation 1996; 94: 1298–1303. |
| [70] | Dohi Y, Thiel MA, Buhler FR, Lüscher TF. Activation of endothelial L-arginine pathway in resistance arteries. Effect of age and hypertension. Hypertension 1990; 16: 170–179. |
| [71] | Hermann M, Flammer A, Lüscher TF. Nitric oxide in hypertension. J Clin Hypertens 2006; 8 (12 Suppl 4): 17–29. |
| [72] | Zeiher AM, Drexler H, Saurbier B, Just H. Endothelium-mediated coronary blood flow modulation in humans. Effects of age, atherosclerosis, hypercholesterolemia, and hypertension. |
| [73] | Safar M, Chamiot-Clerc P, Dagher G, Renaud JF. Pulse pressure, endothelium function, and arterial stiffness in spontaneously hypertensive rats. Hypertension 2001; 38: 1416–1421. |
| [74] | Hayashi T, Yano K, Matsui-Hirai H, Yokoo H, Hattori Y, Iguchi A. Nitric oxide and endothelial cellular senescence. Pharmacol Ther 2008; 120: 333–339. |
| [75] | Farsetti A, Grasselli A, Bacchetti S, Gaetano C, Capogrossi MC. The telomerase tale in vascular aging: regulation by estrogens and nitric oxide signaling. J Appl Physiol 2009; 106: 333–337. |
| [76] | Kamper AM, Spilt A, de Craen AJ, van Buchem MA, Westendorp RG, Blauw GJ. Basal cerebral blood flow is dependent on the nitric oxide pathway in elderly but not in young healthy men. Exp Gerontol.2004; 39: 1245-1248. |
| [77] | Selley M. Increased concentrations of homocysteine and asymmetric dimethyl arginine and decreased concentrations of nitric oxide in the plasma of patients with Alzheimer’s disease. Neurobiol Aging.2003; 24: 903-907. |
| [78] | Selley M. Increased concentrations of homocysteine and asymmetric dimethylarginine and decreased concentrations of nitric oxide in the plasma of patients with Alzheimer’s disease. Neurobiol Aging.2003; 24: 903-907. |
| [79] | Rodríguez‐Mañas L, El‐Assar M, Vallejo S, López‐Dóriga P, Solís J, Petidier R. et al. endothelial dysfunction in aged humans is related with oxidative stress and vascular inflammation. Aging Cell.2009; 8: 226-238. |
| [80] | Domek-Lopacinska KU, Strosznajder JB. Cyclic GMP and nitric oxide synthase in aging and Alzheimer's disease. Mol Neurobiol.2010; 41: 129-137. |
| [81] | Tao J, Wang Y, Yang Z, Tu C, Xu MG, Wang JM. Circulating endothelial progenitor cell deficiency contributes to impaired arterial elasticity in persons of advancing age. J Hum Hypertens. 2006; 20: 490-495. |
| [82] | Clarkson P, Montgomery HE, Mullen MJ, Donald AE, Powe AJ, Bull T, Jubb M, World M, Deanfield JE. Exercise training enhances endothelial function in young men. J Am Coll Cardiol 1999; 33: 1379–1385. |
| [83] | DeSouza CA, Shapiro LF, Clevenger CM, Dinenno FA, Monahan KD, Tanaka H, Seals DR. Regular aerobic exercise prevents and restores age-related declines in endothelium-dependent vasodilation in healthy men. Circulation 2000; 102: 1351–1357. |
| [84] | Adams V, Linke A, Kränkel N, et al. Impact of regular physical activity on the NAD(P)H oxidase and angiotensin receptor system in patients with coronary artery disease. Circulation. 2005; 111 (5): 555-562, |
| [85] | Perticone F, Maio R, Tripepi G, Zoccali C. Endothelial dysfunction and mild renal insufficiency in essential hypertension. Circulation 2004; 110: 821–825. |
| [86] | Wim Van Biesen1, Dirk De Bacquer2 et al, The glomerular filtration rate in an apparently healthy population and its relation with cardiovascular mortality during 10 years. European Heart Journal (2007) 28, 478–483 doi: 10.1093/eurheartj/ehl455. |
| [87] | Eknoyan G, Lameire N, Barsoum R, Eckardt KU, Levin A, Levin N, Locatelli F, MacLeod A, Vanholder R, Walker R, Wang H. The burden of kidney disease: improving global outcomes. Kidney Int 2004; 66: 1310–1314. |
| [88] | K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002; 39 (Suppl.1): S1–S266. |
| [89] | Perticone F, Maio R, Tripepi G, Zoccali C. Endothelial dysfunction and mild renal insufficiency in essential hypertension. Circulation 2004; 110: 821–825. |
| [90] | Cerini C, Dou L, Anfosso F, Sabatier F, Moal V, Glorieux G, De Smet R, Vanholder R, Dignat-George F, Sampol J, Berland Y, Brunet P. P-cresol, a uremic retention solute, alters the endothelial barrier function in vitro. Thromb Haemost 2004; 92: 140–150. |
| [91] | Selamet Tierney ES, Newburger JW, Gauvreau K, Geva J, Coogan E, Colan SD, Ferranti SD. Endothelial Pulse Amplitude Testing: Feasibility and Reproducibility in Adolescents. J Pediatr. 2009; 154 (6): 901-5. |
APA Style
Sunil Kumar Patel, Liangdi Xie, Gong Jin, Xiaoqi Cai. (2017). Changes of Reactive Hyperemia Index (RHI) in Hypertensive Patients. Cardiology and Cardiovascular Research, 1(3), 67-75. https://doi.org/10.11648/j.ccr.20170103.11
ACS Style
Sunil Kumar Patel; Liangdi Xie; Gong Jin; Xiaoqi Cai. Changes of Reactive Hyperemia Index (RHI) in Hypertensive Patients. Cardiol. Cardiovasc. Res. 2017, 1(3), 67-75. doi: 10.11648/j.ccr.20170103.11
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Download@article{10.11648/j.ccr.20170103.11,
author = {Sunil Kumar Patel and Liangdi Xie and Gong Jin and Xiaoqi Cai},
title = {Changes of Reactive Hyperemia Index (RHI) in Hypertensive Patients},
journal = {Cardiology and Cardiovascular Research},
volume = {1},
number = {3},
pages = {67-75},
doi = {10.11648/j.ccr.20170103.11},
url = {https://doi.org/10.11648/j.ccr.20170103.11},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ccr.20170103.11},
abstract = {Recent epidemiological evidences indicates a complex association of hypertension with vascular endothelial dysfunction which causes the development and progression of atherosclerosis leading to adverse cardiovascular and cerebrovascular events due to reduction in nitric oxide (NO) bioavailability. The aim of the study was to investigate the value on reactive hyperemia peripheral arterial tonometry (RH-PAT) as a noninvasive tool to assess and compare endothelial function in between hypertensive and normotensives. Although they do not measure vascular function in the coronary circulation directly, they have been shown to correlate reasonably with its more invasive counterparts. A total of 73 hypertensive patients and 48 normotensive patients were consecutively recruited from Cardiology outpatient department of first affiliated hospital of Fujian medical university. Peripheral endothelial function was measured by using EndoPAT device to assess reactive hyperemia induced vasodilation and expressed by the reactive hyperemia index (RHI) with age, sex, BMI, height with the control subjects and further the relationship between RHI and clinical characteristics laboratory cardiovascular risk factors were also investigated. Statistical analysis were performed using SPSS software version 19.0. The normality of the distribution of variables were performed by the Kolmogorov-Smirnov test and homogeneity test of variance. Continuous variables were expressed as mean ± SD and categorical variables were expressed as percentages. Comparison between two normal groups were made by t-test, for abnormal distributed variables Mann-Whitney U test was used and χ2 test was performed for comparison of categorical variables. Pearson’s correlation analysis was used to assess associations between measured parameters and a p-value < 0.05 was considered to be statistically significant. RHI was significantly lower in hypertensive subjects compared to normotensive subjects (1.69 ± 0.46 vs 2.27 ± 0.60, p < 0.001) and when both groups were divided into different subgroups according to (sex, age < or ≥ 55, smoking, high cholesterol, physical activity, BMI, alcohol habit), significantly low RHI was noted in the hypertensive subgroups, p < 0.05. In the both groups there was no significant difference in normal cholesterol category where as in hypertensive group, subjects with regular physical activity had significantly high RHI as compared to those with no physical activity at all. In a univariate analysis age (r = -0.482, P = 0.001), Systolic BP (r = -0.312, P = 0.001), GFR (r = 0.196, P = 0.031), physical activity (r = 0.536, P = 0.001) were found to significantly correlate with RHI. In a multivariate analysis, only age (β = 0.004, P = 0.001) and SBP (β = 0.003, P = 0.010) significantly and independently correlated with RHI. RHI was significantly attenuated in hypertensive subjects and showed significant correlation between age, SBP, GFR, and physical activity indicating endothelial dysfunction, suggesting RH-PAT may be used as a non-invasive test to identify hypertensive patients with an early endothelial dysfunction.},
year = {2017}
}
TY - JOUR T1 - Changes of Reactive Hyperemia Index (RHI) in Hypertensive Patients AU - Sunil Kumar Patel AU - Liangdi Xie AU - Gong Jin AU - Xiaoqi Cai Y1 - 2017/07/10 PY - 2017 N1 - https://doi.org/10.11648/j.ccr.20170103.11 DO - 10.11648/j.ccr.20170103.11 T2 - Cardiology and Cardiovascular Research JF - Cardiology and Cardiovascular Research JO - Cardiology and Cardiovascular Research SP - 67 EP - 75 PB - Science Publishing Group SN - 2578-8914 UR - https://doi.org/10.11648/j.ccr.20170103.11 AB - Recent epidemiological evidences indicates a complex association of hypertension with vascular endothelial dysfunction which causes the development and progression of atherosclerosis leading to adverse cardiovascular and cerebrovascular events due to reduction in nitric oxide (NO) bioavailability. The aim of the study was to investigate the value on reactive hyperemia peripheral arterial tonometry (RH-PAT) as a noninvasive tool to assess and compare endothelial function in between hypertensive and normotensives. Although they do not measure vascular function in the coronary circulation directly, they have been shown to correlate reasonably with its more invasive counterparts. A total of 73 hypertensive patients and 48 normotensive patients were consecutively recruited from Cardiology outpatient department of first affiliated hospital of Fujian medical university. Peripheral endothelial function was measured by using EndoPAT device to assess reactive hyperemia induced vasodilation and expressed by the reactive hyperemia index (RHI) with age, sex, BMI, height with the control subjects and further the relationship between RHI and clinical characteristics laboratory cardiovascular risk factors were also investigated. Statistical analysis were performed using SPSS software version 19.0. The normality of the distribution of variables were performed by the Kolmogorov-Smirnov test and homogeneity test of variance. Continuous variables were expressed as mean ± SD and categorical variables were expressed as percentages. Comparison between two normal groups were made by t-test, for abnormal distributed variables Mann-Whitney U test was used and χ2 test was performed for comparison of categorical variables. Pearson’s correlation analysis was used to assess associations between measured parameters and a p-value < 0.05 was considered to be statistically significant. RHI was significantly lower in hypertensive subjects compared to normotensive subjects (1.69 ± 0.46 vs 2.27 ± 0.60, p < 0.001) and when both groups were divided into different subgroups according to (sex, age < or ≥ 55, smoking, high cholesterol, physical activity, BMI, alcohol habit), significantly low RHI was noted in the hypertensive subgroups, p < 0.05. In the both groups there was no significant difference in normal cholesterol category where as in hypertensive group, subjects with regular physical activity had significantly high RHI as compared to those with no physical activity at all. In a univariate analysis age (r = -0.482, P = 0.001), Systolic BP (r = -0.312, P = 0.001), GFR (r = 0.196, P = 0.031), physical activity (r = 0.536, P = 0.001) were found to significantly correlate with RHI. In a multivariate analysis, only age (β = 0.004, P = 0.001) and SBP (β = 0.003, P = 0.010) significantly and independently correlated with RHI. RHI was significantly attenuated in hypertensive subjects and showed significant correlation between age, SBP, GFR, and physical activity indicating endothelial dysfunction, suggesting RH-PAT may be used as a non-invasive test to identify hypertensive patients with an early endothelial dysfunction. VL - 1 IS - 3 ER -
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