The relationship of endothelial function and arterial stiffness with subclinical target organ damage in essential hypertension

Yancui Sun, Fei Liu, Ying Zhang, Yan Lu, Zhuolin Su, Haizhe Ji, Yunpeng Cheng, Wei Song, Tesfaldet H Hidru, Xiaolei Yang, Yinong Jiang, Yancui Sun, Fei Liu, Ying Zhang, Yan Lu, Zhuolin Su, Haizhe Ji, Yunpeng Cheng, Wei Song, Tesfaldet H Hidru, Xiaolei Yang, Yinong Jiang

Abstract

This study aimed to explore whether brachial-ankle pulse wave velocity (baPWV) and brachial artery flow-mediated dilation (FMD) or the interaction of both parameters are associated with subclinical target organ damage (STOD) indices in patients with essential hypertension. A total of 4618 patients registered from January 2015 to October 2020 were included. baPWV and FMD were measured to evaluate arterial stiffness and endothelial dysfunction. Whereas left ventricular hypertrophy (LVH), urine albumin-creatinine ratio (UACR), and carotid intima-media thickness (CIMT) were obtained as STOD indicators. On multivariable logistic regression analysis with potential confounders, higher quartiles of baPWV and FMD were significantly associated with an increased risk of STOD. In patients <65 years of age, the odds ratio (OR) of LVH, UACR, and CIMT ≥.9 mm for the fourth versus the first quartile of baPWV were 1.765 (1.390-2.240), 2.832 (2.014-3.813), and 3.075 (2.315-4.084), respectively. In interaction analysis, an increase in baPWV shows a progressively higher risk of STOD across the quartiles of FMD. Also, the estimated absolute risks of LVH, UACR, and CIMT ≥.9 mm for the first to fourth quartile of baPWV increased from 1.88 to 2.75, 2.35 to 4.44, and 3.10 to 6.10, respectively, in patients grouped by FMD quartiles. The addition of baPWV to FMD slightly improved risk prediction for STOD. BaPWV and FMD were independently associated with an increased risk of STOD in patients with essential hypertension especially among patients <65 years of age. Patients with elevated baPWV and decreased FMD parameters are at increased risk of STOD.

Keywords: arterial stiffness; brachial artery flow-mediated dilation; brachial-ankle pulse wave velocity; endothelial function; subclinical target organ damage.

Conflict of interest statement

The authors declare that there is no conflict of interest.

© 2022 The Authors. The Journal of Clinical Hypertension published by Wiley Periodicals LLC.

Figures

FIGURE 1
FIGURE 1
A brief overview of the selection of study participants.
FIGURE 2
FIGURE 2
The risk of STOD based on baPWV quartiles in patients grouped by FMD quartiles. (A). The risk of LVH based on baPWV quartiles in patients grouped by FMD quartiles. (B). The risk of UACR based on baPWV quartiles in patients grouped by FMD quartiles. (C). The risk of CIMT ≥.9 mm based on baPWV quartiles in patients grouped by FMD quartiles. STOD, subclinical target organ damage; baPWV, brachial‐ankle pulse wave velocity; FMD, flow‐mediated dilation; LVH, left ventricular hypertrophy; UACR, urine albumin–creatinine ratio; CIMT, carotid intima‐media thickness
FIGURE 3
FIGURE 3
Receiver‐operating characteristics (ROC) curves for prediction of STOD with baPWV, FMD, and combined with baPWV and FMD. (A) ROC curve for prediction of LVH with baPWV, FMD, and combined with baPWV and FMD, respectively. (B) ROC curve for prediction of eUACR with baPWV, FMD, and combined with baPWV and FMD, respectively. (C) ROC curve for prediction of CIMT ≥.9 mm with baPWV, FMD, and combined with baPWV and FMD, respectively. STOD, subclinical target organ damage; baPWV, brachial‐ankle pulse wave velocity; FMD, flow‐mediated dilation; LVH, left ventricular hypertrophy; UACR, urine albumin–creatinine ratio; CIMT, carotid intima‐media thickness

References

    1. Fuchs FD, Whelton PK. High blood pressure and cardiovascular disease. Hypertension. 2020;75(2):285–292.
    1. Pontremoli R, Leoncini G, Viazzi F, et al. Evaluation of subclinical organ damage for risk assessment and treatment in the hypertensive patient: role of microalbuminuria. J Am Soc Nephrol. 2006;17(4 Suppl 2):S112–114.
    1. Agabiti‐Rosei E, Muiesan ML, Salvetti M. Evaluation of subclinical target organ damage for risk assessment and treatment in the hypertensive patients: left ventricular hypertrophy. J Am Soc Nephrol. 2006;17(4 Suppl 2):S104–108.
    1. Fantin F, Mattocks A, Bulpitt CJ, Banya W, Rajkumar C. Is augmentation index a good measure of vascular stiffness in the elderly? Age Ageing. 2007;36(1):43–48.
    1. Suwaidi JA, Hamasaki S, Higano ST, Nishimura RA, Holmes DR, Jr. , Lerman A. Long‐term follow‐up of patients with mild coronary artery disease and endothelial dysfunction. Circulation. 2000;101(9):948–954.
    1. Shirai K, Saiki A, Nagayama D, Tatsuno I, Shimizu K, Takahashi M. The role of monitoring arterial stiffness with cardio‐ankle vascular index in the control of lifestyle‐related diseases. Pulse (Basel). 2015;3(2):118–133.
    1. Yildiz O. Vascular smooth muscle and endothelial functions in aging. Ann N Y Acad Sci. 2007;1100:353–360.
    1. Laurent S, Boutouyrie P. The structural factor of hypertension: large and small artery alterations. Circ Res. 2015;116(6):1007–1021.
    1. Aggarwal M, Khan IA. Hypertensive crisis: hypertensive emergencies and urgencies. Cardiol Clin. 2006;24(1):135–146.
    1. Tomiyama H, Ishizu T, Kohro T, et al. Longitudinal association among endothelial function, arterial stiffness and subclinical organ damage in hypertension. Int J Cardiol. 2018;253:161–166.
    1. Tomiyama H, Yamashina A. Non‐invasive vascular function tests: their pathophysiological background and clinical application. Circ J. 2010;74(1):24–33.
    1. Higashi Y, Noma K, Yoshizumi M, Kihara Y. Endothelial function and oxidative stress in cardiovascular diseases. Circ J. 2009;73(3):411–418.
    1. Benjamin EJ, Larson MG, Keyes MJ, et al. Clinical correlates and heritability of flow‐mediated dilation in the community: the Framingham Heart Study. Circulation. 2004;109(5):613–619.
    1. Takase H, Dohi Y, Toriyama T, et al. Brachial‐ankle pulse wave velocity predicts increase in blood pressure and onset of hypertension. Am J Hypertens. 2011;24(6):667–673.
    1. Hall JE. Guyton and Hall textbook of medical physiology, 13th ed. Guyton and Hall textbook of medical physiology, 13th ed.
    1. Tanaka A, Tomiyama H, Maruhashi T, et al. Physiological diagnostic criteria for vascular failure. Hypertension. 2018;72(5):1060–1071.
    1. Neves MF, Kasal DA, Cunha AR, Medeiros F. Vascular dysfunction as target organ damage in animal models of hypertension. Int J Hypertens. 2012;2012:187526.
    1. Williams B, Mancia G, Spiering W, et al. 2018 ESC/ESH guidelines for the management of arterial hypertension. Eur Heart J. 2018;39(33):3021–3104.
    1. Li R, Chen Y, Moore JH. Integration of genetic and clinical information to improve imputation of data missing from electronic health records. J Am Med Inform Assoc. 2019;26(10):1056–1063.
    1. Bild DE, Bluemke DA, Burke GL, et al. Multi‐ethnic study of atherosclerosis: objectives and design. Am J Epidemiol. 2002;156(9):871–881.
    1. Ford ES, Giles WH, Mokdad AH. The distribution of 10‐year risk for coronary heart disease among US adults: findings from the National Health and Nutrition Examination Survey III. J Am Coll Cardiol. 2004;43(10):1791–1796.
    1. Levey AS, Stevens LA, Schmid CH, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604–612.
    1. Devereux RB, Dahlof B, Gerdts E, et al. Regression of hypertensive left ventricular hypertrophy by losartan compared with atenolol: the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) trial. Circulation. 2004;110(11):1456–1462.
    1. O'Leary DH, Bots ML. Imaging of atherosclerosis: carotid intima‐media thickness. Eur Heart J. 2010;31(14):1682–1689.
    1. Lee JY, Ryu S, Lee SH, et al. Association between brachial‐ankle pulse wave velocity and progression of coronary artery calcium: a prospective cohort study. Cardiovasc Diabetol. 2015;14:147.
    1. Santulli G, Pascale V, Finelli R, et al. We are what we eat: impact of food from short supply chain on metabolic syndrome. J Clin Med. 2019;8(12).
    1. Mitchell GF, Hwang SJ, Vasan RS, et al. Arterial stiffness and cardiovascular events: the Framingham Heart Study. Circulation. 2010;121(4):505–511.
    1. Vlachopoulos C, Aznaouridis K, Stefanadis C. Prediction of cardiovascular events and all‐cause mortality with arterial stiffness: a systematic review and meta‐analysis. J Am Coll Cardiol. 2010;55(13):1318–1327.
    1. Laurent S, Boutouyrie P, Asmar R, et al. Aortic stiffness is an independent predictor of all‐cause and cardiovascular mortality in hypertensive patients. Hypertension. 2001;37(5):1236–1241.
    1. Tomiyama H, Matsumoto C, Shiina K, Yamashina A. Brachial‐ankle PWV: current status and future directions as a useful marker in the management of cardiovascular disease and/or cardiovascular risk factors. J Atheroscler Thromb. 2016;23(2):128–146.
    1. Tomiyama H, Shiina K. State of the art review: brachial‐ankle PWV. J Atheroscler Thromb. 2020;27(7):621–636.
    1. Flammer AJ, Anderson T, Celermajer DS, et al. The assessment of endothelial function: from research into clinical practice. Circulation. 2012;126(6):753–767.
    1. Asselbergs FW, de Boer RA, Diercks GF, et al. Vascular endothelial growth factor: the link between cardiovascular risk factors and microalbuminuria? Int J Cardiol. 2004;93(2‐3):211–215.
    1. Haffner SM, Stern MP, Gruber MK, Hazuda HP, Mitchell BD, Patterson JK. Microalbuminuria. Potential marker for increased cardiovascular risk factors in nondiabetic subjects? Arteriosclerosis. 1990;10(5):727–731.
    1. Yoshida M, Tomiyama H, Yamada J, et al. Relationships among renal function loss within the normal to mildly impaired range, arterial stiffness, inflammation, and oxidative stress. Clin J Am Soc Nephrol. 2007;2(6):1118–1124.
    1. Lioufas NM, Pedagogos E, Hawley CM, et al. Aortic calcification and arterial stiffness burden in a chronic kidney disease cohort with high cardiovascular risk: baseline characteristics of the impact of phosphate reduction on vascular end‐points in chronic kidney disease trial. Am J Nephrol. 2020;51(3):201–215.
    1. Deedwania PC. Mechanisms of endothelial dysfunction in the metabolic syndrome. Curr Diab Rep. 2003;3(4):289–292.
    1. Tomiyama H, Hirayama Y, Hashimoto H, et al. The effects of changes in the metabolic syndrome detection status on arterial stiffening: a prospective study. Hypertens Res. 2006;29(9):673–678.
    1. Sengstock DM, Vaitkevicius PV, Supiano MA. Arterial stiffness is related to insulin resistance in nondiabetic hypertensive older adults. J Clin Endocrinol Metab. 2005;90(5):2823–2827.
    1. Rutter MK, Meigs JB, Sullivan LM, D'Agostino RB, Sr. , Wilson PW. C‐reactive protein, the metabolic syndrome, and prediction of cardiovascular events in the Framingham Offspring Study. Circulation. 2004;110(4):380–385.
    1. Suh JH, Miner JH. The glomerular basement membrane as a barrier to albumin. Nat Rev Nephrol. 2013;9(8):470–477.
    1. Avolio AP, Kuznetsova T, Heyndrickx GR, Kerkhof PLM, Li JK. Arterial flow, pulse pressure and pulse wave velocity in men and women at various ages. Adv Exp Med Biol. 2018;1065:153–168.
    1. Taddei S, Virdis A, Mattei P, et al. Aging and endothelial function in normotensive subjects and patients with essential hypertension. Circulation. 1995;91(7):1981–1987.
    1. Bruno RM, Duranti E, Ippolito C, et al. Different impact of essential hypertension on structural and functional age‐related vascular changes. Hypertension. 2017;69(1):71–78.
    1. AlGhatrif M, Wang M, Fedorova OV, Bagrov AY, Lakatta EG. The pressure of aging. Med Clin North Am. 2017;101(1):81–101.

Source: PubMed

Sponsorer og samarbejdspartnere

Medicinske tilstande

Narkotikainterventioner

3
Abonner