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Review
. 2019 Jun;30(6):918-928.
doi: 10.1681/ASN.2019020117. Epub 2019 Apr 30.

Arterial Stiffness in the Heart Disease of CKD

Luca Zanoli  1 , Paolo Lentini  2 , Marie Briet  3 , Pietro Castellino  4 , Andrew A House  5 , Gerard M London  6 , Lorenzo Malatino  4 , Peter A McCullough  7 , Dimitri P Mikhailidis  8 , Pierre Boutouyrie  6   9   10
Affiliations
Review

Arterial Stiffness in the Heart Disease of CKD

Luca Zanoli et al. J Am Soc Nephrol. 2019 Jun.

Abstract

CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (i.e., uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.

Keywords: arteries, cardiovascular disease, chronic kidney disease, Chronic inflammation, arteriosclerosis, pulse wave velocity.

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Figures

Figure 1.
Figure 1.
The vascular pathway in CKD. AGEs, advanced glycation end-products; BRS, baroreflex sensitivity; DBP, diastolic BP; LV, left ventricular; MMPs, matrix metalloproteinases; PP, pulse pressure; SBP, systolic BP; SMC, smooth muscle cell; TIMP, tissue inhibitor of matrix metalloproteinases. Modified from reference , with permission.
Figure 2.
Figure 2.
Carotid lesions in patients with CKD. CWS, circumferential wall stress; Einc, Young elastic modulus; IMT, intima-media thickness. Modified from reference , with permission.
Figure 3.
Figure 3.
Arterial stiffness and pulse-wave propagation. DBP, diastolic BP; SBP, systolic BP. Modified from reference , with permission.
See this image and copyright information in PMC

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