Vascular calcification is associated with impaired microcirculatory function in chronic haemodialysis patients
Although vascular calcification (VC) in dialysis patients is associated with increased cardiovascular events, the pathophysiology is still largely obscure. Microcirculatory dysfunction may contribute to demand myocardial ischaemia. We have studied cutaneous microcirculatory function in haemodialysis...
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Published in | Nephron. Clinical practice Vol. 108; no. 2; p. c121 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Switzerland
01.01.2008
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Subjects | |
Online Access | Get more information |
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Summary: | Although vascular calcification (VC) in dialysis patients is associated with increased cardiovascular events, the pathophysiology is still largely obscure. Microcirculatory dysfunction may contribute to demand myocardial ischaemia. We have studied cutaneous microcirculatory function in haemodialysis (HD) patients with and without large-vessel VC. 37 non-diabetic subjects (20 HD and 17 healthy controls) were studied. VC was assessed using CT scanning of a standardised segment of superficial femoral artery (11 VC+, 9 VC-). Laser Doppler imaging was undertaken using a Periscan PIM II(R) at rest and under vasodilator challenge. Baseline perfusion was not statistically different in VC+ patients than VC- patients or controls (1.03 +/- 0.2, 1.08 +/- 0.2, 0.93 +/- 0.3 PU respectively). Overall, the maximum vasodilatory response to both ACh (p < 0.001) and SNP (p = 0.004) was lower in the HD than the control group. In addition, the HD patients took longer to reach a maximum vasodilatation than the controls (p = 0.008 for ACh, n.s. for SNP). Further, the maximum vasodilatory response in the VC+ patients was lower and patients took longer to reach maximum vasodilatation than the VC- group. We have demonstrated, for the first time, impaired and dysregulated microcirculatory function in patients with VC. This may be important in understanding the pathophysiology of the complications and cardiovascular consequences of VC. |
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ISSN: | 1660-2110 |
DOI: | 10.1159/000114202 |