Journal
NEPHROLOGY DIALYSIS TRANSPLANTATION
Volume 20, Issue 6, Pages 1140-1147Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ndt/gfh808
Keywords
arterial stiffness; autonomic neuropathy; baroreflex sensitivity; haemodialysis; vascular calcification
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Introduction. Vascular calcification is a critical determinant of cardiovascular morbidity and mortality in chronic haemodialysis (HD) patients. The pathophysiology underlying this observation remains obscure. Baroreceptor sensitivity (BRS) is important in the maintenance of an appropriate cardiovascular status both at rest and under the physiological stress of HD. BRS is determined by both the mechanical properties of the vascular wall, mediating the transfer of transmural pressure, and afferent and efferent autonomic function. We aimed to study the association between arterial structure, function and BRS in chronic HD patients. Methods. We studied 40 chronic HD patients mean age 62 +/- 2 (26-86) years who had received HD for a mean 40 +/- 4 (9-101) months. Spontaneous BRS was assessed using software studying the relationship between inter-beat variability and beat to beat changes in systolic blood pressure. Functional characteristics of conduit arteries (pulse wave analysis) were studied with applanation tonometry at the radial artery. Arterial calcification was assessed in lower limbs using reconstructed multi-slice computed tomography and quantified with volume-corrected calcification scores within the superficial femoral artery. Results. Mean BRS was 4.43 +/- 0.44 ms/mmHg, with a wide range from 1.0 to 11.5 ms/mmHg. This correlated with arterial stiffness as measured by time to shoulder calculated from the central pulse wave analysis (r = 0.4, P=0.01). BRS was also associated with vascular calcification (P=0.01) but not by other factors such as dialysis vintage, age or pre-dialysis systolic/diastolic blood pressure. Conclusion. The reduction in BRS and the resulting aberrant blood pressure response to the physiological stress and volume changes of HD may be important in the further understanding of the pathophysiology of the increased mortality in HD patients with vascular calcification.
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