Relationship of medial arterial calcinosis to autonomic neuropathy and adverse outcomes in a diabetic veteran population

被引:25
作者
Mayfield, JA
Caps, MT
Boyko, EJ
Ahroni, JH
Smith, DG
机构
[1] Univ Washington, Seattle ERIC VA Puget Sound, Seattle, WA 98108 USA
[2] Vet Affairs Puget Sound Hlth Care Syst, Res & Dev Serv, Seattle, WA USA
[3] Univ Washington, Dept Vasc Surg, Seattle, WA 98195 USA
[4] Vet Affairs Puget Sound Hlth Care Syst, Surg Serv, Seattle, WA USA
[5] Univ Washington, Dept Med, Seattle, WA 98195 USA
[6] Univ Washington, Sch Nursing, Dept Biobehav Nursing & Hlth Syst, Seattle, WA 98195 USA
[7] Univ Washington, Dept Orthoped Surg, Seattle, WA 98195 USA
关键词
autonomic neuropathy; medial arterial calcinosis; ulceration; amputation; mortality;
D O I
10.1016/S1056-8727(01)00178-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Statement of the problem: Medial arterial calcinosis (MAC) is associated with neuropathy, amputation, and mortality through an unknown mechanism. We hypothesized that MAC was a marker of autonomic neuropathy rather than a risk factor and that the outcomes were due to autonomic neuropathy. Methods: All subjects in an ongoing prospective study of diabetic foot conditions in a diabetic veteran cohort who received a foot radiograph between 11/7/90 and 11/5/93 were included. Autonomic neuropathy measured as either heart rate variability with timed respiration or postural hypotension. A logistic model predicted the presence of MAC at baseline and Cox proportional models assessed the relative contribution of autonomic neuropathy and traditional risk factors for the outcomes of ulceration, amputation, and death. Results: MAC was identified in 181 subjects, no MAC in 253 subjects, and 39 were excluded due to disagreement between observers. Both measures of autonomic neuropathy were independent predictors of MAC at baseline, even after adjustment for vibration sensation loss in a logistic model. MAC was associated with an increased risk for ulceration (hazards ratio. HR: 2.1, 95% confidence intervals, CI, 1.4-3.1), amputation (HR 3.3, 95% CI 1.5-7.4), and mortality (HR 1.6, 95% CI 1.1-2.2). The addition of either autonomic measure of neuropathy did not change the MAC HR or significantly improved the fit of the model. Conclusions: Our hypothesis that the excess mortality, amputation, and ulceration in persons with MAC could be explained by autonomic neuropathy measured as postural hypotension or heart rate variability with measured respiration was not supported. (C) 2002 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:165 / 171
页数:7
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