A high ankle brachial index is associated with greater left ventricular mass MESA (Multi-Ethnic Study of Atherosclerosis).

Abstract:

OBJECTIVES:This study sought to determine the association of high ankle brachial index (ABI) measurements with left ventricular (LV) mass, and to compare its strength with that of low ABI with LV mass. BACKGROUND:Arterial stiffness leads to LV mass through nonatherosclerotic pathways in mice. In humans, a high ABI indicates stiff peripheral arteries and is associated with cardiovascular disease (CVD) events. Whether high ABI is associated with LV mass in humans and whether this might reflect consequences of arterial stiffness, atherosclerosis, or both is unknown. METHODS:Among 4,972 MESA (Multi-Ethnic Study of Atherosclerosis) participants without clinical CVD, we used linear regression to evaluate the association of low (<0.90) and high (>1.40 or incompressible) ABI with LV mass by cardiac magnetic resonance imaging (MRI). Intermediate ABIs served as the reference category. To determine the effect of subclinical atherosclerosis, models were adjusted for common and internal carotid intima media thickness (cIMT) and natural log-transformed coronary artery calcification. RESULTS:Compared with subjects with intermediate ABI, LV mass was higher with either low (2.70 g/m(2) higher, 95% confidence interval: 0.65 to 4.75) or high ABI (6.84 g/m(2) higher, 95% confidence interval: 3.2 to 10.47) after adjustment for traditional CVD risk factors, kidney function, and C-reactive protein. However, further adjustment for cIMT and CAC substantially attenuated the association of low ABI with LV mass index (1.24 g/m(2) higher, 95% confidence interval: -0.84 to 3.33), whereas the association of high ABI was minimally altered (6.01 g/m(2) higher, 95% confidence interval: 2.36 to 9.67). CONCLUSIONS:High ABI is associated with greater LV mass; an association that is not attenuated with adjustment for subclinical atherosclerosis in nonperipheral arterial beds. High ABI might lead to greater LV mass through nonatherosclerotic pathways.

journal_name

J Am Coll Cardiol

authors

Ix JH,Katz R,Peralta CA,de Boer IH,Allison MA,Bluemke DA,Siscovick DS,Lima JA,Criqui MH

doi

10.1016/j.jacc.2009.11.010

subject

Has Abstract

pub_date

2010-01-26 00:00:00

pages

342-9

issue

4

eissn

0735-1097

issn

1558-3597

pii

S0735-1097(09)03616-X

journal_volume

55

pub_type

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