Elsevier

Atherosclerosis

Volume 241, Issue 1, July 2015, Pages 36-41
Atherosclerosis

Subclinical atherosclerosis and subsequent cognitive function

https://doi.org/10.1016/j.atherosclerosis.2015.04.813Get rights and content

Highlights

  • We examined the relationship between subclinical atherosclerosis and later cognition.

  • Differences based on demographic factors and APOE4 status were examined.

  • Cognitive scores trended lower with higher positive atherosclerotic indicators.

  • Atherosclerosis was modestly associated with later cognitive status in middle-age.

Abstract

Objective

To examine the relationship between measures of subclinical atherosclerosis and subsequent cognitive function.

Method

Participants from the Dallas Heart Study (DHS), a population-based multiethnic study of cardiovascular disease pathogenesis, were re-examined 8 years later (DHS-2) with the Montreal Cognitive Assessment (MoCA); N = 1904, mean age = 42.9, range 8–65. Associations of baseline measures of subclinical atherosclerosis (coronary artery calcium, abdominal aortic plaque, and abdominal aortic wall thickness) with MoCA scores measured at follow-up were examined in the group as a whole and in relation to age and ApoE4 status.

Results

A significant linear trend of successively lower MoCA scores with increasing numbers of atherosclerotic indicators was observed (F(3, 1150) = 5.918, p = .001). CAC was weakly correlated with MoCA scores (p = .047) and MoCA scores were significantly different between participants with and without CAC (M = 22.35 vs 23.69, p = 0.038). With the exception of a small association between abdominal AWT and MoCA in subjects over age 50, abdominal AWT and abdominal aortic plaque did not correlate with MoCA total score (p ≥ .052). Cognitive scores and atherosclerosis measures were not impacted by ApoE4 status (p ≥ .455).

Conclusion

In this ethnically diverse population-based sample, subclinical atherosclerosis was minimally associated with later cognitive function in middle-aged adults.

Introduction

A relationship between vascular risk factors and the onset and progression of cognitive dysfunction is well established, in large part by the well-known Framingham Study [1] and others [2], [3], [4], [5]. The most common cause of vascular disease is atherosclerosis [6] and atherosclerotic risk has been traditionally assessed based on the sum of predisposing factors such as hypertension [7], diabetes [8], and increased abdominal fat [9]; however, computerized tomography (CT) and magnetic resonance imaging (MRI) provide direct measurement of atherosclerosis. Carotid atherosclerosis has been associated with the onset, severity, and progression of cognitive dysfunction [10], [11], [12], [13]; however, atherosclerosis begins in the abdominal aorta and only later involves the carotid arteries [14]. Therefore, other direct measures may provide a better index of subclinical atherosclerosis [15], such as coronary artery calcium (CAC) [16], abdominal aortic plaque [17], and abdominal aortic wall thickness (AWT) [18], which have been shown to independently predict future adverse cardiovascular events [19].

The extent to which subclinical atherosclerosis is related to cognition is not fully understood, particularly whether these processes exert a detectable effect on cognition in the absence of stroke or prior to the onset of dementing illnesses. The relationship between objective evidence of atherosclerosis and cognition has been studied in convenience samples and studies of the elderly, but has not been widely examined in a population-based sample of adults with a wide age range. Research on subclinical atherosclerosis has recently increased due to advances in imaging, and the majority of this work has utilized carotid measures of atherosclerosis [20], [21]. This is the first study to date to simultaneously examine three direct measures of atherosclerosis (CAC, abdominal aortic plaque, abdominal AWT) in relationship to global cognitive function in a large, ethnically diverse community-based sample. Using a large community-based sample, it was hypothesized that higher levels of atherosclerosis as measured by CAC, abdominal aortic plaque, and abdominal AWT would be moderately related to lower cognitive performance at a later point in life and that an increasing number of positive atherosclerotic indicators would have an incremental negative effect on MoCA scores.

Section snippets

Participants

This investigation was conducted as part of the Dallas Heart Study (DHS), a longitudinal, population-based, multi-ethnic cohort study of factors contributing to cardiovascular disease [22]. All participants provided written informed consent and the study protocol was approved by the Institutional Review Board at the University of Texas Southwestern Medical Center. The first phase of DHS (DHS-1) was initiated in 1999, and participants were drawn from those who returned for follow-up in DHS-2

Sample characteristics

Descriptive information is presented in Table 1. The mean MoCA score for the entire sample was 23.36 (4.03) points. Education was associated with MoCA performance (r = .43, p < .001), as was age (r = −.20, p ≤ .001). After controlling for education and age, there was no difference in MoCA scores by sex (M, SD male: 23.29, 3.95 and female: 23.42, 4.08).

Relationship to cognition

A partial Spearman's correlation controlling for age and education showed a weak but statistically significant correlation between MoCA Total

Discussion

Much of the evidence for an association between cognitive function and atherosclerosis comes from studies of select populations, such as the elderly and those with advanced atherosclerosis, and the majority of this work has utilized carotid measures [13], [36], [37], [38]. This is the first study to simultaneously examine three direct measures of atherosclerosis (coronary artery calcium, abdominal aortic wall thickness, and aortic plaque) in relation to global cognitive function in a

Conflict of interest

None.

Acknowledgment

This work was conducted in part with support from the Wallace, Barbara and Kelly King Charitable Foundation and the National Center for Advancing Translational Sciences of the National Institutes of Health under award Number UL1TR001105. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

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