Lipid profile components and subclinical cerebrovascular disease in the northern manhattan study

Joshua Z. Willey, Hannah Gardener, Yeseon P. Moon, Mitsuhiro Yoshita, Charles DeCarli, Ying Kuen Cheung, Ralph L Sacco, Mitchell S V Elkind, Clinton B Wright

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Background: Subclinical cerebrovascular disease has been associated with multiple adverse events related to aging, including stroke and dementia. The modifiable risk factors for subclinical cerebrovascular disease beyond hypertension have not been well characterized. Our objective was to examine the association between baseline, and changes over time, in lipid profile components and subclinical cerebrovascular disease on magnetic resonance imaging (MRI). Methods: Fasting plasma lipids were collected on participants in the Northern Manhattan Study, a prospective cohort study examining risk factors for cardiovascular disease in a multiethnic elderly urban-dwelling population. A subsample of the cohort underwent brain MRI between 2003 and 2008 (a median of 6.2 years, range = 0-14, after enrollment), when repeat fasting lipids were obtained. We used lipid profile components at the time of initial enrollment (n = 1,256 with lipids available) as categorical variables, as well as change in clinical categories over the two measures (n = 1,029). The main outcome measures were (1) total white matter hyperintensity volume (WMHV) using linear regression and (2) silent brain infarcts (SBI) using logistic regression. Results: None of the plasma lipid profile components at the time of enrollment were associated with WMHV. The association between baseline lipids and WMHV was, however, modified by apolipoprotein E (apoE) status (X2 with 2 degrees of freedom, p = 0.03), such that among apoE4 carriers those with total cholesterol (TC) ≥200 mg/dl had a trend towards smaller WMHV than those with TC <200 mg/dl (difference in log WMHV -0.19, p = 0.07), while there was no difference among apoE3 carriers. When examining the association between WMHV and change in lipid profile components we noted an association with change in high-density lipoprotein cholesterol (HDL-C, >50 mg/dl for women, >40 mg/dl for men) and TC. A transition from low-risk HDL-C (>50 mg/dl for women, >40 mg/dl for men) at baseline to high-risk HDL-C at the time of MRI (vs. starting and remaining low risk) was associated with greater WMHV (difference in logWMHV 0.34, p value 0.03). We noted a similar association with transitioning to a TC ≥200 mg/dl at the time of MRI (difference in logWMHV 0.25, p value 0.006). There were no associations with baseline or change in lipid profile components with SBI. Conclusions: The association of plasma lipid profile components with greater WMHV may depend on apoE genotype and worsening HDL and TC risk levels over time.

Original languageEnglish
Pages (from-to)423-430
Number of pages8
JournalCerebrovascular Diseases
Volume37
Issue number6
DOIs
StatePublished - Jan 1 2014

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Cerebrovascular Disorders
Lipids
Cholesterol
Magnetic Resonance Imaging
Apolipoproteins E
Fasting
Brain
Apolipoprotein E4
Urban Population
HDL Cholesterol
Dementia
White Matter
Linear Models
Cohort Studies
Cardiovascular Diseases
Logistic Models
Stroke
Genotype
Outcome Assessment (Health Care)
Prospective Studies

Keywords

  • Plasma lipids
  • Risk Factors
  • Silent Infarct
  • White Matter

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology
  • Cardiology and Cardiovascular Medicine

Cite this

Willey, J. Z., Gardener, H., Moon, Y. P., Yoshita, M., DeCarli, C., Cheung, Y. K., ... Wright, C. B. (2014). Lipid profile components and subclinical cerebrovascular disease in the northern manhattan study. Cerebrovascular Diseases, 37(6), 423-430. https://doi.org/10.1159/000362920

Lipid profile components and subclinical cerebrovascular disease in the northern manhattan study. / Willey, Joshua Z.; Gardener, Hannah; Moon, Yeseon P.; Yoshita, Mitsuhiro; DeCarli, Charles; Cheung, Ying Kuen; Sacco, Ralph L; Elkind, Mitchell S V; Wright, Clinton B.

In: Cerebrovascular Diseases, Vol. 37, No. 6, 01.01.2014, p. 423-430.

Research output: Contribution to journalArticle

Willey, JZ, Gardener, H, Moon, YP, Yoshita, M, DeCarli, C, Cheung, YK, Sacco, RL, Elkind, MSV & Wright, CB 2014, 'Lipid profile components and subclinical cerebrovascular disease in the northern manhattan study', Cerebrovascular Diseases, vol. 37, no. 6, pp. 423-430. https://doi.org/10.1159/000362920
Willey, Joshua Z. ; Gardener, Hannah ; Moon, Yeseon P. ; Yoshita, Mitsuhiro ; DeCarli, Charles ; Cheung, Ying Kuen ; Sacco, Ralph L ; Elkind, Mitchell S V ; Wright, Clinton B. / Lipid profile components and subclinical cerebrovascular disease in the northern manhattan study. In: Cerebrovascular Diseases. 2014 ; Vol. 37, No. 6. pp. 423-430.
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AU - DeCarli, Charles

AU - Cheung, Ying Kuen

AU - Sacco, Ralph L

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N2 - Background: Subclinical cerebrovascular disease has been associated with multiple adverse events related to aging, including stroke and dementia. The modifiable risk factors for subclinical cerebrovascular disease beyond hypertension have not been well characterized. Our objective was to examine the association between baseline, and changes over time, in lipid profile components and subclinical cerebrovascular disease on magnetic resonance imaging (MRI). Methods: Fasting plasma lipids were collected on participants in the Northern Manhattan Study, a prospective cohort study examining risk factors for cardiovascular disease in a multiethnic elderly urban-dwelling population. A subsample of the cohort underwent brain MRI between 2003 and 2008 (a median of 6.2 years, range = 0-14, after enrollment), when repeat fasting lipids were obtained. We used lipid profile components at the time of initial enrollment (n = 1,256 with lipids available) as categorical variables, as well as change in clinical categories over the two measures (n = 1,029). The main outcome measures were (1) total white matter hyperintensity volume (WMHV) using linear regression and (2) silent brain infarcts (SBI) using logistic regression. Results: None of the plasma lipid profile components at the time of enrollment were associated with WMHV. The association between baseline lipids and WMHV was, however, modified by apolipoprotein E (apoE) status (X2 with 2 degrees of freedom, p = 0.03), such that among apoE4 carriers those with total cholesterol (TC) ≥200 mg/dl had a trend towards smaller WMHV than those with TC <200 mg/dl (difference in log WMHV -0.19, p = 0.07), while there was no difference among apoE3 carriers. When examining the association between WMHV and change in lipid profile components we noted an association with change in high-density lipoprotein cholesterol (HDL-C, >50 mg/dl for women, >40 mg/dl for men) and TC. A transition from low-risk HDL-C (>50 mg/dl for women, >40 mg/dl for men) at baseline to high-risk HDL-C at the time of MRI (vs. starting and remaining low risk) was associated with greater WMHV (difference in logWMHV 0.34, p value 0.03). We noted a similar association with transitioning to a TC ≥200 mg/dl at the time of MRI (difference in logWMHV 0.25, p value 0.006). There were no associations with baseline or change in lipid profile components with SBI. Conclusions: The association of plasma lipid profile components with greater WMHV may depend on apoE genotype and worsening HDL and TC risk levels over time.

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