Fibroblast growth factor 23 is associated with carotid plaque presence and area: The Northern Manhattan study

Nirav H. Shah, Chuanhui Dong, Mitchell S V Elkind, Ralph L Sacco, Armando J Mendez, Barry Hudson, Shonni Silverberg, Myles Wolf, Tatjana Rundek, Clinton B Wright

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Objective - Elevated fibroblast growth factor 23 (FGF23), a hormone that regulates phosphate homeostasis, has been associated with mortality, cardiovascular events, and stroke, and to arterial calcification in chronic kidney disease, but its role in atherosclerosis is unclear and population-based studies are lacking. We hypothesized that elevated FGF23 would associate with carotid plaque presence, area, and echogenicity in the race/ethnically diverse community-based Northern Manhattan Study (NOMAS) sample. Approach and Results - There were 1512 stroke-free NOMAS participants with FGF23 and 2-dimensional carotid ultrasound data (mean age, 68±9 years; 61% women; 62% Hispanic, 18% black, and 18% white). We used multivariable linear and logistic regression to evaluate FGF23, continuously and by quintiles, as a correlate of carotid plaque, plaque area (cubic root transformed), and echogenicity adjusting for sociodemographic and vascular risk factors. Participants with FGF23 levels in the top quintile were more likely to have carotid plaque (odds ratio, 1.49; 95% confidence interval, 1.02-2.19; P=0.04) and larger plaque area (β=0.32 mm<sup>2</sup>, 95% confidence interval, 0.10-0.53 mm<sup>2</sup>; P=0.004) than those in the lowest quintile, adjusting for estimated glomerular filtration rate, demographics, and vascular risk factors. Linear regression models also showed that log transformed FGF23 (LnFGF23) associated with greater odds of plaque presence (odds ratio, 1.26 per LnFGF23; 95% confidence interval, 1.01-1.58; P=0.04), and plaque area (β=0.19 mm<sup>2</sup> per LnFGF23; 95% confidence interval, 0.07-0.31 mm<sup>2</sup>; P=0.002). Conclusions - Higher FGF23 associated with greater likelihood and burden of carotid atherosclerosis independent of CKD. Atherosclerosis may be a mechanism through which FGF23 increases cardiovascular events and stroke.

Original languageEnglish (US)
Pages (from-to)2048-2053
Number of pages6
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume35
Issue number9
DOIs
StatePublished - Sep 28 2015

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Confidence Intervals
Linear Models
Atherosclerosis
Odds Ratio
Myocardial Infarction
Carotid Artery Diseases
fibroblast growth factor 23
Fibroblast Growth Factor 2
Glomerular Filtration Rate
Chronic Renal Insufficiency
Hispanic Americans
Homeostasis
Logistic Models
Stroke
Phosphates
Demography
Hormones
Mortality
Population
vascular factor

Keywords

  • atherosclerosis
  • epidemiology
  • fibroblast growth factors
  • glomerular filtration rate
  • risk factors

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Fibroblast growth factor 23 is associated with carotid plaque presence and area : The Northern Manhattan study. / Shah, Nirav H.; Dong, Chuanhui; Elkind, Mitchell S V; Sacco, Ralph L; Mendez, Armando J; Hudson, Barry; Silverberg, Shonni; Wolf, Myles; Rundek, Tatjana; Wright, Clinton B.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 35, No. 9, 28.09.2015, p. 2048-2053.

Research output: Contribution to journalArticle

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abstract = "Objective - Elevated fibroblast growth factor 23 (FGF23), a hormone that regulates phosphate homeostasis, has been associated with mortality, cardiovascular events, and stroke, and to arterial calcification in chronic kidney disease, but its role in atherosclerosis is unclear and population-based studies are lacking. We hypothesized that elevated FGF23 would associate with carotid plaque presence, area, and echogenicity in the race/ethnically diverse community-based Northern Manhattan Study (NOMAS) sample. Approach and Results - There were 1512 stroke-free NOMAS participants with FGF23 and 2-dimensional carotid ultrasound data (mean age, 68±9 years; 61{\%} women; 62{\%} Hispanic, 18{\%} black, and 18{\%} white). We used multivariable linear and logistic regression to evaluate FGF23, continuously and by quintiles, as a correlate of carotid plaque, plaque area (cubic root transformed), and echogenicity adjusting for sociodemographic and vascular risk factors. Participants with FGF23 levels in the top quintile were more likely to have carotid plaque (odds ratio, 1.49; 95{\%} confidence interval, 1.02-2.19; P=0.04) and larger plaque area (β=0.32 mm2, 95{\%} confidence interval, 0.10-0.53 mm2; P=0.004) than those in the lowest quintile, adjusting for estimated glomerular filtration rate, demographics, and vascular risk factors. Linear regression models also showed that log transformed FGF23 (LnFGF23) associated with greater odds of plaque presence (odds ratio, 1.26 per LnFGF23; 95{\%} confidence interval, 1.01-1.58; P=0.04), and plaque area (β=0.19 mm2 per LnFGF23; 95{\%} confidence interval, 0.07-0.31 mm2; P=0.002). Conclusions - Higher FGF23 associated with greater likelihood and burden of carotid atherosclerosis independent of CKD. Atherosclerosis may be a mechanism through which FGF23 increases cardiovascular events and stroke.",
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author = "Shah, {Nirav H.} and Chuanhui Dong and Elkind, {Mitchell S V} and Sacco, {Ralph L} and Mendez, {Armando J} and Barry Hudson and Shonni Silverberg and Myles Wolf and Tatjana Rundek and Wright, {Clinton B}",
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T1 - Fibroblast growth factor 23 is associated with carotid plaque presence and area

T2 - The Northern Manhattan study

AU - Shah, Nirav H.

AU - Dong, Chuanhui

AU - Elkind, Mitchell S V

AU - Sacco, Ralph L

AU - Mendez, Armando J

AU - Hudson, Barry

AU - Silverberg, Shonni

AU - Wolf, Myles

AU - Rundek, Tatjana

AU - Wright, Clinton B

PY - 2015/9/28

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N2 - Objective - Elevated fibroblast growth factor 23 (FGF23), a hormone that regulates phosphate homeostasis, has been associated with mortality, cardiovascular events, and stroke, and to arterial calcification in chronic kidney disease, but its role in atherosclerosis is unclear and population-based studies are lacking. We hypothesized that elevated FGF23 would associate with carotid plaque presence, area, and echogenicity in the race/ethnically diverse community-based Northern Manhattan Study (NOMAS) sample. Approach and Results - There were 1512 stroke-free NOMAS participants with FGF23 and 2-dimensional carotid ultrasound data (mean age, 68±9 years; 61% women; 62% Hispanic, 18% black, and 18% white). We used multivariable linear and logistic regression to evaluate FGF23, continuously and by quintiles, as a correlate of carotid plaque, plaque area (cubic root transformed), and echogenicity adjusting for sociodemographic and vascular risk factors. Participants with FGF23 levels in the top quintile were more likely to have carotid plaque (odds ratio, 1.49; 95% confidence interval, 1.02-2.19; P=0.04) and larger plaque area (β=0.32 mm2, 95% confidence interval, 0.10-0.53 mm2; P=0.004) than those in the lowest quintile, adjusting for estimated glomerular filtration rate, demographics, and vascular risk factors. Linear regression models also showed that log transformed FGF23 (LnFGF23) associated with greater odds of plaque presence (odds ratio, 1.26 per LnFGF23; 95% confidence interval, 1.01-1.58; P=0.04), and plaque area (β=0.19 mm2 per LnFGF23; 95% confidence interval, 0.07-0.31 mm2; P=0.002). Conclusions - Higher FGF23 associated with greater likelihood and burden of carotid atherosclerosis independent of CKD. Atherosclerosis may be a mechanism through which FGF23 increases cardiovascular events and stroke.

AB - Objective - Elevated fibroblast growth factor 23 (FGF23), a hormone that regulates phosphate homeostasis, has been associated with mortality, cardiovascular events, and stroke, and to arterial calcification in chronic kidney disease, but its role in atherosclerosis is unclear and population-based studies are lacking. We hypothesized that elevated FGF23 would associate with carotid plaque presence, area, and echogenicity in the race/ethnically diverse community-based Northern Manhattan Study (NOMAS) sample. Approach and Results - There were 1512 stroke-free NOMAS participants with FGF23 and 2-dimensional carotid ultrasound data (mean age, 68±9 years; 61% women; 62% Hispanic, 18% black, and 18% white). We used multivariable linear and logistic regression to evaluate FGF23, continuously and by quintiles, as a correlate of carotid plaque, plaque area (cubic root transformed), and echogenicity adjusting for sociodemographic and vascular risk factors. Participants with FGF23 levels in the top quintile were more likely to have carotid plaque (odds ratio, 1.49; 95% confidence interval, 1.02-2.19; P=0.04) and larger plaque area (β=0.32 mm2, 95% confidence interval, 0.10-0.53 mm2; P=0.004) than those in the lowest quintile, adjusting for estimated glomerular filtration rate, demographics, and vascular risk factors. Linear regression models also showed that log transformed FGF23 (LnFGF23) associated with greater odds of plaque presence (odds ratio, 1.26 per LnFGF23; 95% confidence interval, 1.01-1.58; P=0.04), and plaque area (β=0.19 mm2 per LnFGF23; 95% confidence interval, 0.07-0.31 mm2; P=0.002). Conclusions - Higher FGF23 associated with greater likelihood and burden of carotid atherosclerosis independent of CKD. Atherosclerosis may be a mechanism through which FGF23 increases cardiovascular events and stroke.

KW - atherosclerosis

KW - epidemiology

KW - fibroblast growth factors

KW - glomerular filtration rate

KW - risk factors

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