ACE insert/delete polymorphism and atherosclerosis

W. Douglas Scheer; Donald A. Boudreau; James E. Hixson; Henry C. McGill; William P. Newman; Richard E. Tracy; Arthur W. Zieske; Jack P. Strong

doi:10.1016/j.atherosclerosis.2004.09.019

ACE insert/delete polymorphism and atherosclerosis

W. Douglas Scheer, Donald A. Boudreau, James E. Hixson, Henry C. McGill, William P. Newman, Richard E. Tracy, Arthur W. Zieske, Jack P. Strong

Research output: Contribution to journal › Article › peer-review

8 Scopus citations

Abstract

We report on the results of a large autopsy study focusing upon the hypothesis that deletion of the Alu insert in the angiotensin converting enzyme (ACE) gene is associated with: (a) greater prevalence or extent of atherosclerosis in the aorta and coronary arteries; and (b) microscopic qualities of established atherosclerotic plaques in the coronary arteries. This study was conducted in young US black (n = 290) and white (n = 379) males using available materials and data from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, a multi-center cooperative autopsy study organized in 1985 to explore the relationships of known cardiovascular risk factors to atherosclerosis in victims of accidents, homicides, or suicides in the age range of 15-34 years. The results provide strong evidence that ACE genotype may not be a predictor of either the prevalence or the extent of the lesions of atherosclerosis in the right coronary artery or the aorta of young adults, an observation that confirms previous studies that estimated the prevalence and extent of atherosclerosis using coronary angiography. In addition, the results suggest that ACE genotype does not contribute to the formation of atherosclerotic lesions that have the characteristics of vulnerable plaques in the left anterior descending coronary artery of young adults.

Original language	English (US)
Pages (from-to)	241-247
Number of pages	7
Journal	Atherosclerosis
Volume	178
Issue number	2
DOIs	https://doi.org/10.1016/j.atherosclerosis.2004.09.019
State	Published - Feb 2005

Keywords

ACE genotype
Atherosclerosis
PDAY

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1016/j.atherosclerosis.2004.09.019

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@article{5bc63094a1974d279bcc6daf2d8e6587,

title = "ACE insert/delete polymorphism and atherosclerosis",

abstract = "We report on the results of a large autopsy study focusing upon the hypothesis that deletion of the Alu insert in the angiotensin converting enzyme (ACE) gene is associated with: (a) greater prevalence or extent of atherosclerosis in the aorta and coronary arteries; and (b) microscopic qualities of established atherosclerotic plaques in the coronary arteries. This study was conducted in young US black (n = 290) and white (n = 379) males using available materials and data from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, a multi-center cooperative autopsy study organized in 1985 to explore the relationships of known cardiovascular risk factors to atherosclerosis in victims of accidents, homicides, or suicides in the age range of 15-34 years. The results provide strong evidence that ACE genotype may not be a predictor of either the prevalence or the extent of the lesions of atherosclerosis in the right coronary artery or the aorta of young adults, an observation that confirms previous studies that estimated the prevalence and extent of atherosclerosis using coronary angiography. In addition, the results suggest that ACE genotype does not contribute to the formation of atherosclerotic lesions that have the characteristics of vulnerable plaques in the left anterior descending coronary artery of young adults.",

keywords = "ACE genotype, Atherosclerosis, PDAY",

author = "Scheer, {W. Douglas} and Boudreau, {Donald A.} and Hixson, {James E.} and McGill, {Henry C.} and Newman, {William P.} and Tracy, {Richard E.} and Zieske, {Arthur W.} and Strong, {Jack P.}",

note = "Funding Information: Institutions cooperating in the PDAY study and supporting grants from the National Heart, Lung, and Blood Institute and other sources: University of Alabama, Birmingham, AL, HL-33733, HL-33728; Albany Medical College, Albany, NY, HL-33765; Baylor College of Medicine, Houston, TX, HL-33750; University of Chicago, Chicago, IL, HL-33740, HL-45715; The University of Illinois, Chicago, IL, HL-33758; Louisiana State University Health Sciences Center, New Orleans, LA, HL33746, HL-45720; Louisiana Cancer and Lung Trust Fund (2000-02-01); University of Maryland, Baltimore, MD, HL-33752, HL-45693; Medical College of Georgia, Augusta, GA, HL-33772; University of Nebraska Medical Center, Omaha, NE, HL-33778; The Ohio State University, Columbus, OH, HL-33760, HL-45694; Southwest Foundation for Biomedical Research, San Antonio, TX, HL-39913; Gift of Peter and Beth Dahlberg; The University of Texas Health Science Center at San Antonio, TX, HL-33749, HL-45719; Vanderbilt University, Nashville, TN, HL-33770, HL-45718; West Virginia University Health Sciences Center, Morgantown, WV, HL-33748.",

year = "2005",

month = feb,

doi = "10.1016/j.atherosclerosis.2004.09.019",

language = "English (US)",

volume = "178",

pages = "241--247",

journal = "Atherosclerosis",

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publisher = "Elsevier Ireland Ltd",

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AU - Scheer, W. Douglas

AU - Boudreau, Donald A.

AU - Hixson, James E.

AU - McGill, Henry C.

AU - Newman, William P.

AU - Tracy, Richard E.

AU - Zieske, Arthur W.

AU - Strong, Jack P.

N1 - Funding Information: Institutions cooperating in the PDAY study and supporting grants from the National Heart, Lung, and Blood Institute and other sources: University of Alabama, Birmingham, AL, HL-33733, HL-33728; Albany Medical College, Albany, NY, HL-33765; Baylor College of Medicine, Houston, TX, HL-33750; University of Chicago, Chicago, IL, HL-33740, HL-45715; The University of Illinois, Chicago, IL, HL-33758; Louisiana State University Health Sciences Center, New Orleans, LA, HL33746, HL-45720; Louisiana Cancer and Lung Trust Fund (2000-02-01); University of Maryland, Baltimore, MD, HL-33752, HL-45693; Medical College of Georgia, Augusta, GA, HL-33772; University of Nebraska Medical Center, Omaha, NE, HL-33778; The Ohio State University, Columbus, OH, HL-33760, HL-45694; Southwest Foundation for Biomedical Research, San Antonio, TX, HL-39913; Gift of Peter and Beth Dahlberg; The University of Texas Health Science Center at San Antonio, TX, HL-33749, HL-45719; Vanderbilt University, Nashville, TN, HL-33770, HL-45718; West Virginia University Health Sciences Center, Morgantown, WV, HL-33748.

PY - 2005/2

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N2 - We report on the results of a large autopsy study focusing upon the hypothesis that deletion of the Alu insert in the angiotensin converting enzyme (ACE) gene is associated with: (a) greater prevalence or extent of atherosclerosis in the aorta and coronary arteries; and (b) microscopic qualities of established atherosclerotic plaques in the coronary arteries. This study was conducted in young US black (n = 290) and white (n = 379) males using available materials and data from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, a multi-center cooperative autopsy study organized in 1985 to explore the relationships of known cardiovascular risk factors to atherosclerosis in victims of accidents, homicides, or suicides in the age range of 15-34 years. The results provide strong evidence that ACE genotype may not be a predictor of either the prevalence or the extent of the lesions of atherosclerosis in the right coronary artery or the aorta of young adults, an observation that confirms previous studies that estimated the prevalence and extent of atherosclerosis using coronary angiography. In addition, the results suggest that ACE genotype does not contribute to the formation of atherosclerotic lesions that have the characteristics of vulnerable plaques in the left anterior descending coronary artery of young adults.

AB - We report on the results of a large autopsy study focusing upon the hypothesis that deletion of the Alu insert in the angiotensin converting enzyme (ACE) gene is associated with: (a) greater prevalence or extent of atherosclerosis in the aorta and coronary arteries; and (b) microscopic qualities of established atherosclerotic plaques in the coronary arteries. This study was conducted in young US black (n = 290) and white (n = 379) males using available materials and data from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, a multi-center cooperative autopsy study organized in 1985 to explore the relationships of known cardiovascular risk factors to atherosclerosis in victims of accidents, homicides, or suicides in the age range of 15-34 years. The results provide strong evidence that ACE genotype may not be a predictor of either the prevalence or the extent of the lesions of atherosclerosis in the right coronary artery or the aorta of young adults, an observation that confirms previous studies that estimated the prevalence and extent of atherosclerosis using coronary angiography. In addition, the results suggest that ACE genotype does not contribute to the formation of atherosclerotic lesions that have the characteristics of vulnerable plaques in the left anterior descending coronary artery of young adults.

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ACE insert/delete polymorphism and atherosclerosis

Abstract

Keywords

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