Endothelial dysfunction is a feature of atherosclerosis and is associated with CHD (coronary heart disease) risk factors. This study aimed to determine the relationship between the degree of endothelial dysfunction and calculated cardiovascular risk. Endothelial function, as determined by the ACh/NP (acetycholine/sodium nitroprusside response) ratio on brachial plethysmography, was compared with cardiovascular risk as calculated from the Framingham, PROCAM (Prospective Cardiovascular Munster) and MRFIT (Multiple Risk Factor Intervention Trial) algorithms in 246 (187 male) patients, including 44 (22%) with established CHD. Endothelial dysfunction correlated with the total number of risk factors (r2=0.22; P=0.002) and was related to LDL (low-density lipoprotein)-cholesterol in men and triacylglycerols (triglycerides) in women. The ACh/NP ratio correlated with the occurrence of diabetes, CHD and the LDL-cholesterol concentration (r2=0.58; P<0.001). Endothelial dysfunction was associated with presence of CHD on receiver-operating characteristic plot analysis (area=0.706±0.04; P=0.001). There was no correlation between ACh/NP ratio and CHD risk calculated with the Framingham algorithm in men, although both ACh and NP response correlated separately with risk in women. The endothelial ACh/NP ratio correlated with absolute risk in the PROCAM algorithm (r2=0.41; P<0.005). Intermediate results were obtained with MRFIT. Individual risk factors make different contributions to endothelial dysfunction compared with their role in risk calculators. The stronger relationship of endothelial dysfunction with PROCAM risk reflects the contribution of male sex, LDL-cholesterol and triacylglycerols to risk calculated by this algorithm.
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December 2004
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Research Article|
November 24 2004
Cardiovascular risk factors and endothelial dysfunction
Anthony S. WIERZBICKI;
*Department of Chemical Pathology, King's College London (King's, Guy's & St. Thomas' Medical School), St. Thomas' Hospital Campus, Lambeth Palace Road, London SE1 7EH, U.K.
Correspondence: Dr Anthony S. Wierzbicki (email Anthony.Wierzbicki@kcl.ac.uk).
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Philip J. CHOWIENCZYK;
Philip J. CHOWIENCZYK
†Department of Clinical Pharmacology, King's College London (King's, Guy's & St. Thomas' Medical School), St. Thomas' Hospital Campus, Lambeth Palace Road, London SE1 7EH, U.K.
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John R. COCKCROFT;
John R. COCKCROFT
1
†Department of Clinical Pharmacology, King's College London (King's, Guy's & St. Thomas' Medical School), St. Thomas' Hospital Campus, Lambeth Palace Road, London SE1 7EH, U.K.
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Sally E. BRETT;
Sally E. BRETT
†Department of Clinical Pharmacology, King's College London (King's, Guy's & St. Thomas' Medical School), St. Thomas' Hospital Campus, Lambeth Palace Road, London SE1 7EH, U.K.
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Gerald F. WATTS;
Gerald F. WATTS
2
*Department of Chemical Pathology, King's College London (King's, Guy's & St. Thomas' Medical School), St. Thomas' Hospital Campus, Lambeth Palace Road, London SE1 7EH, U.K.
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B. Stephen JENKINS;
B. Stephen JENKINS
‡Department of Cardiology, King's College London (King's, Guy's & St. Thomas' Medical School), St. Thomas' Hospital Campus, Lambeth Palace Road, London SE1 7EH, U.K.
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James M. RITTER
James M. RITTER
†Department of Clinical Pharmacology, King's College London (King's, Guy's & St. Thomas' Medical School), St. Thomas' Hospital Campus, Lambeth Palace Road, London SE1 7EH, U.K.
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Clin Sci (Lond) (2004) 107 (6): 609–615.
Article history
Received:
March 12 2004
Revision Received:
July 19 2004
Accepted:
September 28 2004
Accepted Manuscript online:
September 28 2004
Citation
Anthony S. WIERZBICKI, Philip J. CHOWIENCZYK, John R. COCKCROFT, Sally E. BRETT, Gerald F. WATTS, B. Stephen JENKINS, James M. RITTER; Cardiovascular risk factors and endothelial dysfunction. Clin Sci (Lond) 1 December 2004; 107 (6): 609–615. doi: https://doi.org/10.1042/CS20040078
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