J Korean Med Assoc Search

CLOSE


J Korean Med Assoc > Volume 52(3); 2009 > Article
Han: Control of Dyslipidemia

Abstract

Lipid particles, which can be synthesized in the liver or absorbed through the terminal ileum, are indispensable for maintaining homeostasis. Inadequate life styles together with certain types of genetic background can induce and aggravate the condition of dyslipidemia. The personal status of inflammation, which is reflected by the serum C-reactive protein level, and the status of insulin resistance are considered as emerging risks for cardiovascular diseases. Therefore, together with aggressive management of correctable major risks, maintaining ideal lifestyles may be helpful to prevent the event of cardiovascular diseases. The most important goal of managing dyslipidemic conditions is to reach an ideal level of lipid profile, and aggressive drug management can be tried where indicated.

Acknowledgements

This work was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korean government(MOST) (No. M10748000263-07N4800-26310). KH Han and SH Lim were in part supported by grant A050020 from the Korean Ministry of Health and Welfare, 2009-288 from the Asan Institute for Life Sciences and by the Cardiovascular Research Foundation, Seoul, Korea.

References

1. Thompson GR. A handbook of hyperlipidemia 1990;London: Current Science Ltd.

2. Hovingh GK, de Groot E, van der Steeg W, Boekholdt SM, Hutten BA, Kuivenhoven JA, Kastelein JJ. Inherited disorders of HDL metabolism and atherosclerosis. Curr Opin Lipidol 2005;16:139-145.

3. Brousseau ME, Schaefer EJ, Wolfe ML, Bloedon LT, Digenio AG, Clark RW, Mancuso JP, Rader DJ. Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol. N Engl J Med 2004;350:1505-1515.

4. National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). Third report of the National Cholesterol Education Program (NCEP) Expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III) final report. Circulation 2002;106:3143-3421.

15. Danesh J, Wheeler JG, Hirschfield GM, Eda S, Eiriksdottir G, Rumley A, Lowe GD, Pepys MB, Gudnason V. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med 2004;350:1387-1397.

6. Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ. JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359(21):2195-2207.

7. Griffin BA, Caslake MJ, Yip B, Tait GW, Packard CJ, Shepherd J. Rapid isolation of low density lipoprotein (LDL) subfractions from plasma by density gradient ultracentrifugation. Atherosclerosis 1990;83:59-67.

8. Cho HK, Jang YS. Small dense LDL and atherosclerotic disease. Korean Journal of Lipid and Atherosclerosis 2003;2:360-315.

9. Piepho RW. The pharmacokinetics and pharmacodynamics of agents proven to raise high-density lipoprotein cholesterol. Am J Cardiol 2000;86:35L-40L.

Figure 1
Lipid metabolism: VLDL-IDL-LDL pathway.
jkma-52-299-g001-l.jpg
Figure 2
Lipid metabolism: HDL pathway.
jkma-52-299-g002-l.jpg
Figure 3
Risk assessment in primary prevention of cardiovascular disease (CVD); The effects of high-Sensitivity C-reactive protein and the ratio of total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C)
jkma-52-299-g003-l.jpg
Figure 4
Change of lipid metabolism due to insulin resistance.
jkma-52-299-g004-l.jpg
Figure 5
LDL particle size and apolipoprotein B predict ischemic heart disease: Quebec Cardiovascular Study.
jkma-52-299-g005-l.jpg
Figure 6
Niacin metabolism (9).
jkma-52-299-g006-l.jpg
Table 1
Major risk factors for candiovascular disease other than LDL cholestenol level (NCEP-III guideline)
jkma-52-299-i001-l.jpg

*Diabetes is regarded as a coronary heart disease (CHD) risk equivalent.

HDL cholesterol ≥ 60 mg/dL counts as a "negative" risk factor; its presence removes 1 risk factor from the total count.

Table 2
High risk group (NCEP-III guideline)
jkma-52-299-i002-l.jpg

CHD: coronary heart disease

Table 3
Definition of metabolic syndrome (NCEP-III guideline) (≥ 3 factors fulfills the diagnosis)
jkma-52-299-i003-l.jpg

*Overweight and obesity are associated with insulin resistance and the metabolic syndrome. However, the presence of abdominal obesity is more highly correlated with the metabolic risk factors than is an elevated body mass index (BMI). Therefire, the simple measure of waist circumference is recommended to identify the body weight component of the metabolic syndrome.

Some male patients can develop multiple metabolic risk factors when the waist circumference is only marginally increased, eg, 94~102 cm (37~40 in) Such patients may have strong genetic contribution to insulin resistance and they should benefit from changes in life habits, similarly to men with categorical increases in waist circumference.

Table 4
Target goal of LDL cholesterol level
jkma-52-299-i004-l.jpg

cf. CHD indicates coronary heart disease, LDL: low density lipoprotein

Table 5
Potency of statins and ezetimibe (EZ)
jkma-52-299-i005-l.jpg

TC: total cholesterol, LDL-C: low density lipoprotein cholesterol, Rule of 5s & 7s: Total cholesterol and LDL cholesterol levels are reduced additionally by 5 and 7%, respectively if statin dose is doubled.

Table 6
Guideline of omega-3 fatty acid (AHA)
jkma-52-299-i006-l.jpg

Kris-Etherton, Harris and Appel. Circulation. 2002; 106: 2747-2757.



ABOUT
ARTICLE CATEGORY

Browse all articles >

ARCHIVES
FOR CONTRIBUTORS
Editorial Office
37 Ichon-ro 46-gil, Yongsan-gu, Seoul
Tel: +82-2-6350-6562    Fax: +82-2-792-5208    E-mail: jkmamaster@gmail.com                

Copyright © 2024 by Korean Medical Association.

Developed in M2PI

Close layer
prev next