Review J Lipid Atheroscler 2012;1(2):45-59 JLA Treatment Guidelines for Dyslipidemia: Summary of the Expanded Second Version Jong-Il Son, Sang Ouk Chin, Jeong-Taek Woo Department of Endocrinology and Metabolism, Kyung Hee University Hospital, Seoul, Korea on behalf of The Committee for Developing Treatment Guidelines for Dyslipidemia, Korean Society of Lipidology and Atherosclerosis (KSLA) KSLA published our first version of treatment guidelines for dyslipidemia in 1996, which was based on health examination data gathered by the National Health Insurance Corperation in 1994. A number of academic societies including the Korean Endocrine Society, the Korean Society of Cardiology, the Korean Society for Laboratory Medicine, the Korean Society for Biochemistry and the Korean Nutrition Society participated in the development of this guideline. In 2003, the second version of our guidelines was published based on the Korean National Health and Nutrition Survey (KNHANES) data which was collected in 1998. In 2006, the second version was modified and expanded with using KNHANES data collected in 2005. This article summarizes the recommendations included in the expanded second version of treatment guidelines. The full version of treatment guidelines in Korean is available at the KSLA Homepage (http://www.lipid.or.kr). Key Words: Dyslipidemia, Treatment, Guideline EPIDEMIOLOGY OF DYSLIPIDEMIA IN KOREA which included 115,000 Korean men with a follow-up period of six years demonstrated that hypertension, According to the World Health Organization, approxi- smoking, dyslipidemia and hyperglycemia were risk factors mately 12 million people die every year due to cardio- for CVD and CV disease in Korea (Table 1). However, in vascular diseases (CVD) and cerebrovascular (CV) diseases. this study smoking and dyslipidemia were more associated In Korea, the prevalence of CVD is rapidly increasing, with with CVD than CV, while hypertension was more asso- the mortality rate of 13.8 per 100,000 males in 1995, ciated with CV than CVD. Obesity, alcohol, hyperglycemia which increased to 17.7 in 2005. In women, the mortality and dyslipidemia were not found to have significant rate increased more rapidly with 9.5 per 100,000 females association with hemorrhagic CV. in 1995, increasing to 16.1 per 100,000 in 2005. There Evidence from multiple randomized controlled trials are multiple causative factors for CVD such as smoking, (RCTs) showing that reducing total cholesterol (TC) and lack of physical activity and change in dietary habits leading low density lipoprotein cholesterol (LDL-C) can prevent to the development of central obesity and deterioration CVD is strong and compelling. In Korea, a cohort study of lipid profile, blood pressure and blood sugar. of 310,000 patients with a mean follow-up period of 13 The Korea Medical Insurance Corporation (KMIC) study years was conducted in order to evaluate the association Received: June 22, 2012 Corresponding Author: Jeong-Taek Woo, Department of Endocrinology and Metabolism, Kyung Hee University Revised: July 5, 2012 Hospital, #1 Hoekidong, Dongdaemoon-gu, Seoul 130-702, Korea Accepted: July 12, 2012 Tel: +82-2-958-8128, Fax: +82-2-968-1848, E-mail: [email protected] www.lipid.or.kr 45 J Lipid Atheroscler 2012;1(2):45-59 JOURNAL OF LIPID AND ATHEROSCLEROSIS Table 1. Relative risk of cardiac and cerebrovascular disease associated with various risk factors Risk factor IHD CV CVD+CV Smoking None 1.0 1.0 1.0 Current 2.1 1.1 1.3 Ex-smoker 2.2 1.6 1.6 Blood pressure Normal 1.0 1.0 1.0 High normal 1.4 1.5 1.5 Stage 1 hypertension 1.8 2.6 2.6 Stage 2 hypertension 2.9 4.3 4.3 Stage 3 hypertension 4.4 9.9 8.8 Total cholesterol <200 mg/dL 1.0 1.0 1.0 200-239 mg/dL 1.4 1.0 1.2 ≥240 mg/dL 2.1 1.3 1.6 Fasting blood sugar <126 mg/dL 1.0 1.0 1.0 ≥126 mg/dL 1.6 1.9 1.8 Abbreviations; IHD: ischemic heart disease, CV: cerebrovascular disease, CVD: cardiovascular disease (A) 1.2 1.2 1 1 1 1.0 0.9 1.0 0.9 0.8 0.8 0.8 0.7 0.7 0.8 0.7 0.6 0.6 0.4 0.4 0.2 0.2 0 0 <40 40-49 50-59 60-69 ≥70 <40 40-49 50-59 60-69 ≥70 mg/dL mg/dL (B) 1.6 1.5 1.6 1.4 1.4 1.2 1.2 1.1 1.1 1.1 1.2 1 1.2 1 1.0 1.0 0.8 0.8 0.6 0.6 0.4 0.4 0.2 0.2 0 0 <100 100-129 130-149 ≥150 <100 100-129 130-149 ≥150 mg/dL mg/dL Fig. 1. Relative risk of ischemic heart disease associated with LDL(A) and HDL(B) cholesterol. between lipid profile and CVD. In that study, CVD risk CARDIOVASCULAR RISK ESTIMATION was 1.7 fold higher in patients with TC >230 mg/dL compared to patients with TC <160 mg/dL. The CVD risk All current guidelines on the prevention of CVD in clinical was also associated with elevated LDL-C, triglycerides (TG), practice recommend the assessment of total CVD or CV and low levels of high density lipoprotein cholesterol risk, because in most people atherosclerotic CVD is the (HDL-C) (Fig. 1). product of a number of risk factors. Many risk assessment 46 www.lipid.or.kr Jong-Il Son, et al: Treatment Guidelines for Dyslipidemia: Summary of the Expanded Second Version Table 2. ATP III LDL-C goals and cutpoints for TLC and drug therapy in different risk categories and proposed modifications based on recent clinical trial evidence Risk Category LDL-C Goal Initiate TLC Consider Drug Therapy** High risk: CHD* or CHD risk equivalents† <100 mg/dL ≥100 mg/dL# ≥100 mg/dL†† (10-year risk >20%) (optional goal: <70 (<100 mg/dL: ǁ mg/dL) consider drug options)** Moderately high risk: 2 risk factors‡ <130 mg/dL¶ ≥130 mg/dL# ≥130 mg/dL (10-year risk 10% to 20%)§§ (100–129 mg/dL: consider drug options)‡‡ Moderate risk: 2 risk factors‡ <130 mg/dL ≥130 mg/dL ≥160 mg/dL (10-year risk >10%)§§ Lower risk: 0–1 risk factor§ <160 mg/dL ≥160 mg/dL ≥190 mg/dL (160–189 mg/dL: LDL-lowering drug optional) *CHD includes history of myocardial infarction, unstable angina, stable angina, coronary artery procedures (angioplasty or bypass surgery), or evidence of clinically significant myocardial ischemia. †CHD risk equivalents include clinical manifestations of noncoronary forms of atherosclerotic disease (peripheral arterial disease, abdominal aortic aneurysm, and carotid artery disease transient ischemic attacks or stroke of carotid origin or >50% obstruction of a carotid artery), diabetes, and 2+ risk factors with 10-year risk for hard CHD >20%. ‡Risk factors include cigarette smoking, hypertension (BP ≥140/90 mm Hg or on antihypertensive medication), low HDL cholesterol (<40 mg/dL), family history of premature CHD (CHD in male first-degree relative <55 years of age; CHD in female first-degree relative <65 years of age), and age (men ≥45 years; women ≥55 years). §§Electronic 10-year risk calculators are available at www.nhlbi.nih.gov/guidelines/cholesterol. §Almost all people with zero or 1 risk factor have a 10-year risk <10%, and 10-year risk assessment in people with zero or 1 risk factor is thus not necessary. ǁ Very high risk favors the optional LDL-C goal of <70 mg/dL, and in patients with high triglycerides, non-HDL-C <100 mg/dL. ¶Optional LDL-C goal <100 mg/dL. #Any person at high risk or moderately high risk who has lifestyle-related risk factors (eg, obesity, physical inactivity, elevated triglyceride, low HDL-C, or metabolic syndrome) is a candidate for therapeutic lifestyle changes to modify these risk factors regardless of LDL-C level. **When LDL-lowering drug therapy is employed, it is advised that intensity of therapy be sufficient to achieve at least a 30% to 40% reduction in LDL-C levels. ††If baseline LDL-C is <100 mg/dL, institution of an LDL-lowering drug is a therapeutic option on the basis of available clinical trial results. If a high-risk person has high triglycerides or low HDL-C, combining a fibrate or nicotinic acid with an LDL-lowering drug can be considered. ‡‡For moderately high-risk persons, when LDL-C level is 100 to 129 mg/dL, at baseline or on lifestyle therapy, initiation of an LDL-lowering drug to achieve an LDL-C level <100 mg/dL is a therapeutic option on the basis of available clinical trial results. systems are available, and most guidelines use risk years of follow-up. This risk assessment model, which is estimation systems based on either the Framingham or similar to the SCORE system, estimates the ten-year risk SCORE (Systemic Coronary Risk Estimation) projects. for a fatal atherosclerotic event, whether heart attack, However, these systems are targeted towards Caucasians, stroke, or other occlusive arterial disease, including sudden and the validity of these risk estimation tools in Asian cardiac death. The KCPS model facilitates risk estimation populations that have different lifestyles, social environ- not only in high risk persons who have had a clinical event ments, and genetic backgrounds is less clear. such as CVD, but also in apparently healthy persons with A Korean cancer prevention study (KCPS) developed no signs of clinical disease. Risk estimation charts are a CVD and CV risk assessment model, which was crafted presented separately (Suppl. Fig.