Lipids and lipoproteins Lipids, principally cholesterol and triglycerides, are the water insoluble compounds that require

e larger protein containing complexes called lipoproteins to transport them in blood. The protein components of the lipoprotein are known as apolipoproteins or apoproteins. (See"Lipoprotein classification; metabolism; and role in atherosclerosis".) The determination of what cholesterol level constitutes dyslipidemia has long been the subject of debate, with professional societies publishing statements or guidelines attempting to delineate risk levels and when to consider drug therapy for dyslipidemia (table 4 and table 5 and table 6) [76]. (See "ATP III guidelines for treatment of high blood cholesterol".) The prevalence of dyslipidemia is increased in patients with premature CHD, being as high as 75 to 85 percent compared with approximately 40 to 48 percent in age-matched controls without CHD [63,77]. In the INTERHEART study, dyslipidemia (defined as a raised apo B to apo A-1 ratio) accounted for 49 percent of the population-attributable risk of a first MI [11]. Disturbances in lipoprotein metabolism are often familial. As an example, 54 percent of all patients and 70 percent of those with a lipid abnormality in one reported series had a familial lipid disorder [77]. The most common familial disturbances were Lp(a) excess (alone or with other dyslipidemia), hypertriglyceridemia with hypoalphalipoproteinemia, and combined hyperlipidemia. (See "Inherited disorders of LDL-cholesterol metabolism".) Evidence for the pathogenic importance of serum cholesterol has largely come from randomized trials which showed that reductions in total and LDL-cholesterol levels (almost entirely with statins) reduce coronary events and mortality when given for primary and secondary prevention (figure 4 and figure 5) [78-80]. Factors other than LDL-cholesterol lowering also may contribute to the observed benefit from statin therapy. (See "Clinical trials of cholesterol lowering for primary prevention of coronary heart disease" and "Clinical trials of cholesterol lowering in patients with coronary heart disease or coronary risk equivalents" and "Mechanisms of benefit of lipid-lowering drugs in patients with coronary heart disease".) Recommendations for the treatment of hypercholesterolemia are discussed separately. (See "Treatment of lipids (including hypercholesterolemia) in primary prevention" and "Treatment of lipids (including hypercholesterolemia) in secondary prevention" and "Intensity of lipid lowering therapy in secondary prevention of coronary heart disease".) The following lipid and lipoprotein abnormalities are associated with increased CHD risk. The supportive data are presented elsewhere as noted:

Elevated total cholesterol (figure 6) and elevated LDL-cholesterol (see "Screening guidelines for dyslipidemia", section on 'Association between dyslipidemia and coronary risk') Low HDL-cholesterol (see "HDL metabolism and approach to the patient with abnormal HDL-cholesterol levels", section on 'Low HDL-C as a risk factor for coronary heart disease') Hypertriglyceridemia (see "Approach to the patient with hypertriglyceridemia") Increased non-HDL-cholesterol (see "ATP III guidelines for treatment of high blood cholesterol", section on 'Non-HDLcholesterol') Increased Lp(a) (See "Lipoprotein(a) and cardiovascular disease".) Increased apolipoprotein C-III (see "Lipoprotein classification; metabolism; and role in atherosclerosis") Small, dense LDL particles (see "Inherited disorders of LDL-cholesterol metabolism", section on 'Small dense LDL (LDL phenotype B)') Different genotypes of apolipoprotein E (apoE) influence cholesterol and triglyceride levels as well as the risk of CHD (see "Inherited disorders of LDL-cholesterol metabolism", section on 'Genetics')

The abnormalities discussed above require measurement of lipids or lipoproteins. Proton nuclear magnetic resonance (NMR) spectroscopy of lipoprotein particles has been proposed as an alternative method for predicting cardiovascular disease risk [81]. In a study of over 27,000 women, this techniqu linical trials of cholesterol lowering for primary prevention of coronary heart disease Author Robert S Rosenson, MD Section Editor Mason W Freeman, MD Deputy Editor David M Rind, MD Disclosures All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Mar 2013. | This topic last updated: Mar 7, 2013. INTRODUCTION Treating hypercholesterolemia in patients who do not have clinical evidence of coronary heart disease (CHD) is called primary prevention. The rationale for this approach is based upon epidemiologic data documenting a continuous, graded

relationship between the total plasma cholesterol concentration and CHD events and mortality (figure 1A-B) [1-3]. (See "Overview of the risk equivalents and established risk factors for cardiovascular disease".) The causal role of cholesterol in this relationship is suggested by clinical trials that have demonstrated that targeted lowering of LDLcholesterol in patients with hypercholesterolemia reduces CHD morbidity. Multiple mechanisms that may be involved are discussed elsewhere. (See "Clinical trials of cholesterol lowering in patients with coronary heart disease or coronary risk equivalents".) CLINICAL TRIALS Effect of early trials on mortality Three early trials each showed some benefits in the treated group:

World Health Organization (WHO) Cooperative Trial which used clofibrate10,577 patients [4,5]. Lipid Research Clinics Coronary Primary Prevention Trial which used cholestyramine 3806 patients [6]. Helsinki Heart Study which used gemfibrozil 4081 patients [7].

The mean demographics of the participants were relatively similar in the three trials [8]:

Gender only men were studied Age 46 to 55 years Total cholesterol 248 to 290 mg/dL (6.4 to 7.5 mmol/L) HDL-cholesterol 46 mg/dL (1.2 mmol/L) Triglycerides 159 to 177 mg/dL Blood pressure 121/80 to 141/90 mmHg Percent current smokers 36 to 56 percent

The three initial trials demonstrated significant reductions in coronary events (25, 19, and 34 percent, respectively) (figure 2) [4,6,7]. The time to significant benefit varied from 1.5 years in the Helsinki Heart Study to three years in the WHO Cooperative Trial. These initial trials did not demonstrate a reduction in coronary mortality. This could be explained in part by sample size: in both the Lipid Research Clinics Coronary Primary Prevention Trial and the Helsinki Heart Study, the sample size was calculated on the power to detect all combined (fatal and nonfatal) CHD endpoints, not fatal endpoints alone [6,7]. A more disturbing feature of these early primary prevention trials was an unexpected increase in mortality from noncardiovascular causes in each of the studies. Noncoronary death increased 31 to 42 percent, cancer death increased 18 to 24 percent in the WHO Cooperative Trial and the Helsinki Heart Study, and total mortality increased 25 percent in the WHO Cooperative Trial with no significant change in the other two studies [4-7]. These changes were statistically significant only in the WHO Cooperative Trial, which was also the largest of these studies. The higher death rate from noncardiac causes raised a concern regarding the safety of cholesterol-lowering therapy, particularly in a relatively low-risk population. This concern confounded management guidelines for primary preventive therapy in hypercholesterolemic subjects, until they were addressed in the West of Scotland Coronary Prevention Study [9]. West of Scotland Coronary Prevention Study The WOSCOPS trial was designed to evaluate the effect of pravastatin (40 mg/day) for five years on the rate of nonfatal MI and CHD death in 6595 men with hypercholesterolemia and no prior evidence of MI or cardiac revascularization [9]. The study patient characteristics in this landmark trial included:

Men aged 45 to 64 years. Total cholesterol concentration above 252 mg/dL (6.5 mmol/L) on initial screening. LDL cholesterol above 155 mg/dL (4.0 mmol/L) on visits two and three and above 174 mg/dL (4.5 mmol/L) but below 232 mg/dL (6.0 mmol/L) on one occasion after dietary therapy for four weeks.

Patients who were randomized to pravastatin and were adherent to therapy showed the following change between baseline and end of study lipid levels:

Total cholesterol fell 20 percent from 272 to 218 mg/dL (7.0 to 5.6 mmol/L). LDL-cholesterol fell 26 percent from 192 to 142 mg/dL (5.0 to 3.7 mmol/L). HDL-cholesterol increased 5 percent from 44 to 46 mg/dL (1.14 to 1.19 mmol/L). Triglycerides fell 12 percent from 162 to 143 mg/dL.

The results, based upon intention to treat principles, can be summarized as follows:

Nonfatal MI or CHD death 31 percent risk reduction (p<0.001). Nonfatal MI 31 percent risk reduction (p<0.001). All cardiovascular deaths 32 percent risk reduction (p = 0.033). Total mortality 22 percent risk reduction (p = 0.051).

Coronary interventions with angiography, coronary artery bypass graft, or percutaneous transluminal coronary angioplasty were also reduced by 31 to 37 percent (p<0.01). The above benefits were independent of other predictors of outcome including smoking, diabetes, nitrate consumption, ECG abnormalities, blood pressure, family history of CHD, angina pectoris, and the total cholesterol/HDL cholesterol ratio [10]. Thus, the absolute benefit of therapy was greatest in subjects with the highest baseline risk. The Kaplan-Meier analyses of time to definite nonfatal myocardial infarction (MI) and CHD death and total mortality are shown in the figure (figure 3). The estimated reduction in nonfatal MI or CHD death was from approximately 9.4 to 6.4 percent at six years. Thus, the absolute benefit was 3 percent, ie, for every 100 patients treated, three did not have a coronary event at six years. In addition, it was estimated that the number needed to treat to prevent one death over five years was 146 patients (95 percent confidence interval 90 to 250) [11]. The reduction in clinical events began within six months after randomization, too soon for the benefit to be explained by regression of atherosclerosis. (See"Mechanisms of benefit of lipid-lowering drugs in patients with coronary heart disease".) Another important observation was that, in contrast to the earlier primary prevention trials, there was no difference in noncardiovascular death (56 in thepravastatin group versus 62 in the placebo group [p = 0.54]) or incident (fatal or nonfatal) cancers (115 versus 106 in the placebo group [p = 0.55]). Subgroup analyses showed that the benefits were seen in both younger and older patients and in current smokers and nonsmokers. Furthermore, the treatment effect was proportionately the same regardless of the baseline lipid concentration and the reduction in the LDL cholesterol concentration on therapy [12]. Although there was no risk reduction without a decrease in LDL-cholesterol concentrations, a fall in the range of 24 percent was sufficient to produce the full benefit of pravastatin (figure 4). Thus, LDL cholesterol reduction alone does not appear to account for all of the benefit of pravastatin therapy. (See "Mechanisms of benefit of lipid-lowering drugs in patients with coronary heart disease".) The withdrawal rate from pravastatin was 29.6 percent at five years. This value was not different from the placebo group and the dropouts were not related to adverse side effects. A later report from the WOSCOPS trial identified high-risk groups and compared the absolute benefit of lipid lowering in these patients with the benefits noted in other cardiovascular intervention trials [13]. The following results were noted:

Men with preexisting vascular disease and those over age 55 with at least one other risk factor were at high risk, with an estimated frequency of coronary events of more than 10 percent at five years. The risk was lower in men with no other risk factors (3.5 and 5.3 percent at five years in men aged 45 to 54 and 55 to 64, respectively). The number of patients who had to be treated with pravastatin to prevent one event in five years ranged from 17 in the high-risk group to 66 in those at low risk. Even in the latter group, however, the absolute benefit was still greater than that derived from the treatment of mild hypertension with antihypertensive drugs. On the other hand, the absolute benefit was about three times lower than that seen with the use of simvastatin for secondary prevention in the Scandinavian Simvastatin Survival Study.

In addition to the above benefits, treatment with pravastatin also reduced the number of subjects requiring hospital admission for cardiovascular causes by 21 percent overall and by 27 percent in compliant subjects (figure 5). The number of cardiovascularrelated hospital admissions per 1000 subject years was reduced by 10.8 percent overall and 15.6 percent in compliant subjects [14]. Pravastatin had no effect on noncardiovascular-related hospital admissions. A surprising finding is that pravastatin therapy also resulted in a 30 percent reduction in the risk of developing diabetes, defined as a serum glucose 126 mg/dL (7 mmol/L) [15]. Cost effectiveness The cost effectiveness of pravastatin therapy, based upon the WOSCOPS trial, was analyzed for various countries. Over a broad range of inputs, cost-effectiveness ratios were below $25,000 per life years gained, regardless of the country; cost-effectiveness was better in groups with higher baseline risk [16]. AFCAPS/TexCAPS trial AFCAPS/TexCAPS was a randomized, placebo-controlled trial of lovastatin (20 to 40 mg daily) in 6605 patients without CHD [17]. It differed from WOSCOPS in two major ways: 997 postmenopausal women were included; and the mean serum total and LDL-cholesterol concentration of the participants were near the average value in the general population (221 mg/dL and 150 mg/dL [5.7 and 3.9 mmol/L], respectively); the mean HDL concentration was somewhat low

(36 mg/dL [0.94 mmol/L]) [17]. Lovastatin reduced the serum LDL-cholesterol concentration by 25 percent and increased the HDL cholesterol concentration by 6 percent. After a 5.2 year follow-up, the following absolute benefits were noted in the subjects treated with lovastatin. For every 1000 men and women treated with lovastatin for five years, 19 major coronary events, 12 MIs, and 17 coronary revascularizations could be prevented (figure 6). The total absolute benefit was approximately 2 percent, meaning that 50 patients had to be treated to prevent an event in one at five years. As in WOSCOPS, subgroups with other cardiac risk factors derived the greatest benefit from cholesterol lowering but the benefit was independent of the absolute level of LDL-cholesterol. Role of CRP Measurement of CRP levels, along with analysis of lipid profile, improves risk stratification. (See "C-reactive protein in cardiovascular disease" and "Screening for cardiovascular risk with C-reactive protein".) Statin therapy reduces the level of CRP independently of its effect on cholesterol levels, which suggests that measurement of CRP may be a useful way to identify patients who will benefit from statin therapy. This issue was addressed in analysis of 5742 patients in the AFCAPS/TexCAPS trial [18]. Lovastatinreduced CRP levels by almost 15 percent, independently of its effect on lipid levels. Among patients with a total cholesterol to HDL cholesterol ratio above the median, lovastatin reduced the incidence of coronary events, independently of the CRP level; the number of subjects needed to treat for five years to prevent one event was 47. However, lovastatin was also effective in those with a ratio that was lower than the median who also had a CRP level that was above the median; the number of subjects needed to treat for five years to prevent one event was 43. Lovastatin was ineffective in those with a low ratio and a CRP level below the median. Role of homocysteine Elevated levels of homocysteine predict future coronary events. However, in the AFCAPS/TexCAPS trial, serum homocysteine levels did not identify patients who would benefit from statin therapy [19]. (See "Overview of homocysteine".) Cost effectiveness In the AFCAPS/TexCAPS trial, the cost of lovastatin treatment was $4654 per patient [20]. However, over the duration of the study, lovastatin decreased the frequency of cardiovascular hospitalization by 28 percent and cardiovascular diagnostic and therapeutic procedures (angioplasty and bypass surgery) by 23 and 32 percent, respectively. The net effect was that cardiovascular health care costs were reduced by 27 percent with lovastatin compared to placebo, offsetting the cost of the drug by $524 per patient. ASCOT-LLA trial The ASCOT trial evaluated 19,342 hypertensive patients randomized to one of two antihypertensive regimens [21]. The lipid lowering arm of this trial randomly assigned 10,305 of these patients who had nonfasting total serum cholesterol concentrations of 251 mg/dL (6.5 mmol/L) or less to treatment with atorvastatin (10 mg/day) or placebo. The lipid lowering arm of the study was stopped early (median follow-up of 3.3 years) because of a significant benefit in patients receiving atorvastatin. The study patient characteristics included:

Age 40 to 79 years Sex 1942 women and 8363 men Mean serum total cholesterol 213 mg/dL (5.5 mmol/L) Mean serum LDL cholesterol 131 mg/dL (3.4 mmol/L) Mean serum HDL cholesterol 50 mg/dL (1.3 mmol/L)

Although patients had average serum cholesterol concentrations, they were at high risk for CHD as they were required to have at least three of the following risk factors in addition to hypertension: left ventricular hypertrophy or other specified abnormalities on electrocardiogram, type 2 diabetes, peripheral vascular disease, previous stroke or transient ischemic attack, male sex, age 55 or older, microalbuminuria or proteinuria, smoking, ratio of total to HDL cholesterol of 6 or higher, family history of CHD. Among other exclusion criteria, patients were excluded for prior myocardial infarction, currently treated angina, heart failure, a cerebrovascular event within three months, or a triglyceride level above 399 mg/dL (4.5 mmol/L). The following significant reductions in rates of events per 1000 patient years were seen in patients receiving atorvastatin compared with placebo:

Nonfatal MI plus fatal CHD: 6.0 versus 9.4 Total cardiovascular events and procedures: 24.1 versus 30.6 Fatal and nonfatal stroke: 5.4 versus 7.4

The study did not show statistically significant reductions in all-cause mortality (hazard ratio 0.87 [95% CI 0.71-1.06]) or cardiovascular mortality (hazard ratio 0.90 [95% CI 0.66-1.23]). Patients with diabetes appeared to receive less benefit from atorvastatin than patients without diabetes. This result contrasts with findings in theAFCAPS/TexCAPS trial and several secondary prevention trials.

Subgroups with different baseline total serum cholesterol concentrations seemed to have similar relative reductions in risk for the primary end point of nonfatal MI plus fatal CHD:

Cholesterol concentration less than 193 mg/dL (5.0 mmol/L) hazard ratio 0.63 (p = 0.098) Cholesterol concentration between 193 and 232 mg/dL (5.0 and 5.99 mmol/L) hazard ratio 0.62 (p = 0.011) Cholesterol concentration greater than 232 mg/dL (5.99 mmol/L) hazard ratio 0.69 (p = 0.084)

Although the above hazard ratios are similar, since patients with lower baseline cholesterol concentrations generally have a lower risk of CHD, the absolute benefit of treatment can be expected to be smaller in patients who start with lower cholesterol concentrations. METEOR trial The Measuring Effects on Intima-Media Thickness: an Evaluation of Rosuvastatin (METEOR) trial evaluated the effect of rosuvastatin on carotid intima medial thickness (CIMT) in people at relatively low risk for CHD [22]. Subjects were ages 45 to 70 (men) or 55 to 70 (women) with an LDL-C from 120 to 190 mg/dL (3.1 to 4.9 mmol/L) for those with age as their only CHD risk factor, or from 120 to 160 mg/dL (3.1 to 4.1 mmol/L) for those with two or more CHD risk factors. Subjects with risk factors other than age had to have a projected 10-year risk of CHD events below 10 percent. Subjects were required to have a baseline CIMT between 1.2 and 3.5 mm. This two-year study randomly assigned 984 subjects to rosuvastatin 40 mg daily or placebo in a five to two ratio. The primary endpoint was the annualized rate of change of CIMT. Compared with placebo, subjects treated with rosuvastatin had a marked reduction in LDL-cholesterol (-49 versus -0.3 percent). CIMT stabilized in the rosuvastatin group (-0.0014 mm/year, 95% CI -0.0041 to 0.0014 mm/year), which was significantly different from the increase in CIMT seen in the placebo group (0.0131 mm/year, CI 0.0087 to 0.0174 mm/year). The study was not designed or powered to evaluate clinical events, however all six patients with cardiovascular events were in the rosuvastatin arm (0.86 percent). This was not statistically significantly different from the control arm, and other adverse events were similar for rosuvastatin and placebo. It is uncertain how well changes in CIMT predict clinical events, particularly in this low risk population. While awaiting further data, this study does not convincingly support the use of high dose statins (such as rosuvastatin 40 mg daily) for primary prevention in patients at low risk for CHD events. JUPITER trial The JUPITER trial randomly assigned 17,802 healthy men (aged 50 and older) and women (aged 60 and older) with an LDL-C level below 130 mg/dL (3.4 mmol/L) and a C-reactive protein level of at least 2.0 mg/L to treatment with rosuvastatin 20 mg daily or placebo [23]. The trial was stopped early for benefit after a median follow-up of 1.9 years. After one year of therapy, patients treated with rosuvastatin had lower levels of LDL-C (55 versus 110 mg/dL [1.4 versus 2.8 mmol/L]) and lower levels of C-reactive protein (2.2 versus 3.5 mg/L). The primary endpoint of a first major cardiovascular event (nonfatal MI, nonfatal stroke, hospitalization for unstable angina, arterial revascularization procedure, confirmed death from cardiovascular causes) was lower in patients treated with rosuvastatin (0.77 versus 1.36 events per 100 person-years, HR 0.56, 95% CI 0.46-0.69), as was the risk of all cause mortality (1.00 versus 1.25 deaths per 100 person-years, HR 0.80, CI 0.67-0.97). The number of serious adverse events was similar in the rosuvastatin and placebo arms of the trial, although patients treated with rosuvastatin had a slightly higher rate of newly diagnosed diabetes. One problem with stopping a trial early for significant benefit is that the magnitude of the observed benefit often overestimates the true benefit [24,25]. Thus, the true benefit in patients who fulfilled the JUPITER entry criteria may be lower than the reported results. Effect on stroke Randomized trials of statins as well as their meta-analyses show a 24 to 29 percent reduction in stroke (4.1 versus 5.6 percent for placebo) over a wide range of lipid values in both primary and secondary prevention [21,26-31]. (See "Secondary prevention of stroke: Risk factor reduction", section on 'Dyslipidemia'.) Meta-analysis A 2013 update to a meta-analysis of randomized trials (18 trials; n = 56,934) with a minimum duration of one year, and where 10 percent or fewer patients had a history of CVD, found that statins reduced all-cause mortality (relative risk [RR] 0.86, 95% CI 0.79-0.94) and combined fatal and non-fatal CVD endpoints (RR 0.75, CI 0.70-0.81) [32]. Many of the trials described above and their meta-analyses, as well as trials discussed separately (see "Clinical trials of cholesterol lowering in patients with coronary heart disease or coronary risk equivalents"), included a mix of patients, some of whom had cardiovascular disease (CVD) at baseline and so were not, strictly speaking, pure trials in primary prevention. A meta-analysis of 11 statin trials included data only on 65,229 participants who were free from known CVD at baseline [33]. This meta-analysis examined only all-cause mortality and found a small statistically nonsignificant reduction with statin therapy (risk ratio

0.91, 95% CI 0.83-1.01). This reduction in mortality is somewhat smaller than suggested by the individual trials, and suggests that statin therapy may not substantially decrease all-cause mortality in a true primary-prevention population. The meta-analysis included trials of patients with diabetes who are generally considered to have a coronary risk equivalent (table 1), but excluding those trials did not substantially alter the estimates of effect. Limitations of trials Although lipid-lowering therapy is effective for primary prevention, some frequently seen types of patients have not been included in randomized trials, such as those with desirable total cholesterol but low HDL cholesterol levels, and those with hypertriglyceridemia. In a report from the Framingham Heart Study, as many as 40 percent of men and 80 percent of women had lipid profiles that have not been studied in these large trials; importantly, 25 and 66 percent of men and women, respectively, who developed CHD during follow-up would not have been eligible for these trials, primarily because of isolated hypertriglyceridemia [34]. SUMMARY

Early trials of lipid lowering therapy in primary prevention, conducted with nonstatin medications, demonstrated reductions in coronary events but did not find significant reductions in cardiac mortality. A concerning aspect of these trials were increases in noncardiovascular mortality. (See 'Effect of early trials on mortality' above.) Statin trials in primary prevention, starting with the landmark WOSCOPS trial, have found substantial relative reductions in cardiovascular events without an increase in noncardiovascular mortality. (See 'West of Scotland Coronary Prevention Study' above.) The absolute benefits of statins are smaller in primary prevention than in secondary prevention, and the overall reduction in mortality with statins in primary prevention is quite small even in higher risk patients. (See 'Meta-analysis' above and "Clinical trials of cholesterol lowering in patients with coronary heart disease or coronary risk equivalents".) The clinical implications of these results and the management of lipids in primary and secondary prevention is discussed in detail separately:

(See "Treatment of lipids (including hypercholesterolemia) in primary prevention".) (See "Treatment of lipids (including hypercholesterolemia) in secondary prevention".) (See "Intensity of lipid lowering therapy in secondary prevention of coronary heart disease".) Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES

1.

The Expert Panel. Second Report of the Expert Panel on Detectio

2. Pravastatin for primary prevention of coronary heart disease

3. 4. Kaplan-Meier analysis of the efficacy of pravastatin versus placebo in 6595 middleaged men with hypercholesterolemia (mean serum cholesterol concentration 272 mg/dL [7.0 mmol/L]). At the end of the study, the men treated with pravastatin (red line) had a 32 percent reduction in definite nonfatal myocardial infarction (MI) or death from coronary heart disease (CHD, top panel) and a 22 percent reduction in death from any cause (lower panel).
5. Data from: Shepherd J, Cobbe SM, Ford I, et al. N Engl J Med 1995; 333:1301.

LDL Cholesterol: The Bad Cholesterol

In a world of good cholesterol and bad, LDL cholesterol is the bad boy of the two. LDL collects in the walls of blood vessels, causing the blockages of atherosclerosis. Higher LDL levels put you at greater risk for a heart attack from a sudden blood clot in an artery narrowed by atherosclerosis. Getting your LDL cholesterol checked helps determine your risk for heart disease. If your LDL cholesterol is high, treatment can reduce your chance of having a heart attack.
Related Medications
More information on common Cholesterol drugs from RxList:

Vytorin Lipitor Zetia

What Is LDL Cholesterol? Cholesterol isn't all bad. Its an essential fat that provides support in the membranes of our bodies' cells. Some cholesterol comes from diet and some is made by the liver. Cholesterol can't dissolve in blood, so transport proteins carry it where it needs to go. These carriers are called lipoproteins, and LDL (low-density lipoprotein) is one member of the lipoprotein family. Acting like a microscopic bus fleet, lipoproteins pick up and carry loads of cholesterol through the blood. Each form of lipoprotein has different preferences for cholesterol, and behaves differently with the cholesterol it carries. An LDL particle is a microscopic blob consisting of an outer rim of lipoprotein surrounding a cholesterol center. LDL is called lowdensity lipoprotein because LDL particles tend to be less dense than other kinds of cholesterol particles. What Makes LDL Cholesterol Bad? LDL cholesterol can't help being bad -- it's just its chemical makeup. Here's how high amounts of LDL cholesterol leads to plaque growth and atherosclerosis.

Some LDL cholesterol circulating through the bloodstream tends to deposit in the walls of arteries. This process starts as early as childhood or adolescence. White blood cells swallow and try to digest the LDL, possibly in an attempt to protect the blood vessels. In the process, the white blood cells convert the LDL to a toxic (oxidized) form. More white blood cells and other cells migrate to the area, creating steady low-grade inflammation in the artery wall. Over time, more LDL cholesterol and cells collect in the area. The ongoing process creates a bump in the artery wall called a plaque. The plaque is made of cholesterol, cells, and debris. The process tends to continue, growing the plaque and slowly blocking the artery. An even greater danger than slow blockage is a sudden rupture of the surface of the plaque. A blood clot can form on the ruptured area, causing a heart attack. What LDL Cholesterol Test Results Mean Although heart attacks are unpredictable, higher levels of LDL cholesterol increase your risk. Expert groups define the levels of LDL cholesterol as follows:

An LDL of less than 100 milligrams per deciliter (mg/dL) is optimal. An LDL of 100 to 129 mg/dL is near-optimal. LDL between 130 and 159 mg/dL is borderline high. LDL cholesterol between 160 and 189 mg/dL is high. An LDL of 190 mg/dL or more is very high.