United States - English - NLM (National Library of Medicine)
LOVASTATIN- lovastatin tablet
RPK Pharmaceuticals, Inc.
Lovastatin Tablets, USP
Lovastatin, USP is a cholesterol lowering agent isolated from a strain of Aspergillus terreus. After oral
ingestion, lovastatin, USP, which is an inactive lactone, is hydrolyzed to the corresponding β-
hydroxyacid form. This is a principal metabolite and an inhibitor of 3-hydroxy-3-methylglutaryl-
coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to
mevalonate, which is an early and rate limiting step in the biosynthesis of cholesterol.
Lovastatin, USP is [1S-[1α(R*),3α,7β,8β(2S*,4S*),8aβ]]-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-[2-
(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl]-1-naphthalenyl 2-methylbutanoate. Its structural
H O M.W. 404.55
Lovastatin, USP is a white, nonhygroscopic crystalline powder that is insoluble in water and sparingly
soluble in ethanol, methanol, and acetonitrile.
Lovastatin Tablets, USP are supplied as 10 mg, 20 mg and 40 mg tablets for oral administration. In
addition to the active ingredient lovastatin, USP, each tablet contains the following inactive ingredients:
lactose monohydrate, magnesium stearate, microcrystalline cellulose, and pregelatinized corn starch.
Butylated hydroxyanisole (BHA) is added as a preservative. Lovastatin Tablets USP, 10 mg also contain
FD&C Yellow #6 Aluminum Lake. Lovastatin Tablets USP, 20 mg also contain FD&C Blue #1
Aluminum Lake. Lovastatin Tablets USP, 40 mg also contain D&C Yellow #10 Aluminum Lake, FD&C
Blue #1 Aluminum Lake, and FD&C Yellow #6 Aluminum Lake.
The involvement of low-density lipoprotein cholesterol (LDL-C) in atherogenesis has been well-
documented in clinical and pathological studies, as well as in many animal experiments. Epidemiological
and clinical studies have established that high LDL-C and low high-density lipoprotein cholesterol
(HDL-C) are both associated with coronary heart disease. However, the risk of developing coronary
heart disease is continuous and graded over the range of cholesterol levels and many coronary events
do occur in patients with total cholesterol (total-C) and LDL-C in the lower end of this range.
Lovastatin has been shown to reduce elevated LDL-C concentrations. LDL is formed from very low-
density lipoprotein (VLDL) and is catabolized predominantly by the high affinity LDL receptor. The
mechanism of the LDL-lowering effect of lovastatin may involve both reduction of VLDL-C
concentration, and induction of the LDL receptor, leading to reduced production and/or increased
catabolism of LDL-C. Apolipoprotein B also falls during treatment with lovastatin.
Lovastatin is a specific inhibitor of HMG-CoA reductase, the enzyme which catalyzes the conversion
of HMG-CoA to mevalonate. The conversion of HMG-CoA to mevalonate is an early step in the
biosynthetic pathway for cholesterol.
Lovastatin is a lactone which is readily hydrolyzed in vivo to the corresponding β-hydroxyacid, a strong
inhibitor of HMG-CoA reductase. Inhibition of HMG-CoA reductase is the basis for an assay in
pharmacokinetic studies of the β-hydroxyacid metabolites (active inhibitors) and, following base
hydrolysis, active plus latent inhibitors (total inhibitors) in plasma following administration of lovastatin.
Following an oral dose of
C-labeled lovastatin in man, 10% of the dose was excreted in urine and
83% in feces. The latter represents absorbed drug equivalents excreted in bile, as well as any
unabsorbed drug. Plasma concentrations of total radioactivity (lovastatin plus
C-metabolites) peaked at
2 hours and declined rapidly to about 10% of peak by 24 hours postdose. Absorption of lovastatin,
estimated relative to an intravenous reference dose, in each of four animal species tested, averaged
about 30% of an oral dose. In animal studies, after oral dosing, lovastatin had high selectivity for the
liver, where it achieved substantially higher concentrations than in non-target tissues. Lovastatin
undergoes extensive first-pass extraction in the liver, its primary site of action, with subsequent
excretion of drug equivalents in the bile. As a consequence of extensive hepatic extraction of
lovastatin, the availability of drug to the general circulation is low and variable. In a single dose study in
four hypercholesterolemic patients, it was estimated that less than 5% of an oral dose of lovastatin
reaches the general circulation as active inhibitors. Following administration of lovastatin tablets the
coefficient of variation, based on between-subject variability, was approximately 40% for the area
under the curve (AUC) of total inhibitory activity in the general circulation.
Both lovastatin and its β-hydroxyacid metabolite are highly bound (> 95%) to human plasma proteins.
Animal studies demonstrated that lovastatin crosses the blood-brain and placental barriers.
The major active metabolites present in human plasma are the β-hydroxyacid of lovastatin, its 6′-
hydroxy derivative, and two additional metabolites. Peak plasma concentrations of both active and total
inhibitors were attained within 2 to 4 hours of dose administration. While the recommended therapeutic
dose range is 10 to 80 mg/day, linearity of inhibitory activity in the general circulation was established
by a single dose study employing lovastatin tablet dosages from 60 to as high as 120 mg. With a once-a-
day dosing regimen, plasma concentrations of total inhibitors over a dosing interval achieved a steady
state between the second and third days of therapy and were about 1.5 times those following a single
dose. When lovastatin was given under fasting conditions, plasma concentrations of total inhibitors were
on average about two-thirds those found when lovastatin was administered immediately after a standard
In a study of patients with severe renal insufficiency (creatinine clearance 10 to 30 mL/min), the plasma
concentrations of total inhibitors after a single dose of lovastatin were approximately two-fold higher
than those in healthy volunteers.
In a study including 16 elderly patients between 70 to 78 years of age who received lovastatin 80
mg/day, the mean plasma level of HMG-CoA reductase inhibitory activity was increased approximately
45% compared with 18 patients between 18 to 30 years of age (see PRECAUTIONS, Geriatric Use).
Although the mechanism is not fully understood, cyclosporine has been shown to increase the AUC of
HMG-CoA reductase inhibitors. The increase in AUC for lovastatin and lovastatin acid is presumably
due, in part, to inhibition of CYP3A4.
The risk of myopathy is increased by high levels of HMG-CoA reductase inhibitory activity in plasma.
Strong inhibitors of CYP3A4 can raise the plasma levels of HMG-CoA reductase inhibitory activity and
increase the risk of myopathy (see WARNINGS, Myopathy/Rhabdomyolysis and PRECAUTIONS,
Lovastatin is a substrate for cytochrome P450 isoform 3A4 (CYP3A4) (see PRECAUTIONS, Drug
Interactions). Grapefruit juice contains one or more components that inhibit CYP3A4 and can increase
the plasma concentrations of drugs metabolized by CYP3A4. In one study , 10 subjects consumed 200
mL of double-strength grapefruit juice (one can of frozen concentrate diluted with one rather than 3 cans
of water) three times daily for 2 days and an additional 200 mL double-strength grapefruit juice together
with and 30 and 90 minutes following a single dose of 80 mg lovastatin on the third day. This regimen
of grapefruit juice resulted in a mean increase in the serum concentration of lovastatin and its β-
hydroxyacid metabolite (as measured by the area under the concentration-time curve) of 15 fold and 5
fold, respectively [as measured using a chemical assay — high performance liquid chromatography]. In
a second study, 15 subjects consumed one 8 oz glass of single-strength grapefruit juice (one can of
frozen concentrate diluted with 3 cans of water) with breakfast for 3 consecutive days and a single dose
of 40 mg lovastatin in the evening of the third day. This regimen of grapefruit juice resulted in a mean
increase in the plasma concentration (as measured by the area under the concentration-time curve) of
active and total HMG-CoA reductase inhibitory activity [using an enzyme inhibition assay both before
(for active inhibitors) and after (for total inhibitors) base hydrolysis] of 1.34 fold and 1.36 fold,
respectively, and of lovastatin and its β-hydroxyacid metabolite [measured using a chemical assay —
liquid chromatography/tandem mass spectrometry — different from that used in the first
study] of 1.94
fold and 1.57 fold, respectively. The effect of amounts of grapefruit juice between those used in these
two studies on lovastatin pharmacokinetics has not been studied.
Kantola, T, et al., Clin Pharmacol Ther 1998; 63(4):397-402.
TABLE I: The Effect of Other Drugs on Lovastatin Exposure When Both Were Coadministered
or Grapefruit Juice
AUC Ratio (with/without
coadministered drug) No
Effect = 1.00
600 mg BID for 3 days
200 mg QD for 4 days
40 mg on Day
100 mg QD for 4 days
40 mg on Day
200 mL of double-
80 mg single
8 oz (about 250 mL) of
single-strength for 4
40 mg single
10 mg QD for
5 to 8 fold
or Grapefruit Juice
AUC Ratio (with/without
coadministered drug) No
Effect = 1.00
Total Lovastatin acid
120 mg BID for 14 days
1. Results based on a chemical assay.
2. Lovastatin acid refers to the β-hydroxyacid of lovastatin.
3. The mean total AUC of lovastatin without itraconazole phase could not be determined accurately.
Results could be representative of strong CYP3A4 inhibitors such as ketoconazole, posaconazole,
clarithromycin, telithromycin, HIV protease inhibitors, and nefazodone.
4. Estimated minimum change.
5. The effect of amounts of grapefruit juice between those used in these two studies on lovastatin
pharmacokinetics has not been studied.
6. Double-strength: one can of frozen concentrate diluted with one can of water. Grapefruit juice was
administered TID for 2 days, and 200 mL together with single dose lovastatin and 30 and 90 minutes
following single dose lovastatin on Day 3.
7. Single-strength: one can of frozen concentrate diluted with 3 cans of water. Grapefruit juice was
administered with breakfast for 3 days, and lovastatin was administered in the evening on Day 3.
8. Cyclosporine-treated patients with psoriasis or post kidney or heart transplant patients with stable
graft function, transplanted at least 9 months prior to study.
9. ND = Analyte not determined.
10. Lactone converted to acid by hydrolysis prior to analysis. Figure represents total unmetabolized
acid and lactone.
Clinical Studies in Adults
Lovastatin has been shown to reduce total-C and LDL-C in heterozygous familial and non-familial forms
of primary hypercholesterolemia and in mixed hyperlipidemia. A marked response was seen within 2
weeks, and the maximum therapeutic response occurred within 4 to 6 weeks. The response was
maintained during continuation of therapy. Single daily doses given in the evening were more effective
than the same dose given in the morning, perhaps because cholesterol is synthesized mainly at night.
In multicenter, double-blind studies in patients with familial or non-familial hypercholesterolemia,
lovastatin, administered in doses ranging from 10 mg q.p.m. to 40 mg b.i.d., was compared to placebo.
Lovastatin significantly decreased plasma total-C, LDL-C, total-C/HDL-C ratio and LDL-C/HDL-C
ratio. In addition, lovastatin produced increases of variable magnitude in HDL-C, and modestly
decreased VLDL-C and plasma TG (see TABLES II through IV for dose response results).
The results of a study in patients with primary hypercholesterolemia are presented in TABLE II.
TABLE II: Lovastatin vs. Placebo (Mean Percent Change from Baseline After 6 Weeks)
LDL-C/HDL-C TOTAL-C/HDL-C TG.
10 mg q.p.m.
20 mg q.p.m.
10 mg b.i.d.
40 mg q.p.m.
20 mg b.i.d.
Lovastatin was compared to cholestyramine in a randomized open parallel study. The study was
performed with patients with hypercholesterolemia who were at high risk of myocardial infarction.
Summary results are presented in TABLE III.
TABLE III: Lovastatin vs. Cholestyramine (Percent Change from Baseline After 12 Weeks)
20 mg b.i.d.
40 mg b.i.d.
12 g b.i.d.
Lovastatin was studied in controlled trials in hypercholesterolemic patients with well-controlled non-
insulin dependent diabetes mellitus with normal renal function. The effect of lovastatin on lipids and
lipoproteins and the safety profile of lovastatin were similar to that demonstrated in studies in
nondiabetics. Lovastatin had no clinically important effect on glycemic control or on the dose
requirement of oral hypoglycemic agents.
Expanded Clinical Evaluation of Lovastatin (EXCEL) Study
Lovastatin was compared to placebo in 8,245 patients with hypercholesterolemia (total-C 240 to 300
mg/dL [6.2 mmol/L to 7.6 mmol/L], LDL-C > 160 mg/dL [4.1 mmol/L]) in the randomized, double-blind,
parallel, 48 week EXCEL study. All changes in the lipid measurements (TABLE IV) in lovastatin
treated patients were dose-related and significantly different from placebo (p ≤ 0.001). These results
were sustained throughout the study.
TABLE IV: Lovastatin vs. Placebo (Percent Change from Baseline – Average Values Between
Weeks 12 and 48)
20 mg q.p.m.
40 mg q.p.m.
20 mg b.i.d.
40 mg b.i.d.
1. Patients enrolled
Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS)
The Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS), a double-
blind, randomized, placebo-controlled, primary prevention study, demonstrated that treatment with
lovastatin decreased the rate of acute major coronary events (composite endpoint of myocardial
infarction, unstable angina, and sudden cardiac death) compared with placebo during a median of 5.1
years of follow-up. Participants were middle-aged and elderly men (ages 45 to 73) and women (ages 55
to 73) without symptomatic cardiovascular disease with average to moderately elevated total-C and
LDL-C, below average HDL-C, and who were at high risk based on elevated total-C/HDL-C. In
addition to age, 63% of the participants had at least one other risk factor (baseline HDL-C < 35 mg/dL,
hypertension, family history, smoking and diabetes).
AFCAPS/TexCAPS enrolled 6,605 participants (5,608 men, 997 women) based on the following lipid
entry criteria: total-C range of 180 to 264 mg/dL, LDL-C range of 130 to 190 mg/dL, HDL-C of ≤ 45
mg/dL for men and ≤ 47 mg/dL for women, and TG of ≤ 400 mg/dL. Participants were treated with
standard care, including diet, and either lovastatin 20 to 40 mg daily (n = 3,304) or placebo (n = 3,301).
Approximately 50% of the participants treated with lovastatin were titrated to 40 mg daily when their
LDL-C remained > 110 mg/dL at the 20 mg starting dose.
Lovastatin reduced the risk of a first acute major coronary event, the primary efficacy endpoint, by 37%
(lovastatin 3.5%, placebo 5.5%; p < 0.001; Figure 1). A first acute major coronary event was defined as
myocardial infarction (54 participants on lovastatin, 94 on placebo) or unstable angina (54 vs. 80) or
sudden cardiac death (8 vs. 9). Furthermore, among the secondary endpoints, lovastatin reduced the risk
of unstable angina by 32% (1.8 vs. 2.6%; p = 0.023), of myocardial infarction by 40% (1.7 vs. 2.9%; p =
0.002), and of undergoing coronary revascularization procedures (e.g., coronary artery bypass grafting
or percutaneous transluminal coronary angioplasty) by 33% (3.2 vs. 4.8%; p = 0.001). Trends in risk
reduction associated with treatment with lovastatin were consistent across men and women, smokers and
non-smokers, hypertensives and non-hypertensives, and older and younger participants. Participants with
≥ 2 risk factors had risk reductions (RR) in both acute major coronary events (RR 43%) and coronary
revascularization procedures (RR 37%). Because there were too few events among those participants
with age as their only risk factor in this study, the effect of lovastatin on outcomes could not be
adequately assessed in this subgroup.
In the Canadian Coronary Atherosclerosis Intervention Trial (CCAIT), the effect of therapy with
lovastatin on coronary atherosclerosis was assessed by coronary angiography in hyperlipidemic
patients. In the randomized, double-blind, controlled clinical trial, patients were treated with
conventional measures (usually diet and 325 mg of aspirin every other day) and either lovastatin 20 to 80
mg daily or placebo. Angiograms were evaluated at baseline and at two years by computerized
quantitative coronary angiography (QCA). Lovastatin significantly slowed the progression of lesions as
measured by the mean change per patient in minimum lumen diameter (the primary endpoint) and percent
diameter stenosis, and decreased the proportions of patients categorized with disease progression (33%
vs. 50%) and with new lesions (16% vs. 32%).
In a similarly designed trial, the Monitored Atherosclerosis Regression Study (MARS), patients were
treated with diet and either lovastatin 80 mg daily or placebo. No statistically significant difference
between lovastatin and placebo was seen for the primary endpoint (mean change per patient in percent
diameter stenosis of all lesions), or for most secondary QCA endpoints. Visual assessment by
angiographers who formed a consensus opinion of overall angiographic change (Global Change Score)
was also a secondary endpoint. By this endpoint, significant slowing of disease was seen, with
regression in 23% of patients treated with lovastatin compared to 11% of placebo patients.
In the Familial Atherosclerosis Treatment Study (FATS), either lovastatin or niacin in combination with
a bile acid sequestrant for 2.5 years in hyperlipidemic subjects significantly reduced the frequency of
progression and increased the frequency of regression of coronary atherosclerotic lesions by QCA
compared to diet and, in some cases, low-dose resin.
The effect of lovastatin on the progression of atherosclerosis in the coronary arteries has been
corroborated by similar findings in another vasculature. In the Asymptomatic Carotid Artery
Progression Study (ACAPS), the effect of therapy with lovastatin on carotid atherosclerosis was
assessed by B-mode ultrasonography in hyperlipidemic patients with early carotid lesions and without
known coronary heart disease at baseline. In this double-blind, controlled clinical trial, 919 patients
were randomized in a 2 x 2 factorial design to placebo, lovastatin 10 to 40 mg daily and/or warfarin.
Ultrasonograms of the carotid walls were used to determine the change per patient from baseline to
three years in mean maximum intimal-medial thickness (IMT) of 12 measured segments. There was a
significant regression of carotid lesions in patients receiving lovastatin alone compared to those
receiving placebo alone (p = 0.001). The predictive value of changes in IMT for stroke has not yet
been established. In the lovastatin group there was a significant reduction in the number of patients with
major cardiovascular events relative to the placebo group (5 vs. 14) and a significant reduction in all-
cause mortality (1 vs. 8).
There was a high prevalence of baseline lenticular opacities in the patient population included in the
early clinical trials with lovastatin. During these trials the appearance of new opacities was noted in
both the lovastatin and placebo groups. There was no clinically significant change in visual acuity in the
patients who had new opacities reported nor was any patient, including those with opacities noted at
baseline, discontinued from therapy because of a decrease in visual acuity.
A three-year, double-blind, placebo-controlled study in hypercholesterolemic patients to assess the
effect of lovastatin on the human lens demonstrated that there were no clinically or statistically
significant differences between the lovastatin and placebo groups in the incidence, type or progression
of lenticular opacities. There are no controlled clinical data assessing the lens available for treatment
beyond three years.
Clinical Studies in Adolescent Patients
Efficacy of Lovastatin in Adolescent Boys With Heterozygous Familial Hypercholesterolemia
In a double-blind, placebo-controlled study, 132 boys 10 to 17 years of age (mean age 12.7 yrs) with
heterozygous familial hypercholesterolemia (heFH) were randomized to lovastatin (n = 67) or placebo
(n = 65) for 48 weeks. Inclusion in the study required a baseline LDL-C level between 189 and 500
mg/dL and at least one parent with an LDL-C level > 189 mg/dL. The mean baseline LDL-C value was
253.1 mg/dL (range: 171 to 379 mg/dL) in the lovastatin group compared to 248.2 mg/dL (range: 158.5 to
413.5 mg/dL) in the placebo group. The dosage of lovastatin (once daily in the evening) was 10 mg for
the first 8 weeks, 20 mg for the second 8 weeks, and 40 mg thereafter.
Lovastatin significantly decreased plasma levels of total-C, LDL-C and apolipoprotein B (see TABLE
TABLE V: Lipid-Lowering Effects of Lovastatin in Adolescent Boys With Heterozygous
Familial Hypercholesterolemia (Mean Percent Change From Baseline at Week 48 in
1. data presented as median percent changes
The mean achieved LDL-C value was 190.9 mg/dL (range: 108 to 336 mg/dL) in the lovastatin group
compared to 244.8 mg/dL (range: 135 to 404 mg/dL) in the placebo group.
Efficacy of Lovastatin in Post-Menarchal Girls With Heterozygous Familial Hypercholesterolemia
In a double-blind, placebo-controlled study, 54 girls 10 to 17 years of age who were at least 1 year
post-menarche with heFH were randomized to lovastatin (n = 35) or placebo (n = 19) for 24 weeks.
Inclusion in the study required a baseline LDL-C level of 160 to 400 mg/dL and a parental history of
familial hypercholesterolemia. The mean baseline LDL-C value was 218.3 mg/dL (range: 136.3 to 363.7
mg/dL) in the lovastatin group compared to 198.8 mg/dL (range: 151.1 to 283.1 mg/dL) in the placebo
group. The dosage of lovastatin (once daily in the evening) was 20 mg for the first 4 weeks, and 40 mg
Lovastatin significantly decreased plasma levels of total-C, LDL-C, and apolipoprotein B (see TABLE
TABLE VI: Lipid-Lowering Effects of Lovastatin in Post-Menarchal Girls With
Heterozygous Familial Hypercholesterolemia (Mean Percent Change From Baseline at Week
24 in Intention-to-Treat Population)
1. data presented as median percent changes
The mean achieved LDL-C value was 154.5 mg/dL (range: 82 to 286 mg/dL) in the lovastatin group
compared to 203.5 mg/dL (range: 135 to 304 mg/dL) in the placebo group.
The safety and efficacy of doses above 40 mg daily have not been studied in children. The long-term
efficacy of lovastatin therapy in childhood to reduce morbidity and mortality in adulthood has not been
INDICATIONS AND USAGE
Therapy with Lovastatin Tablets should be a component of multiple risk factor intervention in those
individuals with dyslipidemia at risk for atherosclerotic vascular disease. Lovastatin Tablets should be
used in addition to a diet restricted in saturated fat and cholesterol as part of a treatment strategy to
lower total-C and LDL-C to target levels when the response to diet and other nonpharmacological
measures alone has been inadequate to reduce risk.
Primary Prevention of Coronary Heart Disease
In individuals without symptomatic cardiovascular disease, average to moderately elevated total-C and
LDL-C, and below average HDL-C, Lovastatin Tablets are indicated to reduce the risk of:
- Myocardial infarction
- Unstable angina
- Coronary revascularization procedures
(See CLINICAL PHARMACOLOGY, Clinical Studies in Adults.)
Coronary Heart Disease
Lovastatin Tablets are indicated to slow the progression of coronary atherosclerosis in patients with
coronary heart disease as part of a treatment strategy to lower total-C and LDL-C to target levels.
Therapy with lipid-altering agents should be a component of multiple risk factor intervention in those
individuals at significantly increased risk for atherosclerotic vascular disease due to
hypercholesterolemia. Lovastatin Tablets are indicated as an adjunct to diet for the reduction of
elevated total-C and LDL-C levels in patients with primary hypercholesterolemia (Types IIa and IIb ),
when the response to diet restricted in saturated fat and cholesterol and to other nonpharmacological
measures alone has been inadequate.
Classification of Hyperlipoproteinemias
IDL = intermediate-density lipoprotein.
Adolescent Patients With Heterozygous Familial Hypercholesterolemia
Lovastatin Tablets are indicated as an adjunct to diet to reduce total-C, LDL-C and apolipoprotein B
levels in adolescent boys and girls who are at least one year post-menarche, 10 to 17 years of age, with
heFH if after an adequate trial of diet therapy the following findings are present:
1. LDL-C remains > 189 mg/dL or
2. LDL-C remains > 160 mg/dL and:
there is a positive family history of premature cardiovascular disease or
two or more other CVD risk factors are present in the adolescent patient
Prior to initiating therapy with lovastatin, secondary causes for hypercholesterolemia (e.g., poorly
controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver
disease, other drug therapy, alcoholism) should be excluded, and a lipid profile performed to measure
total-C, HDL-C, and TG. For patients with TG less than 400 mg/dL (< 4.5 mmol/L), LDL-C can be
estimated using the following equation:
LDL-C = total-C - [0.2 x (TG) + HDL-C]
For TG levels > 400 mg/dL (> 4.5 mmol/L), this equation is less accurate and LDL-C concentrations
should be determined by ultracentrifugation. In hypertriglyceridemic patients, LDL-C may be low or
normal despite elevated total-C. In such cases, Lovastatin Tablets are not indicated.
The National Cholesterol Education Program (NCEP) Treatment Guidelines are summarized below:
NCEP Treatment Guidelines: LDL-C Goals and Cutpoints for Therapeutic Lifestyle Changes and
Drug Therapy in Different Risk Categories
LDL Level at Which to Initiate
Therapeutic Lifestyle Changes
LDL Level at Which to
Consider Drug Therapy
CHD or CHD risk
equivalents (10 year risk >
≥ 130 (100 to 129: drug
2+ Risk factors (10 year
risk ≤ 20%)
10 year risk 10 to 20%: ≥
10 year risk < 10%: ≥ 160
0 to 1 Risk factor
≥ 190 (160 to 189: LDL-
lowering drug optional)
1. CHD, coronary heart disease
2. Some authorities recommend use of LDL-lowering drugs in this category if an LDL-C level of <
100 mg/dL cannot be achieved by therapeutic lifestyle changes. Others prefer use of drugs that
primarily modify triglycerides and HDL-C, e.g., nicotinic acid or fibrate. Clinical judgment also
may call for deferring drug therapy in this subcategory.
3. Almost all people with 0 to 1 risk factor have a 10 year risk < 10%; thus, 10 year risk assessment in
people with 0 to 1 risk factor is not necessary.
After the LDL-C goal has been achieved, if the TG is still ≥ 200 mg/dL, non-HDL-C (total-C minus
HDL-C) becomes a secondary target of therapy. Non-HDL-C goals are set 30 mg/dL higher than LDL-
C goals for each risk category.
At the time of hospitalization for an acute coronary event, consideration can be given to initiating drug
therapy at discharge if the LDL-C is ≥ 130 mg/dL (see NCEP Treatment Guidelines above).
Since the goal of treatment is to lower LDL-C, the NCEP recommends that LDL-C levels be used to
initiate and assess treatment response. Only if LDL-C levels are not available, should the total-C be
used to monitor therapy.
Although Lovastatin Tablets may be useful to reduce elevated LDL-C levels in patients with combined
hypercholesterolemia and hypertriglyceridemia where hypercholesterolemia is the major abnormality
(Type IIb hyperlipoproteinemia), it has not been studied in conditions where the major abnormality is
elevation of chylomicrons, VLDL or IDL (i.e., hyperlipoproteinemia types I, III, IV, or V).
The NCEP classification of cholesterol levels in pediatric patients with a familial history of
hypercholesterolemia or premature cardiovascular disease is summarized below:
170 to 199
110 to 129
Children treated with lovastatin in adolescence should be re-evaluated in adulthood and appropriate
changes made to their cholesterol-lowering regimen to achieve adult goals for LDL-C.
Hypersensitivity to any component of this medication.
Active liver disease or unexplained persistent elevations of serum transaminases (see WARNINGS).
Concomitant administration with strong CYP3A4 inhibitors (e.g., itraconazole, ketoconazole,
posaconazole, voriconazole, HIV protease inhibitors, boceprevir, telaprevir, erythromycin,