Long-Term Safety and Efficacy of Pitavastatin in Patients With

Acute Myocardial Infarction (from the Livalo Acute Myocardial

Infarction Study [LAMIS])
Soon Yong Suh, MDa, Seung-Woon Rha, MDb,*, Tae Hoon Ahn, MDa, Eak Kyun Shin, MDa,
Cheol Ung Choi, MDb, Dong Joo Oh, MDb, Jang-Ho Bae, MDc, Seung-Ho Hur, MDd,
Kyung Ho Yoon, MDe, Seok-Kyu Oh, MDe, Jong Hyun Kim, MDf, Sang Wook Kim, MDg,
In Ho Chae, MDh, Kee-Sik Kim, MDi, Young Joon Hong, MDj, and Myung Ho Jeong, MD j, for the
LAMIS Investigators
Pitavastatin is a potent lipophilic statin and may play an important role in acute myocar-
dial infarction (AMI) but there have been limited data on the safety and efficacy of
pitavastatin in AMI. This study consisted of 1,039 consecutive patients with AMI (74.0%
men, mean age 61.4 ⴞ 12.6 years) who presented in 10 major percutaneous coronary
intervention centers in Korea from February 2007 through September 2009. Pitavastatin 2
mg/day was routinely administered in patients with AMI from time of presentation. We
investigated changes of lipid profiles, biochemical markers, adverse events, and clinical
outcomes up to 12 months. During the study 318 events overall occurred in 220 patients
(21.2%) who reported >1 treatment emergent adverse event, although 20 events in 14
patients (1.4%) were treatment-related adverse events. Low-density lipoprotein (LDL)
cholesterol percent change was ⴚ25.6% and LDL cholesterol target attainment was 70.5%
at 12-month follow-up. Levels of creatinine phosphokinase, serum glutamic oxaloacetic
transaminase, glutamic pyruvic transaminase, and high-sensitivity C-reactive protein de-
creased significantly during the first 1 month of pitavastatin treatment and were sustained
to 12-month follow-up. Major adverse cardiac events occurred in 66 patients (7.3%).
All-cause deaths occurred in 32 patients (3.5%) including 19 (2.1%) cardiac deaths and
recurrent MIs occurred in 14 (1.6%) and target lesion revascularizations in 42 (4.7%). In
conclusion, administration of pitavastatin 2 mg/day in patients with AMI showed 70.5%
LDL cholesterol target attainment with good tolerance and was associated with favorable
clinical outcomes up to 12 months. © 2011 Elsevier Inc. All rights reserved. (Am J
Cardiol 2011;108:1530 –1535)

Pitavastatin (Livalo), a potent inhibitor of 3-hydroxy-3- Methods

methyl-glutaryl-coenzyme A reductase, was launched in
Japan in 2003 and currently is commonly used in Asia.1,2 In
the present study we sought to evaluate the long-term effi-
cacy and safety and clinical outcomes after routine admin-
istration of pitavastatin in patients with acute myocardial
infarction (AMI) as a substudy of the Korea Acute Myo-
cardial Infarction Registry (KAMIR).
a
Gachon University of Medicine and Science, Gil Hospital, Incheon,
Korea; bKorea University Guro Hospital, Seoul, Korea; cKonyang Univer-
sity Hospital, Daejeon, Korea; dKyemyung University Hospital, Daegu,
Korea; eWonkwang University Hospital, Iksan, Korea; fPusan HanSeo
Hospital, Busan, Korea; gChung Ang University Hospital, Seoul, Korea;
h
Seoul National University Bundang Hospital, Seongnam, Korea; iDaegu
Catholic University Hospital, Daegu, Korea; jChonnam National Univer-
sity Hospital, Gwangju, Korea. Manuscript received May 24, 2011; revised
manuscript received and accepted July 12, 2011.
All participating centers received an unrestricted research grant from
JW Pharmaceutical, Seoul, Korea.
*ⴱCorresponding author: Tel: 82-2-2626-3020; fax: 82-2-864-3062.
E-mail address: swrha617@yahoo.co.kr (S.-W. Rha).
The Pitavastatin (Livalo) Acute Myocardial Infarction
Study (LAMIS) is a substudy of the KAMIR. LAMIS in-
vestigators were selected from 10 major percutaneous cor-
onary intervention (PCI) centers among the 50 KAMIR sites
and 1,039 consecutive patients with AMI who received
pitavastatin as the sole statin were prospectively enrolled
from February 2007 through September 2009. The KAMIR
is a Korean, prospective, open, observational, multicenter
online registry of AMI with support from the Korean Soci-
ety of Cardiology. These participating hospitals can provide
primary PCI. Details of the KAMIR have been published.3
AMI was diagnosed by characteristic clinical presentation,
serial changes on electrocardiogram suggesting infarction,
and increase in cardiac enzymes. ST-segment elevation MI
was defined by new ST-segment elevation in 2 contiguous
leads measuring 0.2 mV in leads V1 to V3 or 0.1 mV in all
other leads. We enrolled patients if they had an AMI in-
cluding ST-segment elevation MI and non–ST-segment el-
evation MI. Diagnostic angiography and PCI were per-
formed after premedication with aspirin (ⱖ100 mg) and
unfractionated heparin or low-molecular-weight heparin.
Loading of aspirin (200 to 300 mg) and clopidogrel (300 to

0002-9149/11/$ – see front matter © 2011 Elsevier Inc. All rights reserved. www.ajconline.org
doi:10.1016/j.amjcard.2011.07.009
 Coronary Artery Disease/Pitavastatin in Acute Myocardial Infarction 1531

Table 1
Baseline characteristics
Characteristics Pitavastatin
(n ⫽ 1,039)

Age (years) 61.4 ⫾ 12.6

Men 769 (74.0%)
Body mass index (kg/m2) 24.2 ⫾ 3.2
Diabetes mellitus 251 (24.2%)
Hypertension 480 (46.3%)
Dyslipidemia* 102 (9.8%)
Statin use 50 (4.9%)
Previous coronary artery disease† 114 (11.0%)
Current smoker 499 (48.3%)
Systolic blood pressure (mm Hg) 116.6 ⫾ 19.4
Diastolic blood pressure (mm Hg) 71.7 ⫾ 12.4
Heart rate (beats/min) 74.5 ⫾ 14.3
Total cholesterol (mg/dl) 190.9 ⫾ 42.4
Triglyceride (mg/dl) 125.2 ⫾ 91.4
High-density lipoprotein cholesterol (mg/dl) 45.2 ⫾ 11.8
Low-density lipoprotein cholesterol (mg/dl) 122.1 ⫾ 37.1
Figure 1. Study population of LAMIS. High-sensitive C-reactive protein (mg/L) 10.0 ⫾ 29.8
Creatinine phosphokinase, maximum (IU/L) 1,129.5 ⫾ 2,135.0
Type of acute myocardial infarction
600 mg) was performed before PCI. Addition of cilostazol ST-segment elevation myocardial infarction 660 (63.8%)
as a triple antiplatelet and/or glycoprotein IIb/IIIa receptor Non–ST-segment elevation myocardial infarction 375 (36.2%)
Killip classification
inhibitor was left to the physician’s discretion. Coronary
I 817 (80.0%)
angiography was performed through the femoral or radial II 154 (15.1%)
artery. Unfractionated heparin was infused throughout the III 34 (3.3%)
procedure to maintain an activated clotting time of ⱖ250 IV 16 (1.6%)
seconds. Stents were deployed after balloon angioplasty and Onset time of acute myocardial infarction
use of a drug-eluting stent was left to the physician’s dis- Within 12 hours 781 (75.6%)
cretion. We prescribed aspirin 100 mg/day indefinitely and Within 24 hours 93 (9.0%)
clopidogrel 75 mg/day for ⱖ6 months. Pitavastatin 2 mg/ Within 48 hours 44 (4.3%)
day was routinely administered in patients with AMI from After 48 hours 115 (11.1%)
time of presentation. The protocol was approved by the Number of coronary artery narrowed 1,022
0 26 (2.5%)
institutional review board or ethics committee at each par-
1 470 (46.0%)
ticipating centers. 2 341 (33.4%)
Total cholesterol, triglycerides, low-density lipoprotein 3 185 (18.1%)
(LDL) cholesterol, high-density lipoprotein (HDL) choles- Angiographic characteristics
terol, and high-sensitive C-reactive protein were measured. Reference vessel diameter (mm) 3.1 ⫾ 0.6
LDL cholesterol target attainment by the National Choles- Minimal luminal diameter (mm) 0.38 ⫾ 0.45
terol Education Program/Adult Treatment Panel III guide- Lesion length (mm) 23.2 ⫾ 6.2
line was also evaluated at 12 months. The primary study end Stent size (mm) 3.2 ⫾ 0.5
point was all-cause mortality at 12 months after the index Drug-eluting stent 98.8%
PCI. The secondary study end points included individual Bare-metal stent 1.2%
Treatment of acute myocardial infarction 1,014
hard end points and cumulative major adverse cardiac
Percutaneous coronary intervention 959 (94.6%)
events (MACEs) at 12 months. Total MACEs were defined Thrombolysis 51 (5.0%)
as the composite of (1) total death, (2) nonfatal MI, and (3) Coronary bypass 4 (0.4%)
repeated PCI or coronary artery bypass grafting. All deaths Stage of revascularization 982
were considered cardiac deaths unless a noncardiac death No revascularization 58 (5.9%)
could be excluded. Recurrent MI was defined as the devel- Revascularization of single infarct-related artery 511 (52.0%)
opment of pathologic Q wave in ⱖ2 contiguous leads or an Revascularization of only infarct-related artery in 153 (15.6%)
increase in creatine kinase level to ⬎2 times the upper limit multivessel disease
of normal with an increase of creatine kinase-MB isoen- Multivessel coronary revascularization 121 (12.3%)
zyme. Target lesion revascularization was defined as isch- Total coronary revascularization 139 (14.2%)
emia-driven PCI of a target lesion because of restenosis or *Diagnosis previously made by physician or receiving lipid-lowering
reocclusion within the stent or in the adjacent 5 mm of the therapy.
†
distal or proximal segment. Previous angina or myocardial infarction.
Safety assessments consisted of monitoring and record-
ing treatment emergent adverse events, blood chemistry, treatment with pitavastatin and decided whether any
and physical examination including vital signs. The inves- changes were clinically important and related to pitavasta-
tigator decided whether each adverse event was related to tin. Levels of creatinine phosphokinase, serum glutamic
1532 The American Journal of Cardiology (www.ajconline.org)

Table 2
Serial biochemical markers of patients before discharge, at one month, six months, and 12 months
Before Discharge 1 Month 6 Months 12 Months

Total cholesterol (mg/dl) 191 ⫾ 42 154 ⫾ 29 156 ⫾ 34 158 ⫾ 35

Triglyceride (mg/dl) 125 ⫾ 91 145 ⫾ 108 139 ⫾ 77 151 ⫾ 152
High-density lipoprotein cholesterol (mg/dl) 45 ⫾ 12 44 ⫾ 11 44 ⫾ 11 44 ⫾ 10
Low-density lipoprotein cholesterol (mg/dl) 122 ⫾ 37 88 ⫾ 25 91 ⫾ 27 90 ⫾ 28
Creatinine phosphokinase (IU/L) 1,130 ⫾ 2,135 105 ⫾ 95 120 ⫾ 97 117 ⫾ 79
Glutamic oxaloacetic transaminase (IU/L) 91 ⫾ 139 25.1 ⫾ 17.4 26 ⫾ 26 25 ⫾ 10
Glutamic pyruvic transaminase (IU/L) 40 ⫾ 44 28 ⫾ 26 27 ⫾ 29 26 ⫾ 16
High-sensitive C-reactive protein (mg/L) 10.0 ⫾ 29.8 2.0 ⫾ 6.8 2.1 ⫾ 9.4 2.3 ⫾ 13.1

oxaloacetic transaminase, and serum glutamic pyruvic

mg/dl
transaminase were evaluated at baseline, 1 month, 6 months,
and 12 months. 250

Data are expressed as mean ⫾ SD and frequencies are

expressed as percentages. Differences between measure- 200
P < 0.001
ments were tested using t test for continuous variables P=NS P=NS
and chi-square test for categorical variables. A probabil- 150
ity value ⬍0.05 was considered statistically significant. TC
Multivariate logistic regression analysis was performed P < 0.001 LDL-C
P=NS P=NS
100
to determine the independent predictor for MACEs. The
model included all variables with a p value ⬍0.1 in
univariate analysis. All statistical analyses were performed 50

using SPSS 17.0 (SPSS, Inc., Chicago, Illinois).

0
baseline 1month 6month 12month
Results
During the study period 1,128 patients were recruited, Changes in TC & LDL-C
but 89 patients were excluded because of withdrawal of A
informed consent, violation of enrollment criteria, transfer
to another hospital, and in-hospital deaths (Figure 1). There- mg/dl
fore 1,039 patients were enrolled for this study. Baseline 60
characteristics of the overall study population are presented
in Table 1. Mean age was 61.4 ⫾ 12.6 years, 74.0% were
P < 0.05 P=NS
men, mean body mass index was 24.2 ⫾ 3.2 kg/m2, 46.3% P=NS

had hypertension, 24.2% had diabetes, 11.0% had a history

of coronary artery disease, 9.8% had dyslipidemia, 4.9%
P=NS P=NS HDL-C
previously used a statin, and 48.3% were current smokers. 30 P < 0.001 HDL-C<40
Of 1,039 patients with AMI 660 (63.8%) presented with
ST-segment elevation MI and 781 patients (75.6%) were
admitted within 12 hours onset of AMI (Table 1). As the
initial therapeutic strategy for ST-segment elevation MI 532
patients underwent primary PCI, 45 patients underwent fa-
0
cilitating PCI, 37 patients received thrombolytics, and 35 baseline 1month 6month 12month
patients were managed by conservative treatment. Of 375
patients (36.2%) with non–ST-segment elevation MI 244 pa- Changes in HDL-C
tients received early invasive therapy and the other 124 patients
received early conservative therapy. B
Not all efficacy data were always available during the Figure 2. Serial changes in (A) total cholesterol (diamonds) and low-
study period. Thus lipid changes were analyzed in patients density lipoprotein cholesterol (squares) and (B) high-density lipoprotein
whose data were available at 12 months. Of the total 1,039 cholesterol (triangles) and high-density lipoprotein cholesterol⬍40 mg/dl
patients 340 patients had data available for total cholesterol, (squares) in LAMIS.
319 for triglycerides, 318 for HDL cholesterol, and 319 for
LDL cholesterol. Baseline mean total cholesterol, triglycer-
ide, HDL cholesterol, and LDL cholesterol levels were 191 ⫾ (Table 2). We found that total cholesterol and LDL choles-
42, 125 ⫾ 91, 45 ⫾ 12, and 122 ⫾ 37 mg/dl, respectively. terol were decreased significantly during the first 1 month of
At 12 months mean total cholesterol, triglyceride, HDL pitavastatin treatment (total cholesterol 191 ⫾ 42 vs 154 ⫾
cholesterol, and LDL cholesterol levels were 158 ⫾ 35.0, 29 mg/dl, p ⬍0.001; LDL cholesterol 122 ⫾ 37 vs 88 ⫾ 25
151 ⫾ 152, 44 ⫾ 10, and 90 ⫾ 29 mg/dl, respectively mg/dl, p ⬍0.001) and sustained throughout the 12-month
 Coronary Artery Disease/Pitavastatin in Acute Myocardial Infarction 1533

Table 3
Low-density lipoprotein cholesterol target attainment by National Cholesterol Education Program guideline (low-density lipoprotein ⬍100 mg/dl)
Before Discharge 1 Month 6 Months 12 Months
(n ⫽ 1,007) (n ⫽ 540) (n ⫽ 438) (n ⫽ 319)

Low-density lipoprotein attainment 274 (27.2%) 378 (70.0%) 293 (66.9%) 225 (70.5%)
Diabetic patients 78 (31.7%) 96 (74.4%) 62 (69.7%) 45 (67.2%)
Nondiabetic patients 196 (25.9%) 281 (68.7%) 231 (66.6%) 180 (71.7%)

Table 5
mg/l Cumulative clinical outcomes up to 12 months
100 Variables 1 Month 6 Months 12 Months
(n ⫽ 1,039) (n ⫽ 963) (n ⫽ 901)

Total deaths 8 (0.8%) 20 (2.1%) 32 (3.6%)

Cardiac deaths 6 (0.6%) 13 (1.4%) 19 (2.1%)
10
P < 00.05
05 Noncardiac deaths 2 (0.2%) 7 (0.7%) 13 (1.4%)
P=NS P=NS Recurrent myocardial
CRP infarction
ST-segment elevation 1 (0.1%) 5 (0.5%) 8 (0.9%)
1
myocardial infarction
Non–ST-segment elevation 1 (0.1%) 5 (0.5%) 6 (0.7%)
myocardial infarction
Repeat percutaneous
0.1 coronary intervention
baseline 1month 6month 12month
Target lesion 1 (0.1%) 18 (1.8%) 42 (4.7%)
revascularization
Figure 3. Serial changes in high-sensitive C-reactive protein in LAMIS. Target vessel 2 (0.1%) 26 (2.7%) 59 (6.5%)
revascularization
Table 4 Coronary bypass grafting 0 0 2 (0.2%)
Overall summary of treatment emergent adverse events Total major adverse cardiac 8 (0.8%) 34 (3.5%) 66 (7.3%)
event
Category Number of Number of
Patients (%) Events (%)

With any treatment emergent 220 (21.2%)
adverse event
With any serious treatment
emergent adverse event
Death or life-threatening
Need admission
Other
With any treatment-related 14 (1.4%)
adverse event
follow-up (Figure 2). Mean HDL cholesterol was decreased
2.4% from baseline to 12 months (45 ⫾ 12 vs 44 ⫾ 10
mg/dl, p ⬍0.05) in all patients. Interestingly, for the low
HDL group (HDL cholesterol ⬍40 mg/dl, n ⫽ 99 pa-
tients) HDL cholesterol was increased by 13.5% (34 ⫾ 4
vs 39 ⫾ 8 mg/dl, p ⬍0.001; Figure 2). Percent changes of
mean total cholesterol, mean LDL cholesterol, and mean
HDL cholesterol showed decreases of 16.7%, 25.6%, and
2.4%, respectively, in all patients. In addition, 70.5% of
patients had achieved the LDL cholesterol target defined
by National Cholesterol Education Program criteria and
LDL cholesterol target attainment for diabetic patients
was 67.2% (Table 3). The inflammatory marker high-
sensitive C-reactive protein was remarkably high at base-
line but normalized during the first 1 month of pitavas-
tatin treatment and was sustained up to 12-month
follow-up (10.0 ⫾ 29.8 vs 2.3 ⫾ 13.1 mg/dl, p ⬍0.05;
Figure 3).
318 (30.6%) In total 1,039 patients were evaluated for safety through-
out the follow-up period. Overall 318 events (30.6%) in 220
42 patients (21.2%) were reported including ⱖ1 treatment
emergent adverse event and 20 events in 14 patients were
17 treatment-related adverse events. Investigators considered
24 that 15 events (4.7%) were related to pitavastatin and 5
1 events (1.6%) were probably related to pitavastatin treat-
20 (1.92%)
ment (Table 4). Furthermore, 11 events caused a hold of
pitavastatin treatment and 32 events ended in withdrawal
from the study. Most treatment emergent adverse events
(276 of 318, 86.8%) were classified as not serious, whereas
42 of 318 events (13.2%) were classified as serious treat-
ment emergent adverse events. We also found that mean
creatinine phosphokinase, glutamic oxaloacetic transami-
nase, and glutamic pyruvic transaminase levels normalized
during the first 1 month of pitavastatin treatment and was
sustained up to 12-month follow-up (Table 2). Common
adverse treatment-related adverse events were 4 cases of
serum glutamic oxaloacetic transaminase/glutamic pyruvic
transaminase increase, 3 cases of myalgia, and 1 case of
creatinine phosphokinase increase. There were no reports of
myopathy, myositis, or rhabdomyolysis throughout the 12-
month follow-up period.
At 12 months after index admission 138 patients (13.2%)
were lost to clinical follow-up. During the 12-month follow-up
period there were 32 all-cause deaths (3.5%) including 19
cardiac deaths (2.1%) and 13 noncardiac deaths (1.4%).
Recurrent MIs developed in 14 (1.6%), target lesion revas-
cularization in 42 (4.7%), and MACE occurred in 66 pa-
1534 The American Journal of Cardiology (www.ajconline.org)
tients (7.3%) at 12 months (Table 5). In univariate analysis
age, body mass index, onset time of AMI, and diabetes
mellitus were significantly associated with risk of 12-month
MACEs. To rule out confounding effects from baseline
biases, multivariate logistic analysis was performed. Con-
founding factors included age, gender, body mass index,
conventional cardiovascular risk factors (hypertension, dia-
betes mellitus, dyslipidemia, smoking, history of coronary
artery disease, onset time of AMI, and major treatment
strategies, i.e., PCI or thrombolysis). Multivariate logistic
regression analysis showed that diabetes (odds ratio 2.464,
95% confidence interval 1.58 to 3.84, p ⬍0.001) was only
the significant independent predictor for 12-month MACEs.
Discussion
Mortality after AMI has continued to decrease during the
previous 30 years, most recently with the introduction of
immediate reperfusion therapy with fibrinolytics and pri-
mary PCI and powerful medications such as antiplatelets,
angiotensin-converting enzyme inhibiters, ␤ blockers, and
statins. Currently almost all patients with acute coronary
syndrome are treated with statin but it is still unclear
whether the clinical benefits are attributable to lipid lower-
ing or independent lipid-lowering effects.4,5 Swedish regis-
try results have indicated that initiation of statin treatment at
or before hospital discharge in survivors of AMI is associ-
ated with a lower subsequent 1-year mortality rate.6 Other
previous studies have also suggested that early statin treat-
ment is beneficial in stabilizing vulnerable plaque after
acute coronary events.7–15 In contrast, statin discontinuation
rates in routine care are significantly higher than those
observed in clinical trials.16 Discontinuation rates of statin
for life-long treatment are usually high, approximately 30%
within the first year of prescription, and are broadly similar
with all statin drugs. Previous studies have shown that statin
discontinuation after AMI has a short-term harmful effect
on survival.17
LAMIS is a substudy of the KAMIR and a large long-
term prospective observational study of patients with AMI
and pitavastatin treatment. Pitavastatin was proved to have
as strong as LDL cholesterol-lowering effect as atorvastatin
in the Japan Assessment of Pitavastatin and Atorvastatin in
Acute Coronary Syndrome (JAPAN-ACS) study.18 In LA-
MIS pitavastatin showed favorable effects on lipid profiles
and high-sensitive C-reactive protein for 12 months of
follow-up. Even high-sensitive C-reactive protein was de-
creased significantly and was not significantly associated
with risk of 12-month MACEs. LDL cholesterol target
attainment was 70.5% in the total study population and LDL
target attainment for diabetic patients was 67.2% during the
12-month follow-up (Table 3). In particular HDL cholesterol
was increased by 13.5% in patients with lower HDL choles-
terol. Therefore pitavastatin may be beneficial to prevent fur-
ther cardiovascular events and decrease mortality because of
LDL cholesterol decrease and HDL cholesterol increase in
patients with low HDL even in the AMI setting.19
LAMIS is the first study on the safety and efficacy of
pitavastatin use in patients with AMI and it aimed to pro-
vide an insight into predictors that are associated with
MACEs at 12 months. The Cholesterol and Recurrent
Events Trial (CARE) showed that lowering cholesterol with
pravastatin significantly decreases the number of recurrent
coronary events (10.2% for pravastatin group vs 13.2% in
placebo group) after AMI.20 The Lescol Intervention Pre-
vention Study (LIPS) also showed that fluvastatin treatment
after PCI significantly decreases the risk of MACEs (21.4%
for fluvastatin vs 26.7% for placebo) in stable or unstable or
silent ischemia.21 In this 12-month observational study total
mortality was only 3.5% and the MACEs were 7.3%. Dia-
betes mellitus was the only independent predictor of 12-
month MACEs. We assume that this favorable 1-year cu-
mulative clinical outcome is closely associated with
pitavastatin as the sole statin in patients with AMI.
During the 12 months pitavastatin treatment in patients
with AMI produced a low rate of adverse events and reliable
safety and exerted potent LDL cholesterol-lowering effects.
Statins may be associated with adverse events including
myopathy, gastrointestinal disturbance, headache, paresthe-
sia, and hypersensitivity reactions. Because statins are used
mostly as for long-term therapy, safety is very important in
long-term statin therapy. In LAMIS the incidence of in-
creased liver enzymes ⬎3 times the upper normal limit
occurred in only 4 patients and the incidence of discontin-
uation of the study drug because of an adverse reaction was
3.07% of patients (32 of 1,039). However, there were no
reports of clinically significant myopathy, myositis, or rhab-
domyolysis during follow-up. This 12-month observational
study revealed no particular safety problem associated pi-
tavastatin use in patients with AMI.
LAMIS is a substudy of the KAMIR and a large long-
term prospective observational study of patients with AMI
and exclusive use of pitavastatin. However, this is a single-
arm nonrandomized observational study with an inherited
chance of selection bias. A randomized trial would be re-
quired to truly provide more relevant scientific data. In total
138 patients (13.2%) were lost to final clinical follow-up at
12 months for different reasons and this limits the clear
analysis of clinical outcome assessment at 12 months. Fur-
ther, LDL cholesterol target attainments were evaluated in
only 30.7% of the study population (319 of 1,039) because
of missing laboratory test results.
Acknowledgment: We thank the 1,039 patients and 10
investigators for participating in this study. We appreciate
the great devotion of Myung Ho Jeong, MD, as the principal
investigator of this study.
Appendix
LAMIS investigators and centers: Seung-Woon Rha,
Cardiovascular Center, Korea University Guro Hospital,
Seoul, Korea; Tae Hoon Ahn, Cardiovascular Center, Ga-
chon University of Medicine and Science, Gil Hospital,
Incheon, Korea; Jang Ho Bae, Cardiovascular Center,
Konyang University Hospital, Daejeon, Korea; Seung Ho
Hur, Cardiovascular Center, Keimyung University, Dong-
san Medical Center, Daegu, Korea; Kee Sik Kim, Cardio-
vascular Center, Daegu Catholic University Hospital,
Daegu, Korea; In Ho Chae, Cardiovascular Center, Seoul
National University Bundang Hospital, Seongnam, Korea;
 Coronary Artery Disease/Pitavastatin in Acute Myocardial Infarction
Jong Hyun Kim, Busan HanSeo Hospital, Busan, Korea;
Kyung Ho Yoon, Cardiovascular Center, Wonkwang Uni-
versity Hospital, Iksan, Korea; Sang Wook Kim, Cardio-
vascular Center, Chungang University Hospital, Seoul, Ko-
rea; and Myung Ho Jeong (principal investigator of
LAMIS), Cardiovascular Center, Chonnam National Uni-
versity Hospital, Gwangju, Korea.
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