J Cardiol 2007 Mar; 49（3）: 115 – 123

Impact of Statin Therapy on
Coronary Intervention for Non-ST
Elevation Acute Coronary Syndrome With Decreased Low-Density
Lipoprotein Cholesterol
Hidehiko

HARA, MD

Masato NAKAMURA, MD＊1
Itaru YOKOUCHI, MD＊1
Keiko

KIMURA, MD＊2

Naohiko

NEMOTO, MD＊1

Shingo

ITO, MD＊1

Tsuyoshi

ONO, MD＊1

Masanori

SHIBA, MD＊1

Masamichi

WADA, MD＊1

Takahiro

TSUJI, MD＊1

Hirotaka

KOMATSU, MD＊1

Raisuke

IIJIMA, MD＊1

Rintaro

NAKAJIMA, MD＊1

MasayaYAMAMOTO, MD＊1

Masato

YAMAMOTO, MD＊1

Takashi

YOSHITAMA, MD1

TakuroTAKAGI, MD＊1

Hisao

HARA, MD＊1

Kaoru

SUGI, MD, FJCC＊1

Abstract ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
Objectives. The benefits of treating patients with acute coronary syndrome（ACS）
with statins are wellestablished. This study investigated the effects of statins on patients who presented with low levels of lowdensity lipoprotein（LDL）cholesterol, were diagnosed with non-ST elevation ACS, and subsequently
underwent percutaneous coronary interventions（PCI）.
Methods. From 2000 to 2003, 87 patients（mean age 68 ± 10 years, 69 males, 18 females）underwent
PCI because of non-ST elevation ACS, and had low LDL cholesterol on presentation. These patients weredivided into two groups : those who had been taking statins（S-group, n ＝ 46）, and those not taking statins,
or controls（C-group, n ＝ 41）. Only patients whose LDL cholesterol was ＜ 100 mg/dl at admission（average : 82 ± 12 mg/dl）were included in the study. Troponin-T（TnT）, creatine kinase（CK）, CK-MB, andhigh-sense C reactive protein（hs-CRP）were measured before and 6 hr after PCI. The two groups were──────────────────────────────────────────────
ミネアポリス心臓研究財団, 米国 ; ＊ 1 東邦大学大橋医療センター 循環器内科 : 〒 153−8515 東京都目黒区大橋 2−17−6 ;＊ 2 モ
ンテフィオーレ医療センター 老年病科, 米国
Minneapolis Heart Institute and Foundation, Minneapolis, MN, USA ; ＊ 1Department of Cardiovascular Medicine, Toho University
Ohashi Medical Center, Tokyo ; ＊ 2Division of Geriatrics, Montefiore Medical Center, New York, NY, USA
Address for correspondence : HARA H, MD, Minneapolis Heart Institute and Foundation, 920 East 28th Street Suite 620, Minneapolis,
MN 55407, USA ; E-mail : harahide@aol.com
Manuscript received September 20, 2006 ; revised December 23, 2006 ; accepted December 25, 2006

115

116

Hara, Nakamura, Yokouchi et alevaluated at 6 months clinical follow-up.
Results. There was no difference in these markers before PCI in both groups. TnT and CK-MB in the Sgroup at 6 hr post-PCI were significantly decreased compared to those of the C-group（0.45 ± 1.34 vs1.40 ± 2.37 ng/ml, respectively, for TnT, p ＝ 0.04 ; 17.2 ± 45.5 vs 81.3 ± 157.2 IU/l, respectively, for
CK-MB, p ＝ 0.02）. Major adverse cardiac events（MACE）defined as death, myocardial infarction, congestive heart failure and target lesion revascularization were evaluated after 6 months. There was no difference in MACE between the two groups.
Conclusions. Statin treatment before PCI in patients with non-ST elevation ACS demonstrated beneficial effects such as less myocardial damage, even though both groups presented with low LDL cholesterollevels. However, no significant effect on MACE was seen at 6 months after PCI.
─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────J Cardiol 2007 Mar; 49（3）: 115−123

Key Words
Coronary artery disease
Lipoproteins, LDL
Angioplasty
ST segments

INTRODUCTION
Statins, or 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, have been shown to
reduce ischemic cardiovascular events by 25 to
30%, and to reduce low-density lipoprotein
（LDL）
1−3）
cholesterol levels by 25 to 35%.
Some of thebeneficial effects of statins may be due to thepleiotropic effects on anti-inflammation, 4−8）
antithrombosis,9, 10）and vasculature.11）Acute coronary syndrome（ACS）
is considered to be an indicator for high risk of early recurrent cardiovascular
events.12, 13）Therefore, we investigated the effect ofstatin therapy on patients with non-ST elevation
ACS who presented with low levels of LDL cholesterol on admission.
SUBJECTS AND METHODSPatient population
We evaluated 87 patients（69 males, 18 females,mean age 68 ± 10 years）who underwent percutaneous coronary interventions（ PCI）at Toho
University Ohashi Medical Center from September
2000 to March 2003. All patients had low LDL
cholesterol on admission. All patients had non-ST
elevation ACS that included high-risk unstableangina and non-ST elevation myocardial infarction,
except for serum creatine kinase（CK）level ＞−3times than upper limit of normal on admission. We
excluded patients based on the following criteria :left bundle-branch block or paced ventricularrhythm, severe congestive heart failure, cardiogenic
shock, severe anemia, renal failure requiring dialysis, hepatic dysfunction, and administration of othercholesterol-lowering drugs before admission. In
addition, patients with obvious side branch occlu-

Lipid modifying agentssion after PCI were excluded. We divided the study
group patients into two groups : previously treatedwith statin treatment group（S-group, n ＝ 46）, andnon-statin treatment control group（C-group, n ＝41）. The clinical course after PCI was monitored.
Percutaneous coronary intervention procedure
PCI was performed in a standard manner.
Angiographic success was defined by a final resultof ＜ 50% residual stenosis by visual estimation.
Stent implantation was performed according to current clinical practice, and limited to bare metal
stents. All patients received aspirin 81 mg/dl or
more before PCI, and ticlopidine 200 mg/dl or
cilostazol 200 mg/dl for at least 2 weeks after stentplacement. All patients received 100 IU/kg bolus of
intravenous heparin before PCI, and activated clotting time was maintained at ＞ 250 sec during theprocedure. Thrombolysis in Myocardial Infarction（TIMI）grade was assessed at the end of the procedure.
Quantitative coronary angiographic analysis
Quantitative angiographic measurements were
performed with an automated computer-based system（CMS, Medis Medical Imaging System）byexperienced interventional cardiologists.
Quantitative coronary angiography was performed
before and immediately after the procedure usingedge detection algorithms. Minimal luminal diameter, reference vessel diameter, and diameter ofstenosis were measured.
Measurement of lipid profile and inflammatory
markers
LDL cholesterol was measured on admission and
J Cardiol 2007 Mar; 49（3）: 115 – 123

Statin for Acute Coronary Syndrome

only patients with LDL ＜ 100 mg/dl were includedin this study. Troponin-T（TnT）, high-sense C-reactive protein（ hs-CRP）, CK, and CK-myocardialband（CK-MB）were measured before and 6 hr after
PCI.
Clinical follow-up
Clinical follow-up for major adverse cardiac
events（MACE）
was assessed at 6 months after PCI.
The definition of MACE was death, acute myocardial infarction（ AMI）, congestive heart failure（CHF）, and target lesion revascularization（TLR）.
Aspirin 81 mg/dl or more was prescribed duringfollow-up except for intolerance. Management ofstatin treatment was left to individual physicians
after PCI.
Statistical analysis
Statistical analysis was performed using commercial software（ Statview TM, Version 5.0, SAS
Institute Inc）. All data were analyzed as mean ± 1
standard deviation. Categorical variables werecompared by the χ2 or Fisher s exact test.
Unpaired Student s t-test was performed to compare continuous variables between the two groups（Table 1）. A probability value ＜ 0.05 was considered statistically significant.
RESULTS
Baseline characteristics
Patient characteristics are compared between thetwo groups in Table 1. There was no difference interms of age, sex, prevalence of diabetes mellitus
and hypertension. The level of total cholesterol at
admission was 161 ± 19 mg/dl in the S-group and
154 ± 17 mg/dl in the C-group（NS）. High-density
lipoprotein（ HDL）cholesterol level was slightly
higher in the S-group than in the C-group, but was
not statistically significant（ 52 ± 14 vs 46 ±14 mg/dl, respectively ; p ＝ 0.09）. LDL cholesterollevel was 82 ± 13 mg/dl in the S-group, and 82 ±12 mg/dl in the C-group（NS）on admission, andtriglyceride level was 135 ± 65 and 129 ±74 mg/dl, respectively, which were also not different（NS）. Statins known and taken by the patientsin the S-group were as follows : atorvastatin in 10
patients（21.7%）, pravastatin in 10（21.7%）, simvastatin in 3（6.5%）, and fluvastatin in 3（6.5%）.
Left ventricular ejection fraction was not statistically different.

J Cardiol 2007 Mar; 49（3）: 115 – 123

Table 1

117

Baseline patient characteristics
S-groupC-group（n＝46） （n＝41）

p value

Age（yr）

69±10

68±12

0.71

Male

34（73.9） 35（85.4）

0.19

Smoking22（47.8） 21（51.2）

0.75

Diabetes mellitus

24（52.2） 16（39.0）

0.22

Hypertension

32（69.6） 32（78.1）

0.37

Total cholesterol（mg/dl）

161±19154±170.11

HDL cholesterol（mg/dl）

52±14

46±14

0.09

LDL cholesterol（mg/dl）

82±13

82±12

0.90

Triglyceride（mg/dl）

135±65129±740.68

Prior-MI13（28.3）8（19.5）

0.38

LVEF
（%）

59±11

57±18

0.56

Continuous values are mean ± SD.（ ）: %.
HDL＝high-density lipoprotein ; LDL＝low-density lipoprotein ; MI＝myocardial infarction ; LVEF＝left ventricular ejection fraction.

Angiographic results
The reference diameter in the S-group and Cgroup before angioplasty was not significantly different（2.9 ± 0.7 vs 3.0 ± 0.8 mm, respectively ;NS）. Minimal luminal diameter before PCI was
also not significant（0.9 ± 0.3 vs 0.7 ± 0.5 mm,
respectively ; NS）. Left anterior descending artery,left main coronary artery, and saphenous vein graft
were treated in more patients in the S-group compared to the C-group, but there was no statisticaldifference between the two groups（Table 2）. The
right coronary artery was treated in more patients in
the C-group, but no significant difference wasfound（29.3% vs 10.9%, respectively ; p ＝ 0.06）.
Regarding devices used in the procedure（Table 3）,
stent implantation was used more in the C-groupthan the S-group, though there was no significant
statistical difference（ 65.9% vs 54.3%, respectively ; NS）. Rotational atherectomy was used
more frequently in the C-group than the S-group（19.5% vs 13.0%, respectively ; NS）, whereas
directional coronary atherectomy was used more
frequently in the S-group than the C-group（15.2%
vs 2.4% ; respectively, p ＝ 0.07）. Both interventions were not significantly different between
the two groups. Aspiration catheter and/or distal
protection devices were used more in the S-groupthan the C-group, but no significance was foundbetween the two groups（28.3% vs 22.0%, respectively ; NS）. Most treated lesions were de novo,
and the prevalence of de novo lesion was lower in118Hara, Nakamura, Yokouchi et al

Table 2

Lesion characteristics and procedural data
S-groupC-group（n＝46） （n＝41）

p value

Pre-PCI reference

2.9±0.7

3.0±0.8

0.21

Pre-PCI MLD

0.9±0.3

0.7±0.5

0.69

Post-PCI reference

3.2±0.9

3.3±0.7

0.16

Post-PCI MLD

2.9±0.92.8±1.0

0.19

De novo

36（78.3） 35（85.4）

0.39Type B2, C

26（56.5） 29（70.7）

0.17

LAD

25（54.3） 15（36.6）

0.09

RCA

5（10.9） 12（29.3）

0.06

LCX

11（23.9） 13（31.7）

0.57

LMT

3（6.5）

0

0.10

SVG

2（4.3）

1（2.4）

0.62

2.8±0.5

2.8±0.5

0.82

QCA analysis（mm）

Type of lesion

Culprit vessel

Post-PCI TIMI gradeFig. 1 Comparison of box plots illustrating creatine（C-group）, andkinase levels in the control groupthe statin treatment group（S-group）
Both groups were compared in the pre-percutaneous
coronary intervention and 6 hr post-PCI periods.
CK ＝ creatine kinase. Other abbreviation as in Table 2.

Continuous values are mean ± SD.（ ）: %.
QCA ＝ quantitative coronary angiography ; PCI ＝ percutaneous coronary intervention ; MLD ＝ minimal luminal diameter ;LAD ＝ left anterior descending artery ; RCA ＝ right coronary
artery ; LCX ＝ left circumflex artery ; LMT ＝ left main trunk ;SVG ＝ saphenous vein graft ; TIMI ＝ Thrombolysis in Myocardial
Infarction.

Table 3 Procedural characteristics
S-groupC-groupp value（n＝46） （n＝41）
BA29（63.0）33（80.5）

0.14

Stent

25（54.3）

27（65.9）

0.27

CBA

15（32.6）

7（17.1）

0.13

RA6（13.0）8（19.5）0.55

DCA

7（15.2）1（2.4）

0.07

Aspiration/distal protection 13（28.3）

9（22.0）

0.52

（ ）
: %.
BA＝balloon angioplasty ; CBA＝cutting balloon angioplasty; RA＝rotational atherectomy; DCA＝directional coronary
atherectomy

the S-group than the C-group, but did not reach statistical difference（78.3% vs 85.4%, respectively ;NS）. The prevalence of type B2, C lesion was
higher in the C-group, but there was no statisticalsignificance（56.5% vs 70.7% ; NS）. Post angioplasty TIMI grade was the same in both groups（2.8 ± 0.5 vs 2.8 ± 0.5 ; NS）.

Fig. 2 Comparison of creatine kinase midband
between the S-group and the C-group in the prePCI and 6 hr post PCI periods
CK-MB ＝ creatine kinase midband. Other abbreviation
as in Table 2.

Myocardial enzyme and inflammation marker
CK and CK-MB were measured in both groups
before and 6 hr after PCI（Figs. 1, 2）. The CK
value was similar pre-PCI（ 137 ± 331 IU/l, Sgroup vs 111 ± 110 IU/l, C-group ; NS）, but higher in the C-group post PCI（295 ± 882 vs 452 ±783 IU/l ; NS）, but this did not reach statistical difference. CK-MB showed no difference in thegroups pre-PCI, but CK-MB was significantly
higher in the C-group than in the S-group（81.3 ±
157.2 vs 17.2 ± 45.5 IU/l, respectively, p ＝ 0.02）
J Cardiol 2007 Mar; 49（3）: 115 – 123

Statin for Acute Coronary Syndrome

119

Table 4 Comparison of medication during follow-up
S-groupC-groupp value（n＝46） （n＝41）
Aspirin44（95.7） 39（95.1）

0.91

Ticlopidine

29（63.0） 21（51.2）

0.27

Cilostazol5（10.9）6（14.6）

0.60

Nitrates

13（28.3） 10（24.4）

0.68

Calcium blocker

19（41.3） 13（31.7）

0.35

Beta-blocker

12（26.1） 12（29.3）

0.74

ACE-I/ARB

30（65.2） 32（78.1）

0.19

Nicorandil

13（28.3）

0.07

Statin use during follow-up 40（87.0）

Fig. 3 High-sense C-reactive protein in the S-groupand the C-group in the pre-PCI and 6 hr postPCI periods（12.2）
5

6（14.6） ＜0.0001

（ ）
: %.
ACE-I＝angiotensin converting enzyme inhibitor ; ARB＝angiotensin receptor blocker.

Hs-CRP ＝ high-sense C-reactive protein. Other abbreviation as in Table 2.

in the C-group post-PCI（0.45 ± 1.34 vs 1.40 ±2.37 IU/l, respectively, p ＝ 0.04）.

Fig. 4 Comparison of troponin-T in the S-group andthe C-group in the pre-PCI and 6 hr post-PCI
periods
TnT ＝ troponin-T. Other abbreviation as in Table 2.

post-PCI. The hs-CRP was measured before and 6
hr after PCI in both groups. The value of hs-CRP
was a little higher in the S-group than the C-grouppre-PCI（Fig. 3）, but there was no significant difference between the two groups（0.57 ± 1.22 vs0.45 ± 1.01 ng/ml, respectively ; NS）. Hs-CRP
value at 6 hr after PCI was higher in the C-groupthan the S-group, but was not significant（0.63 ±1.71 vs 0.47 ± 1.02 ng/ml ; NS）. TnT was alsomeasured before and 6 hr after PCI（Fig. 4）. No
difference was seen in the both groups pre-PCI, but
TnT in the S-group was significantly less than thatJ Cardiol 2007 Mar; 49（3）: 115 – 123

Comparison of medical treatment during followup
Medical treatments during follow-up are shownin Table 4. Most patients kept taking aspirin duringfollow-up except for intolerance（95.7% in S-groupvs 95.1% in C-group ; NS）. Ticlopidine or cilostazol were used for at least for 2 weeks after PCI, butwere discontinued in some cases. So 63.0% of
patients in the S-group and 51.2% in the C-group
continued ticlopidine during the follow-up period.
There was no significant difference between the Sgroup and the C-group regarding the use of medical
treatments such as cilostazol, nitrates, calcium
blocker, beta-blocker, and angiotensin converting
enzyme inhibitor/angiotensin receptor blocker. The
usage of nicorandil was more frequent in the Sgroup, but was not significant statistically（28.3%
vs 12.2%, respectively ; p ＝ 0.07）. Six patients（14.6%）started statin treatment in the C-group, and40 patients（87.0%）continued statin therapy duringfollow-up（p ＜ 0.0001）. The 6 patients who started
statin treatment had 2 TLR（33.3%）during followup, and the 35 patients in the C-group who did notreceive statin had 13 MACE（37.1% ; 1 AMI, 2
CHF, and 10 TLR）
, so there was no difference inthe frequency of MACE between these two groups（33.3% vs 37.1%, respectively ; NS）.
Clinical follow-up after 6 months
The characteristics of clinical follow-up 6

120Hara, Nakamura, Yokouchi et al

Table 5Major adverse cardiac events at 6-monthfollow-up
S-group（n＝46）

C-group（n＝41）

p value

Death

0

0

1.00

AMI

2（4.3）

1（2.4）

0.63

CHF

1（2.2）

2（4.9）

0.49

TLR

9（19.6）

12（29.3）

0.29

（ ）
: %.
AMI＝acute myocardial infarction ; CHF＝congestive heart
failure ; TLR＝target lesion revascularization.

months after PCI are shown in Table 5. There wasno death in both groups. Acute myocardial infarction, which was defined as CK value greater than 3times the upper limit of normal, occurred in 2
patients（4.3%）in the S-group, and 1 patient（2.4%）
in the C-group. There was no significant difference
between the two groups. Congestive heart failure
resulting in hospital re-admission occurred less in
the S-group than the C-group, but there was no difference（2.2% vs 4.9%, respectively ; NS）. TLR inthe S-group was less than in the C-group, but thisdid not reach statistical significance（ 19.6% vs29.3%, respectively ; NS）.
DISCUSSION
Our results from this study demonstrate thatpatients who took statin before their non-ST elevation ACS event had a more favorable post PCI
course, compared to those who were not taking
statin, even though both groups of patients presented with low levels of LDL cholesterol. These
results support recent studies on the benefits ofstatin administration before coronary intervention.14, 15）While the precise underlying mechanismof inhibition of elevated myocardial enzymes bystatins is not yet known, many hypothesize that thepleiotropic effects of statins contribute, by reducing
inflammation, improving vascular endothelial functions, inhibiting thrombosis, and remodeling ofplaque composition in the diseased vessel.4−11）Our
results did not reveal any difference in inflammatory markers such as hs-CRP after PCI. Although thevalue of hs-CRP in the S-group tended to be lower
than that in the C-group, this did not reach statistical significance, likely because of the small study
population.
In this study, statins inhibited the rise in CK-MB
and TnT, likely through favorable remodeling on

plaque composition and volume. 16） Coronary
microembolization occurs more frequently among
ACS patients.17） Statins may not only reduce thisphenomenon, but also improve endothelial functionin the microcirculation, as well as provide direct
myocardial protection.18）
During coronary intervention, myocardial injury
is estimated to occur in 10 to 40% of cases, and the
myocardial injury sustained during the procedure isoften characterized by a slight increase of markers
of myocardial necrosis without symptoms, electrocardiographic changes or impairment of cardiac
function.19）However, even small increases of CKMB signify a real and measurable myocardial
injury and may be associated with a higher followup mortality.20）Most instances of minor CK-MB
elevation occur in patients with uncomplicated procedures with excellent final angiographic results, as
shown by the final TIMI flow grade. This was thecase with our study. Myocardial injury seen during
successful PCI may be explained by distal
microembolization of plaque components, anenhanced inflammatory state or total plaque burden
and/or instability.21）
Different treatments have been proposed to prevent myocardial injury during coronary intervention, including nitrate infusion, intracoronary betablockers,22）adenosine, verapamil,23）nicorandil24）
and b/ a inhibitors,25）but none of these havebeen routinely introduced into clinical practice. The
ARMYDA（ Atorvastatin for Reduction of
MYocardial Damage during Angioplasty）
trial evaluated the effects of atorvastatin on post-procedural
release of markers of myocardial damage inpatients with stable angina, and the results suggest
a beneficial effect of pre-treatment with statins.26）
Our study design differed from ARYMDA, inthat we exclusively studied a population with lowlevel of LDL cholesterol. We enrolled non-ST elevation ACS patients who presented with low LDL
cholesterol, and had a control group not being treated with statins. Our study subjects presented with
ACS, and consequently had more coronary risk factors such as hypertension, diabetes mellitus, andsmoking history, compared to the general population used in mega-trials.27, 28）Most of the patients in
the S-group had hypercholesterolemia, as they werereceiving statin treatment before PCI. Despite thisadditional risk factor, the S-group had more favorable results post PCI, compared with the control
group.
J Cardiol 2007 Mar; 49（3）: 115 – 123

Statin for Acute Coronary Syndrome

The results of the present study did not show any
significant difference in terms of 6 months clinicaloutcome between two groups, but CHF and TLR
tended to occur more in the C-group. This trend
may reach statistical significance with a larger
patient population and a longer follow-up duration.
Study limitations
This was a non-randomized, retrospective study
at a single center, with a small number of subjects,
and the follow-up period was limited to 6 months.
The two groups had comparable patient demographics and lesion characteristics. The lipid profile
was similar in both groups. We were unable toobtain the data regarding duration and dosage ofstatin treatment before PCI. However, the results ofthis study emphasize the favorable effect of statins要

on reducing myocardial injury after PCI, regardlessof type, dosage, and duration of administration.
CONCLUSIONS
Statin treatment before PCI appears to confer
benefits on patients with low LDL cholesterol who
present with non-ST elevation ACS. Patients who
took statins prior to their ACS event had lessmyocardial damage, compared with those who did
not take statin. However, there was no significant
difference in MACE between the two groups at 6
months follow-up.
Acknowledgment
We are indebted to Mitsubishi Kagaku Bio-Clinical Laboratories,
Inc., Tokyo, Japan for their generous assistance in analyzing thespecimens used in this study.

約

LDL コレステロール低値の非 ST 上昇型急性冠症候群に対する冠動脈インターベンション: スタチン療法の効果

目

原

英 彦

中村

正人

伊藤

信吾

小 野

剛

小松

宏貴

飯島

吉 玉

隆

横 内

到

木村

啓子

根本

尚彦

昌 徳

和田

昌道

辻

貴 裕

雷輔

中島林太郎

山本

正也

山本

雅人

高木

拓郎

久 男

杉

薫

柴

原

的 : 急性冠動脈症候群に対するスタチン療法は有用であることが知られている．我々は低比

重リポ蛋白（LDL）コレステロール低値でありながら，非 ST 上昇急性冠動脈症候群を生じ経皮的冠動脈形成術（PCI）を施行された患者群に対し，以前からスタチン療法を行われていた群とそうでない群とを比較し，その効果を検討した．
方

法 : 2000−2003 年に，非 ST 上昇急性冠動脈症候群を生じたが，入院時の LDL コレステロー

ル値 100 mg/dl 未満の 87 例の患者（平均年齢 68 ± 10 歳，男性 69 例，女性 18 例，平均 LDL 82 ±12 mg/dl）を調査した．スタチン治療群（46 例），および非スタチン治療対照群（41 例）の 2 群に分け，PCI 術前，術後 6 時間にクレアチンキナーゼ（CK）, CK-MB, およびトロポニン T, 高感度 C 反応性蛋白を測定した．また，PCI 施行 6 カ月後の主要心事故（死亡，急性心筋梗塞，心不全，病変部の再血行再建術）の割合を両群について調べた．
結果 : PCI 施行前では両群に各測定項目の差異を認めなかった．しかし，トロポニン T と CK-

MB に関し，治療 6 時間後の値はスタチン治療群が有意に対照群よりもおのおの低値をとった（トロポニン T 値 : 0.45 ± 1.34 vs 1.40 ± 2.37 ng/ml, p ＝ 0.04 ; CK-MB 値 : 17.2 ± 45.5 vs 81.3 ± 157.2 IU/l,
p ＝ 0.02）．6 ヵ月後の主要心事故には両群で差を認めなかった．
結論: LDL コレステロール低値の患者群において，非 ST 上昇急性冠動脈症候群に対して行われる PCI 施行前のスタチン療法は，術後心筋障害を軽減し有用であることが示唆された．しかし，6 ヵ月後の主要心事故には有意な差は認められなかった．

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121

122

Hara, Nakamura, Yokouchi et al

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