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Received:Revised:Accepted:

August 12, 2013 October 23, 2013November 8, 2013

Corresponding Author: Myung Ho Jeong, Director of the Cardiovascular Convergence Research Center Nominatedby Korea Ministry of Health and Welfare, Chonnam National University Hospital, 42 Jaebong-ro, Donggu, Gwangju501-757, KoreaTel: +82.62-220-6243, Fax: +82.62-228-7174, E-mail: myungho@chollian.net

This is an Open Access article distributed under the terms of the creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Case Report

http://dx.doi.org/10.12997/jla.2013.2.2.91pISSN 2287-2892 • eISSN 2288-2561 JLASuccessful Percutaneous Coronary Intervention in a Young Male Systemic Lupus Erythematosus Patient with Acute Myocardial InfarctionZhe Hao Piao, Myung Ho Jeong, Hae Chang Jeong, Shi Hyun Rhew, Ki Hong Lee, Keun Ho Park, Doo Sun Sim, Young Joon Hong, Ju Han Kim, Youngkeun Ahn, Jeong Gwan Cho, Jong Chun Park

Cardiovascular Research Center, Chonnam National University Hospital, Gwangju, Regeneromics Research Center, Chonnam National University, Gwangju, Korea

Acute myocardial infarction is a rare but potentially lethal complication of systemic lupus erythematosus. There are several proposed mechanisms for acute myocardial infarction in lupus patients: atherosclerosis and endothelial injury leading to plaque rupture, coronary vasculitis and inflammation of the vessel wall causing aneurismal dilatation or spasm, and acute thrombosis and embolism. We report a-37-year-old man with systemic lupus erythematosus who developed myocardial infarction twice.Potential mechanisms for acute myocardial infarction for this patient are discussed in this report.

Key Words: Percutaneous coronary intervention, Myocardial infarction, Systemic lupus erythematosus

INTRODUCTION

Systemic lupus erythematosus (SLE) is a chronic systemic

autoimmune disease. Acute myocardial infarction (AMI)

is an uncommon initial presentation for systemic lupus

erythematosus. The incidence of myocardial infarction is

5 times as high in patients with lupus as in the general

population, and in young women the age-specific

incidence is increased by a factor of as much as 50.1 There

are several proposed mechanisms for AMI in lupus

patients, including traditional risk factors and nontradi-

tional risk factors. We report a case of AMI in a young

man with SLE who developed recurrent AMI and received

percutaneous coronary intervention (PCI) and also aim

to discuss the mechanisms.

CASE REPORT

A 37-year-old man with a 12-year history of SLE had

been treated with a corticosteroid since being diagnosed

as having SLE at the age of 25 years. He had history of

hypertension, hyperlipidemia and current smoking.

In August 2005, at the age of 30 years, the patient

was admitted to the hospital with chest pain of 12-hour

duration. Physical examination showed normal results and

no murmur or rales were auscultated. His initial electro-

cardiogram (ECG) showed normal sinus rhythm and

T-wave inversion in leads II, III, aVF. An emergent

echocardiogram demonstrated hypokinesia of the inferior

walls. On the laboratory studies, the white blood count

was 4.6×103/μL, the hemoglobin was 14.2 g/dL, and the

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Fig. 1. Twelve-lead electrocardiogram showed normal sinus rhythm and T-wave inversion in leads III, aVF and V5-V6.

platelets were 169×103/μL. The erythrocyte sedimentation

rate (ESR) was 19 mm/hr (normal 0 to 20) and the

C-reactive protein (CRP) concentration was 0.1 mg/L

(normal 0 to 0.3). The initial coagulation studies showed

a partial thromboplastin time of 39.4 seconds (normal

26.5 to 41.1) and an international normalized ratio of

1.02 (normal 0 to 1.2). The peak level of creatine kinase

(CK) was 2,347 U/L (normal 35 to 172), CK-MB 95.4 U/L

(normal 2.3 to 9.5) and troponin-I 19.0 ng/mL (normal

0 to 0.05). The antinuclear antibody test was positive at

1：160 with a homogeneous pattern. The double-

stranded DNA was negative and the antiphospholipid

antibody (APLA) panel was negative. The levels of

complement were low, with the levels of Complement

(C) 3 at 58 mg/dL (normal 90 to 180) and C4 at 9.31

mg/dL (normal 10 to 40). The lipid profile showed total

cholesterol (TC) 125 mg/dL (normal 150 to 200), trigly-

cerides (TG) 89 mg/dL (normal 0 to 200), high density

lipoprotein-cholesterol (HDL-C) 26.1 mg/dL (normal 40

to 80), and low-density lipoprotein-cholesterol (LDL-C)

88 mg/dL (normal 0 to 120).

Coronary angiogram (CAG) revealed huge aneurysmal

dilatations of the three proximal coronary arteries with

slow Thrombolysis in the myocardial infarction (TIMI) flow

(TIMI 2 antegrade flow). An intravascular ultrasound

(IVUS) revealed huge anerysmal dilatations with thrombi

in all three coronary arteries. The patient received

aggressive anti-thrombotic medical therapy including the

standard regimen of aspirin, clopidogrel and heparin

without PCI. He had good recovery and there were no

cardiac events during clinical follow-up. Follow-up CAG

was performed at 8-months after discharge and it revealed

good distal flow and huge multiple aneurysms in the three

coronary arteries, but without thrombus.

In February 2013, at the age of 37 years, the patient

suffered from severe chest pain and presented to our

hospital again. On admission, physical examination

showed blood pressure was 120/80 mmHg and heart rate

was 70 beats/min, and no murmur or rales were detected.

The ECG showed normal sinus rhythm and T-wave

inversion in leads III, aVF and V5-V6 (Fig. 1). The

echocardiogram showed good left ventricular systolic

function and akinesia in the inferior walls. The white blood

count was 9.6×103/μL, the hemoglobin was 14.5 g/dL and

the platelets were 204×103/μL. The ESR was 22 mm/hr

and the CRP concentration was 0.19 mg/L. The cardiac

enzymes were elevated, with CK of 253 U/L, CK-MB of

104.2 U/L, and troponin I of 12.9 ng/ml. The levels of

C3 at 99.2 mg/dL and C4 at 19.1 mg/dL. The lipid profile

was favorable with levels of TC 154 mg/dL, TG 193 mg/dL,

HDL-C 38 mg/dL, and LDL-C 97 mg/dL.

CAG revealed total occlusion in the distal left circumflex

artery (LCX), and more aggravated stenosis in the middle

left anterior descending coronary artery (Fig. 2). After

pre-dilation with a 1.0×5 mm balloon and the residual

stenosis is 75%. So 3.0X19 mm bare-metal stent (Coroflex

stent, B. Broun, Germany) was implanted (Fig. 3A). The

final angiogram showed TIMI 3 flow without residual

Zhe Hao Piao, et al: AMI in SLE

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Fig. 2. Coronary angiogram on second admission. (A) huge dilatations in the proximal three coronary arteries and softplaque in the left anterior descending, (B) left circumflex artery, (C) right coronary artery, and total occlusion in the distalleft circumflex artery.

Fig. 3. (A) A bare-metal stent (Coroflex stent) was implanted in the distal left circumflex artery, (B) The final angiogramshowed good distal flow without residual stenosis.

stenosis (Fig. 3).

He was discharged 1 week after presentation, and

with aspirin, clopidogrel, bisoprorlol, candesartan, and

atorvastatin. At 1-month follow-up visit, he did not

complain of any recurrence of chest pain.

DISCUSSION

SLE is a chronic and multi-systemic autoimmune

disorder occurring predominantly in women. SLE has many

clinical manifestations, one of which is coronary artery

disease including AMI. The most common cause of death

in SLE patients affected by disease for more than 5 years

is cardiovascular disease.2 Coronary artery disease (CAD)

is one of the cardiovascular manifestations observed in

young SLE patients. The clinical manifestations of CAD

in SLE can result from several pathophysiologic mecha-

nisms, including atherosclerosis, arteritis, thrombosis,

A B C

A B

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embolization, spasm, and abnormal coronary flow.3,4

Patients with SLE have increased risks of AMI. Recent

case-control series have confirmed that the risk of

myocardial infarction in patients with SLE is increased

between 9- and 50-fold over that in the general

population.4-6

Korkmaz et al.,7 in a review of the English literature

from 1975 to 2006, found records of 50 SLE patients

with AMI under 35 years old. According to the charac-

teristics of their coronary lesions, the 50 patients were

divided into 3 groups: 16 with normal coronary arteries

or coronary thrombosis (group I), 12 with coronary

aneurysm or arteritis (group II), and 22 with coronary

atherosclerosis (group III). Five patients in group I showed

normal coronary arteries, and three patients exhibited

anti-cardiolipin antibodies and/or lupus anticoagulant; the

other 11 patients showed isolated coronary thrombosis.

Most patients in the group I (93%) were positive for

Antiphospholipid antivodies (APLAs), but among the 22

patients in group III, only one patient was positive for

APLAs.

In this case, our young patient experienced AMI twice.

The major cause of the first AMI may be attributed to

coronary artery thrombi within multiple coronary

aneurysms. Coronary artery thrombosis is often related

to the presence of APLAs in SLE patient. The presence

of APLAs predisposes some patients to thrombosis, and

it has also has been associated with valvular thickening

and nonbacterial endocarditis.8 Coronary aneurysm is rare

in SLE and confirmation of etiology is usually made at

postmortem examination and likely to result in myocardial

infarction. The precise mechanisms of coronary aneurysm

in patients with SLE are unknown. The vascular endothelial

dysfunction and vascular inflammation may play an

important role in coronary aneurysm.9

The major cause of the second AMI may be attributed

to coronary artery atherosclerosis and endothelial injury

leading to plaque rupture. The young age of many of

the patients with lupus, atherosclerosis remains the most

common cause of AMI.10 Our patient had traditional risk

factors for atherosclerosis, including hypertension, dyslipi-

demia as well as smoking. However, evidence suggests

that traditional risk factors alone do not explain the

increase in CAD observed.11,12 The nontraditional CAD risk

factors in SLE are Lupus nephritis, presence of pro-

inflammatory cytokines, some of inflammatory media-

tors, APLAs, anti-oxidative modified low-density lipo-

proteins antibodies, long-term use of corticosteroid and

cumulative dose of glucocorticoids.13

The optimal treatment of AMI from each etiology may

be different. For AMI from atherosclerotic disease, the

early PCI, angioplasty, and stent placement to achieve

revascularization is the best treatment. Coronary vasculitis,

on the other hand, may be a specific manifestation of

systemic inflammation in SLE, and conventional throm-

bolysis may fail to achieve reperfusion. Instead, treatment

for vasculitis with systemic steroids may be more

appropriate. For non-atherosclerosis acute thrombosis,

aggressive anti-platelet therapy is the best treatment. For

coronary vasospasm treatment with intracoronary nitrate

administration can resolve both symptoms of chest pain

and angiographic occlusion.14

In conclusion, our patient with SLE developed AMI twice

with different causes. We believe that the best treatment

of AMI may be different according to its etiology.

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