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Arch Iranian Med 2009; 12 (3): 313 – 316
Archives of Iranian Medicine, Volume 12, Number 3, May 2009
313
Acute Myocardial Infarction in a Patient with Behçet’s
Disease
Mohammad-Reza Beyranvand MD•*, Mohammad-Hassan Namazi MD*, Yusef
Mohsenzadeh MD*, Mohammad Assadpour Piranfar MD**
A 37-year-old man, a known case of Behcet's disease with its
vascular complications such as abdominal and thoracic artery
aneurysms, was admitted with the diagnosis of acute anterior
myocardial infarction and received thrombolytic therapy. Coronary
angiography and percutaneous coronary intervention via transradial
approach were performed for the patient on the eighth day of
admission. The patient did not suffer from any symptoms, myocardial
infarction, or readmission in the nine-month follow-up. About 25
cases of myocardial infarction associated with Behcet's disease
have been reported previously. Although coronary involvement is
rare in Behcet's disease, it is especially important because it
affects young individuals and often presents as acute coronary
syndromes.
Archives of Iranian Medicine, Volume 12, Number 3, 2009: 313 –
316.
Keywords: Acute myocardial infarction • aortic aneurysm •
Behçet’s disease • percutaneous coronary intervention (PCI) •
transradial approach
Introduction
ehçet’s disease (BD) is an inflammatory disorder of unknown
cause, characterized by recurrent oral aphthous
ulcers, genital ulcers, uveitis, and skin lesions.1 Large venous
or arterial lesions occur in about 25% (7 to 38%) of
patients.2,3
Vascular lesions are most likely to involve the venous system;
however, arterial lesions are the greater risk. Involvement of a
major artery is seen in 1.5% to 2.2% of patients, often as a
rapidly expanding aneurysm.4 Large vessels are affected by a
vasculitis of the vasa vasorum. The vascular injuries are
superimposed on the hypercoagul-ability state that is also
characteristic of BD and may be in part due to activated
endothelial cells and platelets.1 Endothelial function is also
impaired in Behçet’s syndrome.2 Here, we describe a patient with BD
and acute myocardial infarction (AMI) treated with percutaneous
coronary
intervention (PCI) via the left radial artery approach.
Case Report
A 37-year-old man with back pain at T12 level
came to our emergency room. He had had chest discomfort the day
before. He didn't complain of nausea, sweating, dyspnea, or
palpitation. The pulse rate and blood pressure were 80 bpm and
120/80 mmHg, respectively. The electrocardio-gram (ECG) showed ST
elevation in leads V1-V6 and ST depression in inferior leads
(Figure 1). He was admitted with the diagnosis of acute anterior MI
and received 1.5 million IU streptokinase in addition to aspirin,
morphine sulfate, IV nitroglycerin, and a beta-blocker. The routine
laboratory tests were within normal limit except for increased
white blood cell count (11300/mL). HBS and HCV were negative.
Troponin level was 3.46 µg/L. CRP was also negative.
Coronary angiography via transradial approach was performed for
the patient on the eighth day of admission. At first, the right
radial artery was attempted but guide wire (even hydrophilic guide
wire) didn't pass beyond the brachial artery because of a stenosis
possibly due to sequel of previous transbrachial coronary
angiography
Case Report
B
Authors' affiliations: *Cardiovascular Department, Shaheed
Moddarres Hospital, **Taleghani Hospital, Tehran, Iran.
•Corresponding author and reprints: Mohammad-Reza Beyranvand MD,
Cardiovascular Department, Moddarres Hospital, Saadat Abad, Tehran,
Iran. E-mail: beyran4@ yahoo.com Accepted for publication: 14
January 2008
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Acute myocardial infarction in a patient with BD
Archives of Iranian Medicine, Volume 12, Number 3, May 2009
314
(Figure 2); so, we tried the left radial artery. The left main,
left circumflex (LCX), and right
coronary arteries (RCA) were normal, but the left anterior
descending (LAD) coronary artery showed 80% stenosis at the
proximal portion and left ventriculography showed antero-apical
akinesia with ejection fraction of 35% (Figure 3). Aortography
revealed normal ascending and descending thoracic aorta and normal
brachiocephalic, left carotid, and left subclavian arteries, but
there was an irregularity at the abdominal aorta, and aorta was cut
off beyond the renal arteries with good collateral flow to the
iliac arteries and other arteries (Figure 4).
The patient scheduled for PCI at the same session. Direct
stenting with vision (Guidant) 3 – 18 mm was performed (Figure 5).
The patient was discharged after two days without any
complications. The patient did not experience any
further episodes of chest pain or complications in the
nine-month follow-up.
Past history
He was a smoker for 16 years (8 pack/year) and opium addicted
without a history of hypertension, diabetes mellitus, dyslipidemia,
or positive family history of premature atherosclerosis. He was a
known case of BD (oral aphthous ulcers, genital ulcers, and skin
lesions) for 15 years and was under treatment with betamethasone
tablets 0.5 mg/day at the time of admission.
He felt a pulsatile mass in his periumbilical area six years ago
and was admitted to the hospital and underwent abdominal surgery
with the diagnosis of abdominal aortic aneurysm. Seven months later
he underwent abdominal laparotomy again because of the graft
infection and a fistula to the duodenum. Consequently because of
the right femoral artery embolization his right thigh above the
knee was amputated. Eight months later he went to emergency room
with severe chest pain and back
Figure 1. Electrocardiogram of the patient in the emergency
room.
Figure 2. Right brachial artery stenosis.
Figure 3. Coronary arteriography: significant stenosis at the
proximal portion of the left anterior descending coronary
artery.
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M. R. Beyranvand, M. H. Namazi, Y. Mohsenzadeh, et al.
Archives of Iranian Medicine, Volume 12, Number 3, May 2009
315
pain, muffling of the left lung sounds, and cardiomegaly in CXR.
Coronary angiography and aortography were performed via the right
brachial artery and showed a huge aneurysm in the descending
thoracic aorta after isthmus, normal carotid and subclavian
arteries, 50% stenosis in the midportion of the LAD, normal LCX and
RCA, and 60% ejection fraction. Four days later he underwent left
extensive thoracotomy, resection and unroofing of aneurysmal
capsule, and patch aortoplasty (Dacron patch). For five years after
this surgery he was stable with no more events until the recent
episode of AMI.
Discussion
Although vascular Behçet’s disease (VBD) involves all types of
vessels, coronary involvement is extremely rare.5 About 25 cases of
MI associated with BD have been reported previously, some of them
have had normal coronary and some have had stenosis in the culprit
artery.5–22 They are young, usually male individuals, without
vascular risk factors except smoking in some of them. The
vasculitis of BD alone may be responsible for stenosis, thrombosis,
and false arterial aneurysms. Arterial complications are mostly
aneurysmal and thrombotic in type.23 The physiopathologic
mechanisms involved (reduction of endothelial or systemic
fibrinolytic activity, rise in fibrinogen, and factor VIII) are
still unclear.6 Also etiopathogeny, the causal relationship, and
the treatment are yet unknown.7
The patient was a complicated case of VBD with the descending
thoracic and abdominal aorta aneurysms and coronary artery stenosis
and infarction.
Involvement of the coronary artery in our patient may be another
manifestation of VBD beside extensive involvement of the aorta, or
may be a manifestation of atherosclerotic disease (like a patient
without BD), or probably a combination of these situations.
Accelerated atherosclerosis due to betamethasone also may play a
role in our patient. Etiopathogeny of AMI in a patient with BD may
be important because of treatment strategy. Drugs such as
corticosteroids may help to subside symptoms and signs in a patient
with VBD but worsen myocardial heeling in a patient with AMI and
without VBD. Appropriate approach in a patient with AMI and BD is
not clear currently. Some authors report using high dose of
corticosteroids,15 some using thrombolytic agents,14 and some
others doing primary PCI.11 We treated our patient with
streptokinase at the emergency room and didn't increase the dose of
betamethasone that he was taking before. To the best of our
knowledge this is the first report of transradial PCI in a patient
with BD and AMI. We used a bare metal stent and not a drug eluting
stent because there isn't any data regarding the choice stent in
BD. AMI has high mortality and morbidity especially in a young
patient with BD; so, careful attention in diagnosis and treatment
of this vascular complication even in the absence of known risk
factors is imperative.
Figure 4. Aortography of the patient showing cut off of aorta
beyond the renal arteries.
Figure 5. LAD coronary artery after stent angioplasty on the
proximal portion with no residual stenosis.
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Acute myocardial infarction in a patient with BD
Archives of Iranian Medicine, Volume 12, Number 3, May 2009
316
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