A Case Report of Acute Myocardial Infarction Induced
by Coronary Spasm
Hideaki Ota,1 MD, Yoshiaki Kawase,1 MD, Hiroki Kondo,1 MD, Taiji Miyake,1 MD,
Shigeshi Kamikawa,1 MD, Munenori Okubo,1 MD, Kunihiko Tsuchiya,1 MD,
Hitoshi Matsuo,1 MD, Junko Honye,1 MD, and Katsumi Ueno,1 MD
A 53-year-old male complaining of chest pain was admitted to our hospital with suspected acute myocardial infarc-
tion (AMI). Emergent coronary angiography (CAG) determined a totally occluded middle right coronary artery (RCA).
Thrombus aspiration was conducted, followed by intravascular ultrasound (IVUS) imaging. Diffuse intima plus media
thickness was identified at the obstruction site and a thrombus was observed proximally to the occlusion site on IVUS.
Following isosorbide dinitrate (ISDN) administration, dilatation of the RCA was confirmed. IVUS study indicated the
luminal dilatation was achieved by the release of the diffuse intima plus media thickening. Of note, plaque volume
showed no significant difference after administration of ISDN at any vessel site. These results clearly show that luminal
dilatation and vessel dilatation were achieved from the redistribution of plaque volume (intima plus media). A follow-up
CAG showed no significant stenosis in the RCA. After a provocation test using methylergometrine maleate, the RCA
was totally occluded at the very site of the initial event. The involvement of vasospasm as a cause of AMI in the present
case was doubly confirmed with characteristic IVUS images of vasospasm in the acute phase and with a provocation test
at follow-up. (Int Heart J 2013; 54: 237-239)
Key words: Intravascular ultrasound, Intima and media thickening
ventricular arrhythmia.1-3) Previous studies have shown that the
etiology of spasm is due to transient abnormal or hypersensi-
tive response of vascular smooth muscle to various stimuli and
that the atherosclerosis is invariably present at the site of focal
Previous intravascular ultrasound (IVUS) and optical co-
herence tomography (OCT) studies have reported the morpho-
logical features of vasospastic lesions.6-11) However, most of
the data were obtained in a spastic lesion that was artificially
induced by the administration of a vasoconstrictor (acetylcho-
line or ergonivine). In the present report, we report IVUS im-
ages from a patient with ST elevation type acute myocardial
infarction (STEMI) due to vasospasm.
oronary artery vasospasm has been shown to play an
important role in the pathogenesis of ischemic heart
disease, variant angina, myocardial infarction, and
A 53-year-old male complaining of chest pain at rest was
admitted to our hospital.
The patient had experienced 2-3 minutes of similar epi-
sodes once a month for 2 to 3 years. This time, his chest pain
had lasted for more than 3 hours prior to the admission.
Laboratory data showed a white blood cell count of
14460/mm3, creatine kinase (CK) of 3075 IU/L, CK-MB of
86.9 IU/L, and troponin-I of 16.2 ng/mL. An electrocardio-
gram (ECG) showed ST elevation in the II, III, and aVF leads
and ST depression in the aVL lead. The data indicated an acute
myocardial infarction. Emergent coronary catheterization was
Emergent coronary angiography showed a totally occlud-
ed RCA (Figure 1A). Immediate percutaneous coronary inter-
vention (PCI) for the RCA was conducted. After a guide wire
crossed the lesion, a thrombectomy was performed. Following
thrombus aspiration, an IVUS catheter (View It, Terumo Co.,
Tokyo, Japan) was inserted to visualize the characteristics of
the lesion (Figure 1B and a,b,c).
Diffuse intima plus media thickness was identified at the
obstruction site by IVUS imaging. A thrombus was observed
proximal to the obstruction site. Five mg of ISDN was injected
into the RCA. Following administration of 5 mg ISDN, dilata-
tion of the RCA was confirmed by both coronary angiography
and IVUS (Figure 2A and a,b,c).
The IVUS findings indicated the luminal dilatation was
achieved by the release of the diffuse intima plus media thick-
ening. The residual thrombus was still observed proximal to
From the 1 Department of Cardiology, Gifu Heart Center, Gifu, Japan.
Address for correspondence: Hideaki Ota, MD, Department of Cardiology, Gifu Heart Center, 4-14-4 Yabuta-minami, Gifu City, Gifu 500-8384, Japan.
Received for publication February 7, 2013.
Revised and accepted March 14, 2013.