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Soonchunhyang Medical Science 19(2):115-119, December 2013
pISSN: 2233-4289 I eISSN: 2233-4297
CASE REPORT
Acute Myocardial Infarction with Simultaneous Occlusions of Left Anterior
Descending Artery and Right Coronary Artery
Kyu-Yong Ko, Dae-Hyeok Kim, Tae-Hyeon Hwang, Sun-Young Lee, Sung-Ill Woo, Ho-Yeon Joo, Jin-Chul Kim
Division of Cardiology, Department of Internal Medicine, Inha University School of Medicine, Incheon, Korea
Acute myocardial infarctions involving multiple coronary arteries simultaneously are infrequent and causative risk factors of the occlusions are unclear. However, severe complications arise, such as congestive heart failure or death. We report a case of two simultaneously occluded coronary arteries. A 39-year-old Korean man with simultaneous total occlusion of the left anterior descending artery and the right coronary artery presented with chest discomfort and cardiogenic shock. Immediate percutaneous coronary intervention was performed and a transvenous temporary pacemaker and intra-aortic balloon counterpulsation catheter were inserted. Through continuous effort he was discharged 8 days post intervention without any complaints.
Keywords: Coronary occlusion; Myocardial infarction; Cardiogenic shock
INTRODUCTION
heart rate was 114/min, and his blood pressure was 80/60 mmHg.
An electrocardiogram (ECG) was immediately applied and showed
Acute myocardial infarction (AMI) involving two or more cor-
ST elevation in the inferior (II, III, and aVF) leads and anterior (V1-
onary arteries simultaneously has worse prognosis than a single
V6) leads, and a Q wave in the anterior (V1-V3) leads (Fig. 1), which
artery occlusion regarding a high risk of death [1-3]. We report a
was suggested inferior and anterior AMI. Smoking was the only
39-year-old Korean man with simultaneous total occlusion of the
risk factor for coronary artery disease. A chest X-ray revealed no
left anterior descending artery and right coronary artery, present-
pulmonary congestion. The patient was given 300 mg of aspirin,
ing with chest discomfort, cardiogenic shock, ventricular tachy-
600 mg of clopidogrel and an intravenous heparin infusion as per
cardia and finally asystole. After successful percutaneous coro-
primary PCI protocol, while waiting for emergent PCI. Initial lab-
nary intervention (PCI), the patient was discharged 8 days post in-
oratory data showed Troponin-I < 0.10 ng/mL (range, 0.00 to 0.16
tervention.
ng/mL), creatinine kinase (CK) 193 IU/L (range, 56 to 244 IU/L),
CK-MB isoenzyme 3.2 ng/mL (range, 0.0 to 5.0 ng/mL), myoglobin
CASE REPORT
164 ng/mL (range, 0 to 72 ng/mL), and glucose 437 mg/dL (range,
70 to 100 mg/dL). When the patient arrived at the angiography
In November 2012, a 39-year-old Korean male was referred to
the emergency room (ER) after losing consciousness. While he
room, his heart rate was 40 beats/min and a temporary transvenous pacemaker was inserted (VVI 70 bpm, 10 mA, and 2.0 mV).
was playing baseball, he felt chest pain and soon fainted. When his
Coronary angiography revealed two-vessel coronary disease,
friends noticed that he was pulseless, they started cardiac massage
with a thrombus and total occlusion of the middle right coronary
for about 5 minutes, which led to the regaining of his pulse. A phys-
artery (RCA) (Fig. 2A) and proximal left anterior descending ar-
ical examination showed that his respiratory rate was 20/min, his
tery (LAD). A minimal stenosis at the left main coronary artery
Correspondence to: Dae-Hyeok Kim
Division of Cardiology, Department of Internal Medicine, Inha University School of Medicine, 366 Seohae-daero, Jung-gu,
Incheon 400-103, Korea
Tel: +82-32-8902-2440, Fax: +82-32-890-2447, E-mail: [email protected]
Received: Sep. 9, 2013 / Accepted after revision: Oct. 21, 2013
© 2013 Soonchunhyang Medical Research Institute
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/).
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115
Ko KY, et al. • Simultaneous Double Coronary Artery Occlusion
Fig. 1. Initial electrocardiogram on arrival shows ST elevation in the inferior (II, III, and aVF) leads and anterior (V1-V6) leads, and a Q wave in the anterior (V1-V3) leads.
was also observed (Fig. 2B). There was no significant luminal nar-
hemodynamically stable in New York Heart Association class II,
rowing of the left circumflex artery. We could not find any collat-
and recovered to the normal state of consciousness, maintaining
eral circulation to the RCA or LAD. An intervention was perform-
good urine output, without evidence of ventricular arrhythmias
ed first on the middle RCA. The lesion was crossed with a Runth-
on the monitor. To find out other co-existing diseases which could
rough NS (Terumo, Tokyo, Japan) guidewire easily and smoothly.
create a thrombus formation, we examined the chest computed
After the balloon was dilated, a thrombus formation was revealed.
tomography (CT) and blood tests including anti-phospholipid im-
An angioplasty was performed with an implantation of a 2.75 × 18
munoglobulin G (IgG), anti-cardiolipin IgG, anti-cardiolipin im-
mm Resolute integrity (Medtronic, Galway, Ireland) stent (Fig. 2C).
munoglobulin M, lupus anticoagulant, anti-β2 glycoprotein IgG,
There was neither slow-flow nor no-reflow in the RCA after the
protein C activity, protein S activity, homocysteine and anti-throm-
intervention. However, there was no collateral circulation from
bin III. The examination results showed no thrombus on the chest
the RCA to the LAD and an intervention at the proximal LAD le-
CT or any abnormality in the blood tests. The echocardiogram af-
sion was also performed. The guidewire for LAD lesion was also
ter the procedure showed moderate dysfunction of the left ventric-
easily and smoothly passed. An implantation with a 2.75 × 22 mm
ular systolic function with a mean ejection fraction of 37%, akine-
Resolute integrity stent followed by balloon dilatation was done at
sia of the mid to apical anteroseptal wall, left ventricle apex and
the proximal LAD (Fig. 2D). We did not administer intravenous
basal inferior wall, and severe hypokinesia of the mid inferior wall.
glycoprotein (GP) IIb/IIIa inhibitor as the thrombus was not seen
Eight days later, he was discharged home without chest pain or pul-
in the culprit lesions after the final intervention.
monary congestion. The ECG at the time of discharge showed no
The blood pressure was 60/40 mmHg after the PCI, when an in-
ST elevation (Fig. 3). The patient is free of symptoms and is visiting
tra-aortic balloon counterpulsation (IABP) was introduced (1:1
the out-patient clinic prescribed with aspirin, clopidogrel, statin,
triggered by ECG). However, about 10 minutes after the PCI, all of
angiotensin-receptor blocker, beta-blocker, furosemide, and spi-
a sudden the patient lost consciousness with ECG alterations, no-
ronolactone.
tably in the ventricular tachycardia and then entered asystole. Cardiopulmonary resuscitation with cardioversion was initiated and
DISCUSSION
a spontaneous rhythm of the patient was recovered. After removal
of IABP and the pacemaker, 2 days after admission, the patient
The main causes of the ST segment elevation myocardial infarc-
had no sign of recurrence of chest pain and was electrically and
tion were the plaque rupture and the subsequent thrombosis of a
116
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Soonchunhyang Medical Science 19(2):115-119
Simultaneous Double Coronary Artery Occlusion • Ko KY, et al.
A
B
C
D
Fig. 2. Emergent coronary angiograms during percutaneous coronary intervention. (A) Total occlusion and thrombus formation (arrow) at the middle right coronary artery (RCA). (B) Total occlusion and thrombus formation (arrow) at proximal left anterior descending artery (LAD) and minimal stenosis (arrow head) at the left main coronary artery. (C, D) After intervention, no residual stenosis at the RCA and at the LAD.
single culprit vessel. However, simultaneous occlusions involving
sulting in blood stasis and acute occlusion in another artery with a
more than 2 coronary arteries are not due to local plaque patholo-
severe underlying lesion [4,5], hypercoagulable states, such as ma-
gy. The causative factors involved in the acute and simultaneous
lignancy or thrombocytosis [6,7], and antithrombin III deficiency
thrombosis of multiple coronary vessels are unclear; there are some
[8]. However, when a patient comes to the ER with the impression
reported possible causative factors. These are hemodynamic insta-
of AMI, it is very difficult to verify these causative factors. There-
bility and hypotension due to occlusion of one coronary artery, re-
fore early administration of an ECG and timely angiography are
Soonchunhyang Medical Science 19(2):115-119
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117
Ko KY, et al. • Simultaneous Double Coronary Artery Occlusion
Fig. 3. Electrocardiogram before discharge shows a remaining Q wave in the anterior leads (V1, V2 and V3), but no ST elevation in the inferior leads (II, III, and aVF) and
anterior leads (V1-V6).
important. In this case, an initial ECG taken in the ER showed ST
but has a poorer prognosis than a single vessel disease [6,8]. In one
elevation of two coronary vessel territories (inferior and anterior)
review article, more than 50% of the patients in the previous re-
which made us suspect double vessel occlusion and the following
ports suffered from cardiogenic shock [9]. In addition, an autopsy
angiography confirmed this speculation. As the patient was al-
series in patients who died from AMI report that a thrombotic oc-
ready in cardiogenic shock, thrombolysis was not indicative. An
clusion of more than one major coronary artery is not rare, occur-
emergency PCI for the RCA was primarily done since the patient
ring in up to 50% of the patients [10]. This may suggest the fact
displayed bradycardia. After successful intervention of the RCA,
that AMI with multivessel occlusion often leads to massive myo-
no-reflow or slow-flow was not observed and collateral circulation
cardial damage and death before the patient arrives at the hospital.
to the LAD was not found, therefore we decided to perform a PCI
Fortunately in this case, the patient came to hospital immediately
at the LAD lesion, also. As both lesions were passed by guidewire
and intervention was done promptly. Also, treatment using an
easily and smoothly and there was no collateral circulation from
IABP was effective enough to allow the patient to be discharged
other vessels to the RCA or the LAD, we are sure it is the case of si-
soon after gaining back normal vital signs. Therefore, an early di-
multaneous double vessel occlusion. After coronary intervention
agnosis and proper management are the most important things in
of both the LAD and RCA lesions, neither no-reflow nor slow-flow
the therapeutic course.
was observed and residual thrombus was not seen and therefore
In conclusion, patients with multiple occlusive coronary artery
we did not use GP IIb/IIIa inhibitor. However, we feel at odds about
disease are often in a devastating condition. Cautious attention
the occurrence of cardiac arrest which might have been prevented
must be given for the accurate diagnosis in an abnormal ECG show-
by using GP IIb/IIIa inhibitor. This patient had only one risk fac-
ing ST segment elevation. Further, early diagnosis and proper ma-
tor—smoking. Further, there were no laboratory abnormalities
nagement including timely intervention are the most important
which could cause coagulation problems or other systemic condi-
things in the therapeutic course.
tions such as a pulmonary embolism. In this case, a hemodynamically unstable condition such as cardiac arrest, before arriving at
REFERENCES
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An AMI with simultaneous two or more vessels occurs rarely
118
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