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Soonchunhyang Med Sci > Volume 21(1); 2015 > Article
Yim, Kim, Kim, Kim, Kim, and Kim: Acute Myocardial Infarction with Simultaneous Thrombosis of Multiple Coronary Arteries

ABSTRACT

Simultaneous thrombosis of multiple coronary arteries in acute myocardial infarction is very rare in clinical settings. Its mechanism is not yet clear, but patients displaying multivessel simultaneous thrombosis tend to have poor clinical outcomes. Hence, it is important to recognize this condition and provide timely and proper management. We report a case of simultaneous thrombosis involving multiple coronary arteries in a patient with ST-segment elevation myocardial infarction.

INTRODUCTION

Acute myocardial infarction (AMI) simultaneously involving multiple coronary arteries is rare [1,2]. Many patients with multivessel thrombosis in AMI are clinically ill and have a poor prognosis, including death [3]. Therefore, it is very important to recognize this condition and provide prompt and appropriate management for patients. We report a case of documented multivessel thrombosis in ST-segment elevation myocardial infarction (STEMI).

CASE REPORT

A 41-year-old male came to our emergency room (ER) with tight anterior chest pain lasting for several hours. His vital signs showed his blood pressure to be 100/70 mmHg, with a heart rate of 80/min and a respiration rate 26/min. The oxygen saturation in the room air was 100%. The rest of the physical examination, including the breathing sound and chest X-ray, was unremarkable. Electrocardiography (ECG) revealed ST-segment elevation in the inferior leads (II, III, and aVF) and anterior leads (V3-V5), and ST-segment depression in the lateral leads (I and aVL) (Fig. 1). Findings detected in portable echocardiography in the ER were severe left ventricular (LV) systolic dysfunction with left ventricular ejection fraction (LVEF) of 25% to 35% and akinesia of left anterior descending artery (LAD) territory. Initial laboratory tests showed: troponin-I 0.23 ng/mL, creatinine kinase (CK)-myocardial band (MB) isoenzyme 4.90 ng/mL, CK 164 IU/L, glucose 274 mg/dL, aspartate aminotransferase 64 IU/L, alanine aminotransferase 74 IU/L, cholesterol 210 mg/dL, low density lipoprotein cholesterol 136.6 mg/dL, high density lipoprotein cholesterol 46 mg/dL, and white blood cell 15.2 ×103 /μL. He has had hypertension and type 2 diabetes mellitus and has been smoking half a pack of cigarettes per day for 20 years.
We moved him to a coronary angiography (CAG) room for intervention, just after seeing his ECG and portable echocardiographic findings. When arriving at the CAG room, he collapsed with dropped blood pressure at 80/50 mmHg, and his consciousness changed to a drowsy state. We began resuscitation with intravenous dopamine at a rate of 2.2 μg/kg/min, and then performed his coronary angiogram. Its findings were multiple coronary artery thrombotic occlusions; total occlusions of the proximal LAD, right coronary artery (RCA), and left circumplex artery (LCX) (Fig. 2A-C). In addition, we could not find any collateral flow to LAD, RCA, and LCX territories. Fortunately, the flow to the ramus intermedius artery (RI) and obtuse marginal artery (OM) were preserved with thrombosis in myocardial infarction (TIMI) flow 2. We first performed the intervention on the proximal LAD which we thought was the culprit vessel for this STEMI. The LAD lesion was passed smoothly with a 0.03556 cm guidewire (Runthrough; Terumo, Tokyo, Japan). A Xience prime stent (Abbott Vascular, Sana Clara, CA, USA) 3.5×33 mm was deployed after ballooning, resulting in TIMI flow 3 and weak collateral flow from LAD to LCX territory (Fig. 3A). However, his chest pain was becoming aggravated, and his blood pressure (BP) dropped to 60/50 mmHg, despite the successful coronary angioplasty on the proximal LAD. Immediately, we were able to maintain systolic BP above 90 mmHg with volume infusion and intracoronary epinephrine injection. We moved to the second intervention of the proximal RCA. Wire-passing using 0.03556 cm guidewire (Runthrough, Terumo, Tokyo, Japan) to the lesion at RCA was also smooth. Another Xience prime stent (Abbott Vascular) 3.5×38 mm was well positioned after ballooning. After successful intervention on the proximal RCA, the flow of RCA was good (TIMI flow 3) and the patient’s chest pain was relieved (Fig. 3B). Furthermore, we could not find any collateral flow from the RCA to LCX territory.
We also tried to perform the third intervention on the proximal LCX using 0.03556 cm guidewire (Runthrough, Terumo), but we failed to pass through the lesion (Fig. 3C). Moreover, the BP of the patient was unstable, dropping again to 80/60 mmHg with hemodynamic support, including inotropics and intravenous volume infusion. We decided to defer the intervention on the proximal LCX and moved the patient to the intensive care unit.
The day after the intervention, the echocardiography revealed LV systolic dysfunction with EF of 28%, akinesia of inferior and septal walls, including apex, and hypokinesia of the anterior wall from base to mid LV. The serial cardiac enzyme reached the peak level, troponin-I 146.74 ng/mL and CK-MB isoenzyme 530.75 ng/mL, and then began to decrease. He was discharged after an inhospital treatment of 6 days. The EKG before discharge showed ST-segment resolution (Fig. 4). He has visited our out-patient clinic regularly without any symptoms for several months.

DISCUSSION

Multiple coronary thromboses involving two or more epicardial coronary vessels in previously normal coronary arteries are very rare [1,2]. In pathological studies, multiple coronary thromboses were found in about 10% of patients who died from AMI [4]. The patients with multiple coronary artery thromboses tend to have more severe clinical outcomes, including cardiogenic shock and death [3]. Moreover, the presence of coexisting chronic total occlusion (CTO) lesions in patients with AMI is associated with poor prognosis. In one study, 1-year mortality rates of patients with multivessel disease (MVD) and concomitant CTO lesions undergoing rescue percutaneous coronary intervention is higher than those with MVD without CTO lesions (27% and 13%, respectively) [5]. In another study, patients with CTO lesions were more likely to be associated with cardiogenic shock, lower LVEF and frequent use of assist devices as compared to patients without CTO lesions in AMI [6].
In our case, when the patient arrived at the ER, he complained about chest pain. His ECG and portable echocardiography showed a high possibility of AMI involved in LAD and/or RCA. However, the coronary angiogram revealed total occlusions of LCX, LAD, and RCA, findings which were more severe than we expected. Immediate angioplasty on LAD and RCA was done successfully within 4 hours from the time of the development of his chest pain, and it took about 40 minutes to finish the entire procedure in the angioroom. We used 200 mL of contrast agent during angioplasty.
Initially, we thought that the patient might suffer a more severe clinical course because he displayed total occlusion of three coronary vessels and cardiogenic shock. However, he recovered better than we expected without severe cardiopulmonary complications. We believe that the flow from OM or RI might contribute to the survival and better outcome of the patient. Moreover, the timely angioplasty might influence positive effects on the better outcome of the patient.
Pathophysiologic conditions causing multiple coronary thromboses are unclear. However, several possible mechanisms for multiple coronary artery thromboses have been suggested, including the thrombus due to multivessel spasm [7], the state of hypercoagulability [8], the decreased blood flow to other coronary arteries after AMI [2], and diabetes mellitus (DM) [9]. Smoking and alcohol are also related to increased risks of coronary artery thrombosis by accelerating platelet aggregation and adhesion and by impairing endothelium dependent vasodilation [10]. In our case, the patient had a risk factor of coronary artery disease, including type 2 DM, hypertension, and smoking, which might be involved in the development of acute simultaneous occlusion of multiple coronary arteries by causing a hypercoagulable state.
We speculate that both LAD and RCA total occlusions were caused by simultaneous thrombosis of coronary arteries because there was no collateral circulation from other vessels to LAD and RCA territories, and both LAD and RCA lesions were passed easily by guide wire. However, LCX lesions might be considered as CTO, as it had the collateral flow from LAD to LCX territories after intervention on the proximal LAD, and it was too firm for the guide wire to pass through, despite several attempts.
In conclusion, AMI involving multiple coronary arteries is a very rare but life-threatening condition. Moreover, it is not easy to differentiate multivessel coronary thrombosis from AMI in the ER. If we recognize such a condition and provide timely and appropriate management, we might exert a good influence of the prognosis of patients with mutivessel coronary artery thrombosis.

Fig. 1.
Electrocardiogram on arrival shows ST-segment elevation in the anterior leads and inferior leads, and ST-segment depression in the lateral leads.
sms-21-1-24f1.tif
Fig. 2.
Coronary angiogram. (A) Total occlusion of the proximal LAD (thick arrow). There seen RI (black arrow head) and OM (white arrowhead). (B) Total occlusion of the proximal right coronary artery (thick arrow). (C) Total occlusion of the proximal left circumplex artery (thin arrow) and LAD (thick arrow). The flow to the RI (black arrow head) and OM (white arrowhead) were preserved with thrombosis in myocardial infarction flow 2 each. LAD, left anterior descending artery; RI, ramus intermedius artery; OM, obtuse marginal artery
sms-21-1-24f2.tif
Fig. 3.
Coronary angiogram after intervention. (A) Successful implantation of everolimus-eluting stent at the proximal LAD resulted in TIMI flow 3 (thick arrow) and weak collateral flow from LAD to LCX territory (not seen in this figure). (B) Successful implantation of everolimus-eluting stent at the proximal right coronary artery resulted in TIMI flow 3 (thick arrow). (C) Stent implantation was failed as the guidewire could not passthrough the LCX lesion. Therefore, blood flow could be seen only in the obtuse marginal artery (white arrow head), ramus intermedius artery (black arrow head), and revasculized LAD (thick arrow). LAD, left anterior descending artery; TIMI, thrombosis in myocardial infarction; LCX, left circumplex artery.
sms-21-1-24f3.tif
Fig. 4.
Electrocardiogram before discharge shows ST-segment resolution.
sms-21-1-24f4.tif

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