• Full Screen
  • Wide Screen
  • Narrow Screen
  • Increase font size
  • Default font size
  • Decrease font size

Acute double vessel myocardial infarction from the territory of te Left Anterior Descending artery (LAD) and the Right Coronary Artery (RCA), complicated by dissection of Left Main Coronary Artery (LMCA). A Case report.


Borislav Atzev, Yordan Dzhumean, Georgi Lyutov, Dima Vasenska
Clinic of Cardiology, MHAT “Puls”, 62 Slavyanska Str., Blagoevgrad 2700, Bulgaria
Tel. +359-88-8755-370
e-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

Summary: Acute myocardial infarction of two vascular territories is known as double or combined myocardial infarction. In this case report we have represented a fourty year old man with anterior and inferior myocardial infarction. Emergency coronary angiography showed thrombotic occlusion in the Left Anterior Descending artery (LAD) mid segment as well as subtotal thrombotic occlusion in the Right Coronary Artery (RCA) mid segment. Emergency coronary angiography was performed to the infarct related arteries. Due to iatrogenic dissection of the Left Main Coronary Artery (LMCA) we undertook percutaneous coronary intervention (PCI) of LMCA with good angiographic result. After one month, control coronary angiography showed no significant stenosis of the LAD, RCA and LM.

Key words: double vessel myocardial infarction, coronary artery disease, PCI.

Acute myocardial infarction (AMI) involving acute transmural ischemia of two vascular territories at the same time, is known as double or combined infarction [1]. It has been reported rarely in most series of patients admitted for AMI due to its poor clinical outcomes. The iatrogenic dissection of LMCA is uncommon, but potentially serious complication that requires prompt management using angioplasty.

We report a case of a 40-year old man who presented in the emergency department with constricting chest pain with onset at rest and of around two hours.


His risk factors for coronary artery disease was smoking (20 cigarettes/day for the last 10 years). The patient had no prior coronary artery disease history and no family history of cardiovascular disease. On admission, he was symptomatic, in Killip class II. Physical examination showed pale and wet skin, his blood pressure was 100/60 mmHg and his heart rate was 105 beat per min. The 12-lead electrocardiogram (ECG) showed sinus rhytm, ST-elevation in I, II, III, aVF, V1-V6 indicating recent acute anterior and inferior acute myocardial infarction (AMI) (Fig.1). The blood tests at admission did not show the abnormal elevation of creatinine phosphokinase (CPK), MB fraction and Troponin I. The echocardiography showed diffuse hypokinesia, left ventricular ejection fraction (LVEF) was calculated as 20% by the 2-dimensional Simpson's method. The patient was given Aspirin 325 mg as well as Clopidogrel 600mg. Emergency coronary angiography was performed using the right femoral approach. It showed thrombotic occlusion in the LAD, mid segment with Trombolysis in Myocardial Infarction (TIMI) grade 0 flow, as well as subtotal thrombotic occlusion in the RCA with TIMI grade I flow. We undertook emergency percutaneous transluminal coronary angioplasty (PTCA) for the LAD and RCA lesion. After triple thrombus aspiration and predilatation a bare metal stent (BMS) 3.00/24mm was inserted in the LAD, inflated to 12 atm (Fig.2). Due to iatrogenic dissection of LM, we directly inserted another BMS 4.00/8mm (Fig.3). After that, two BMS were inserted in RCA – 4.00/16mm and 4.00/8mm, inflated to 16 atm (Fig.4). Finally, TIMI grade III flow was observed in both LAD and RCA. The patient was entirely pain free at the end of the intervention. He was transferred to the intensive care unit where he was treated with intravenous Heparin (1000 U/hr), Eptifibatide. The hospital course was uneventful. Serum creatine phosphokinase peaked at 2287 IU /l, its MB fraction at 286 IU/l, Troponin I 1,8ng/ml. The patient was discharged without a cardiac episode on dual antiplatelet therapy. ECG indicated poor R-wave progression in the anterior leads as well as abnormal Q waves in the inferior leads. The left ventricular ejection fraction was 30% with akinesia of the apical area. After one month, control coronary angiography showed no significant stenosis of the LAD, RCA and LM.

Discussion: AMI commonly occurs through occlusion of a coronary artery by atheromatous plaque rupture followed by thrombus formation [2]. Acute simultaneous occlusion of two or three coronary vessels is very uncommon, difficult to diagnose without angiography and shows poor prognosis and high mortality. There have been reported several predisposing factors such as multivessel spasm [3,4], state of hypercoagulability [5], hyperhomocysteinaemia [6,7], and essential thrombocythaemia [8,9], hormone therapy [10], in some patients with amphetamine abuse [11] and gastric cancer [12]. The decrease of coronary pressure after single vessel occlusion at the onset of myocardial infarction has been thought to be involved in the mechanism of combined myocardial infarction [13]. It has been established that heightened inflammatory response and catecholamine surge during AMI may lead to a second coronary arterial occlusion [3]. Autopsy studies reveal that thrombotic occlusion of more than one major epicardial coronary artery is not uncommon, occurring in up to 50% of patients with infarction [14]. On the other hand Pollak et al. found 18 cases (2.5%) of multiple culprit arteries in a series of 711 patients undergoing primary PCI [15]. This discordance can be explained by the fact that the development of multiple coronary occlusions is often fatal, resulting in sudden cardiac death. Pollak et al. emphasize the seriousness of this condition due to the fact that a third of the patients were presented in cardiogenic shock and a quarter of them had life threatening arrhythmias. In addition to the listed above predisposing factors, Pollak et al. discuss the influence of additional comorbidities such as atrial fibrillation, a history of cancer, HIV infection that can lead to this life threatening condition [15]. It has been reported that double vessel myocardial infarction involves mostly the RCA and LAD. There is only one case to describe the involvement of the LAD and RCx [15]. The main question that arised during the emergent coronary intervention was which of the infarcted vessels to be treated first with angioplasty. Because of the fact that the LAD had TIMI grade 0 flow, whereas the RCA showed TIMI grade I flow we performed immediate PCI of the LAD.

The case presented here is unusual because it shows a young patient with combined myocardial infarction, complicated by iatrogenic dissection of LM. The incidence rate of this life threatening complication has been reported of 0.02% [16]. Some authors have established that the dissection of LM should be treated immediately using stenting even in case of initial TIMI grade III flow and hemodynamic stability [16]. There have been described very few cases with conservative treatment of LMCA in case of low-grade dissection and asymptomatic and hemodynamically stable patients [17].

We suppose that emergency coronary angiography with full revascularization prevents the development of cardiogenic shock and life threatening arrhythmia, and is associated with excellent short-term outcome. In emergency conditions due to the necessity of immediate technical actions there is an increased risk of complications, in our case dissection of LM. These complications should be treated according to the hemodynamic status of the patient, clinical outcome and prognosis.













1. Sia, S.K., C.N. Huang, K.C. Ueng, et al. Double vessel acute myocardial

infarction showing simultaneous total occlusion of left anterior descending artery and right coronary artery. - Circ J., 72, 2008, 1034-1036.


2. Goldstein, J.A., D.Demetriou, C.L. Crines, M. Pica, M. Shoukfeh, W.W. O’Neill. Multiple complex coronary plaques in patients with acute myocardial infarction. - New Eng J Med., 343, 2000, 915–922.


3. Vincent, G.M., J.L.Anderson, H.W.Marshall. Coronary spasm producing coronary thrombosis and myocardial infarction. - N Engl J Med., 309, 1983, 220-223.


4. Benacerraf, A., J.M. Sholl, F. Achard, M. Tonnelier, G. Lavergne. Coronary spasm and thrombosis associated with myocardial infarction with nearly normal coronary arteries. – Circulation, 67, 1983, 1147-1150.


5. Reiner, A.P., D.S. Siscovick, F.R. Rosendaal. Hemostatic risk factors and arterial thrombotic disease. - Thromb Haemost, 85, 2001, 584-595.


6. Glueck, C.J., R.N. Fontain, A.Gupta, M.Alasmi. Myocardial infarction in a 35-year-old man with homocysteinemia, high plasminogen activator inhibitor activity, and resistance to activated protein C. – Metabolism, 46, 1997, 1470-1472.


7. Politi, L., D.E.Monopoli, M. G. Modena. ST-segment elevation myocardial infarction with concomitant multiple coronary arteries thromboses in a young patient with hyperhomocysteinaemia. - Heart, 94, 2008, 1180-1188.


8. Terada, H., H.Satoh, A.Uehara. Multivessel coronary thrombosis, acute myocardial infarction, and no reflow in a patient with essential thrombocythaemia. – Heart, 83, 2000, 1180-1189.


9. Virmani, R., M.A. Popovsky, W.C. Roberts. Thrombocytosis, coronary thrombosis and acute myocardial infarction. - Am J Med., 67, 1979, 498-506.


10. Nakagawa, T., M.Yasuno, H.Tanahashi, S.Ohnishi, M.Nishino, Y.Yamada, H.Abe. A case of acute myocardial infarction. Intracoronary thrombosis in two major coronary arteries due to hormone therapy. – Angiology, 45, 1994, 333-338.


11. Wei-Ren, Lan, H.-I. Yeh, Ch.Jia-Yin Hou, Y.Chou. Acute Thrombosis of Double Major Coronary Arteries Associated with Amphetamine Abuse. - Acta Cardiol Sin., 23, 2007, 268-272.


12. Tokita, YYS, N.Hata, M.Takano. Acute myocardial infarction due to simultaneous occlusion of two main coronary arteries in a patient with advanced gastric cancer—a case report. – Int.J.Angiol., 13, 2004, 127-130.


13. Antman, E.M., E.Braunwald. Acute myocardial infarction. A textbook of cardiovascular medicine. Philadelphia, Pennsylvania, 2001.


14. Davies, M.J., A.Thomas. Thrombosis and acute coronary-artery

lesions in sudden cardiac ischemic death. - N Engl J Med., 310, 1984, 1137-1140.


15. Pollak, P.M., S.V. Parikh. Multiple culprit arteries in patients with ST segment elevation myocardial infarction referred for primary percutaneous coronary intervention. - Am J Cardiol., 104, 2009, 619-623.


16. Namazi, M., R. Rostami. Iatrogenic left main artery dissection: A catastrophic complication. – Exp. Clin. Cardiol., 4, 2012, 254–256.


17. Celik, M., U. Cagdas. Conservative treatment of iatrogenic left main coronary artery dissection: report of two cases. – Cardiovasc. Diagn. Ther., 4, 2013, 244–246.


You are here: Articles Acute double vessel myocardial infarction from the territory of te Left Anterior Descending artery (LAD) and the Right Coronary Artery (RCA), complicated by dissection of Left Main Coronary Artery (LMCA). A Case report.