Multiple Coronary Artery Thrombosis in a 41-Year-Old Male Patient Presenting with ST-Segment Elevation Myocardial Infarction

ABSTRACT: Simultaneous occlusion of multiple epicardial coronary arteries is an uncommon finding in patients presenting with ST-segment elevation myocardial infarction (STEMI). We describe a 41-year-old male Asian patient who presented with inferior and anterior STEMI complicated by cardiogenic shock and frequent life-threatening ventricular arrhythmias. The patient was subsequently found to have acute occlusion of the proximal right coronary artery (RCA) and proximal left anterior descending coronary artery (LAD). The patient was treated with primary percutaneous coronary interventions for RCA and LAD, and intra-aortic balloon pump placement showed excellent results. Based on the available literature, early PCI for this very rare condition is paramount for patient survival.

J INVASIVE CARDIOL 2012;24(3):E43-E46

Key words: ST-segment elevation myocardial infarction, multiple coronary artery occlusions, percutaneous coronary intervention, intra-aortic balloon pump

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Acute coronary syndromes (ACS) are clinical events that cause considerable immediate morbidity and mortality.^1,2 Atherosclerotic plaque rupture with a broken or eroded capsule seems to be the trigger for acute thrombotic occlusion on one coronary artery.^3-5 Simultaneous occlusion of more than one coronary artery is an uncommon clinical finding in patients with ST-segment elevation myocardial infarction (STEMI) and patients are usually critically ill at presentation; the recognition of this condition is paramount for appropriate management, specifically immediate percutaneous coronary intervention (PCI).^6-35 Herein, we present a case and review the literature about reported cases of multiple coronary artery thromboses. 

Case Report. A 41-year-old male Asian patient admitted to the hospital in early 2011 with severe central chest pain. The patient had diabetes mellitus, hypertension, and was a cigarette smoker. The patient had no prior coronary artery disease history and no family history of cardiovascular disease. He denied illicit drug use. On physical examination, the patient was drowsy, pale, and sweating. He had a regular heart rate of 48 BPM. The patient was hypotensive with systolic blood pressure of 60 mmHg and diastolic blood pressure of 40 mm Hg. ECG demonstrated initially normal sinus rhythm, ST-segment elevation in leads II, III, aVF, and in leads V1-4 (Figure 1). The patient received aspirin, 600 mg of clopidogrel, unfractionated heparin, and front loading of glycoprotein IIb/IIIa inhibitor (tirofiban) followed by infusion. He was referred for urgent cardiac catheterization. Upon arrival to the cardiac catheterization laboratory, an intra-aortic balloon pump was placed for hemodynamic support. Coronary angiography showed occlusion of the proximal right coronary artery (RCA) and the proximal left anterior descending (LAD) coronary artery (Figure 2). The procedure was complicated by more than 20 episodes of ventricular fibrillation requiring resuscitation. Percutaneous balloon angioplasty and placement of 2 stents resulted in TIMI III flow in both the LAD and RCA. Echocardiography immediately after PCI showed a left ventricular ejection fraction of 46% with hypokinetic anterior wall. He was maintained on dual antiplatelet therapy with aspirin and clopidogrel.

Initial laboratory data showed hemoglobin of 12.6 h/dL. The patient’s white cell count was 19.1/mm³, and his creatinine was 66 μmol/L. His peak troponin T level was 327 ng/mL. The patient was extubated on day 3, and remained clinically stable. Evaluation for hypercoagulability including lupus anticoagulant, anticardiolipin IgM, Ig G, homocysteine, and Factor V Leiden, were all negative. The patient was discharged 9 days later. On the day of discharge, repeat echocardiography showed normal left ventricular ejection fraction of 64% with no regional wall motion abnormalities.

Discussion. We present an infrequent clinical and angiographic finding in a young patient with STEMI. The patient had concomitant occlusion of the LAD and RCA resulting in simultaneous anterior and inferior STEMI, which resulted in cardiogenic shock and life threatening ventricular arrhythmias. Despite the unstable presentation, early PCI and IABP resulted in excellent recovery.

Atherosclerotic plaque rupture or erosion was originally thought to occur only in the culprit vessel and at a specific site. More recently, several investigators using coronary angiography, intravascular ultrasound, and angioscopy showed that multiple plaque ruptures are frequent in acute coronary syndromes and can be detected in different coronary arteries.^3,4,36 Goldstein et al reported 39.5% of patients to have multiple complex plaques after analyzing coronary angiograms of 253 patients presenting with acute myocardial infarction (MI). When compared to patients with single complex plaques, patients with multiple complex plaques were at increased risk of repeat ACS, PCI, particularly of the non-infarct related lesions and coronary artery bypass grafting.⁴ The investigators concluded that plaque instability may be due to a widespread process throughout the coronary vessels, which may have implications in the clinical management of ACS. In an angioscopic evaluation of all major coronary arteries of 21 Japanese patients presenting with acute MI, Asakura et al revealed equal prevalence of vulnerable plaques in culprit and non-culprit arteries,³⁶ suggesting that acute MI represents the pan-coronary process of vulnerable plaque development. Rioufol et al reported similar observations using intravascular ultrasound evaluation of the coronary arteries in 24 patients presenting with ACS.³

Despite the fact that multiple vulnerable coronary plaques are commonly observed among patients presenting with ACS, thrombotic occlusion of more than one coronary artery is very uncommon. In a retrospective review of all patients treated with primary PCI at 2 university medical centers in the United States (University of Virginia, Charlottesville [2000-2006] & University of Texas Southwestern Medical centers, Dallas [2004-2007]), Pollack et al7 identified 18 patients (2.5%) with angiographically documented multiple culprit arteries. Most patients were Caucasians (61%), male (89%), and had histories of current tobacco use (56%). Similar to our finding, the investigators reported high incidence of clinical and hemodynamic instability in these patients: 28% of patients were in cardiogenic shock; 22% had life threatening ventricular arrhythmias; and 22% of patients required IABP. Moreover, consistent with our finding, despite their unstable presentations and large extents of myocardial damage, nearly all patients survived to hospital discharge with few major in-hospital adverse events.

Several possible underlying conditions for multiple coronary thromboses have been reported including: hypercoagulable state due to malignancy or thrombocytosis, hyperhomocysteinemia, human immune deficiency syndrome, coronary artery spasm, atrial fibrillation, and illicit drug use such as cocaine and amphetamine (Table 1). However, in the vast majority of reported cases, there were no underlying conditions apart from the usual cardiovascular risk factors.

Conclusion

Simultaneous coronary artery thrombosis in the setting of STEMI is very rare and is usually associated with cardiogenic shock and life threatening arrhythmia. Early PCI is associated with excellent short-term outcome.

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From the Department of Cardiology and Cardiovascular Surgery, Hamad Medical Corporation (HMC), Qatar.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted August 3, 2011, provisional acceptance given September 7, 2011, final version accepted September 12, 2011.
Address for correspondence: Jassim Al Suwaidi, MB, ChB, FACC, FSCAI, FESC, Department of Cardiology and Cardiovascular Surgery, Hamad General Hospital (HMC), P.O Box 3050, Doha, Qatar. E-mail: Jha01@hmc.org.qa; jalsuwaidi@hotmail.com