Introduction
Coronary embolism (CE) is an underrecognized, nonatherosclerotic cause of acute myocardial infarction (AMI). Its true prevalence is likely underestimated because diagnosis is challenging in the acute setting, with Shibata et al reporting a prevalence of 2.9% in patients with de novo AMI and Popovic et al reporting 4.3% among patients presenting with ST-segment elevation myocardial infarction (STEMI).1,2 Atrial fibrillation (AF) is the most frequently identified predisposing condition, although cardiomyopathy, valvular heart disease, infective endocarditis, malignancy, prosthetic valves, and hypercoagulable states have also been identified.3,4 The Shibata criteria provide a structured framework for identifying coronary embolism based on angiographic findings, the extent of underlying coronary atherosclerosis, and the presence of potential embolic sources.1 Distinguishing coronary embolism from plaque-mediated coronary thrombosis can nevertheless remain challenging when histopathological confirmation or intracoronary imaging is unavailable. We report a case of inferolateral STEMI with suspected coronary embolism involving the distal right posterolateral ventricular branch (RPLV) in a patient with paroxysmal AF and minimal underlying coronary atherosclerotic disease, illustrating the diagnostic challenge posed by an abrupt distal occlusion and unsuccessful attempts at revascularization.
Case Presentation
A 76-year-old man with a history of paroxysmal atrial fibrillation on apixaban, hypertension, hyperlipidemia, and prior cerebrovascular accident presented with sudden-onset substernal pressure-like chest pain that was nonradiating and not relieved by aspirin 324 mg or sublingual nitroglycerin 0.4 mg. On arrival, his blood pressure was 146/84 mmHg, heart rate 114 beats/min, respiratory rate 15/min, and oxygen saturation 97% on room air. Examination was notable for an irregularly irregular tachycardic rhythm. Initial electrocardiogram demonstrated atrial fibrillation with rapid ventricular response and findings consistent with an inferolateral STEMI (Figure 1). Troponin rose from 10 ng/L initially to 125,000 ng/L. Chest radiography showed mild cardiomegaly and pulmonary vascular congestion without focal consolidation or pleural effusion.
Figure 1 (A) Initial electrocardiography (ECG) showing atrial fibrillation with rapid ventricular rate, ST-segment elevations in leads ii, iii, aVF, V4-V6, and ST-segment depressions in leads V1-V2 consistent with an inferolateral STEMI. (B) ECG on hospital day 3 showing atrial fibrillation with controlled ventricular rate and resolution of prior inferior ST-segment elevations with evolving T-wave inversions consistent with post-infarction changes.
The patient received ticagrelor 180 mg and heparin 5000 units before undergoing emergent coronary angiography. Angiography demonstrated 100% thrombotic occlusion of the distal RPLV branch with Thrombolysis in Myocardial Infarction (TIMI) 0 flow. The remaining coronary arteries showed nonobstructive coronary artery disease, and left ventricular end-diastolic pressure was 9 mmHg. Balloon percutaneous transluminal coronary angioplasty followed by mechanical thrombectomy of the distal RPLV lesion failed to restore distal perfusion, and no stent was implanted (Figures 2 and 3). Because the culprit lesion involved a small distal branch supplying a limited myocardial territory, further aggressive thrombectomy was deferred. No thrombotic material was retrieved for histopathological examination, and intracoronary imaging with intravascular ultrasound or optical coherence tomography was not performed.
Figure 2 Coronary angiographic views of the right coronary artery in the left anterior oblique cranial (LAO-CRA) and right anterior oblique cranial (RAO-CRA) projections. The right posterolateral ventricular (RPLV) branch is a large-caliber vessel that bifurcates at its midportion. The red arrow indicates the site of 100% distal RPLV occlusion with thrombolysis in myocardial infarction (TIMI) 0 flow. The right posterior descending artery (RPDA) is a large-caliber vessel without significant angiographic disease.
Figure 3 Coronary angiographic images of attempted revascularization of the distal right posterolateral ventricular (RPLV) branch. (A) Balloon angioplasty with a 2.0 × 12 mm balloon failed to restore flow, with persistent 100% occlusion and TIMI 0 flow in the distal RPLV. (B) Mechanical thrombectomy of the distal RPLV lesion was also unsuccessful, with no angiographic improvement.
Transthoracic echocardiography demonstrated a left ventricular ejection fraction of 40% to 45% with regional wall motion abnormalities involving the inferolateral territory and no evidence of left ventricular thrombus. Transesophageal echocardiography was not performed. During hospitalization, the patient continued to have episodes of atrial fibrillation with tachycardia, and his metoprolol succinate dose was increased from 25 mg to 50 mg daily, which he tolerated well. According to the Shibata criteria, the patient met one major criterion (angiographic evidence of coronary artery thrombosis without an atherosclerotic component) and two minor criteria (<25% stenosis in nonculprit coronary vessels and the presence of paroxysmal AF as a thromboembolic risk factor), thereby fulfilling the criteria for definite coronary embolism.1 However, this represented a criteria-based clinical classification, as histopathological and intracoronary imaging confirmation of an embolic mechanism was unavailable. The patient was treated medically with apixaban 5 mg twice daily, amiodarone 200 mg daily, clopidogrel 75 mg daily, atorvastatin 40 mg daily, and metoprolol. Given a CHA2DS2-VASc score of 5, long-term anticoagulation with apixaban was continued for thromboembolic prevention. His hospital course was otherwise unremarkable, and he was discharged on hospital day 5. At 1-month outpatient cardiology follow-up, the patient remained asymptomatic, with no recurrent chest pain, dyspnea, or palpitations.
Discussion
According to the Fourth Universal Definition of Myocardial Infarction (2018), acute myocardial infarction is defined as acute myocardial injury in the setting of clinical evidence of acute myocardial ischemia.5 Coronary embolism is categorized in the classification proposed by De Lemos et al as a type C subgroup of Type 1 myocardial infarction (Type 1C MI), reflecting acute coronary obstruction in the absence of plaque rupture.6 In the present case, the patient met diagnostic criteria for acute MI, and the subsequent angiographic and clinical findings raised suspicion for an embolic rather than atherosclerotic mechanism.
Coronary embolism is broadly classified into three etiologic subtypes: direct, paradoxical, and iatrogenic. Among these, atrial fibrillation is the most frequently identified underlying cause and accounts for 73% of cases in the Shibata cohort.1 In our patient, paroxysmal AF was considered the most plausible embolic risk factor, although no definite intracardiac embolic source was identified.
AF-related coronary embolism presenting as STEMI has been described previously. Shah et al reported a patient with paroxysmal AF and anterior STEMI caused by thrombotic occlusion of the left anterior descending artery in the setting of minimal underlying coronary disease, in whom thrombosuction retrieved a substantial thrombus.7 In contrast, our patient had an abrupt distal RPLV occlusion with minimal underlying atherosclerotic disease, unsuccessful attempts at revascularization, and no thrombotic material available for histopathological confirmation. Therefore, the clinical value of this case lies not in the rarity of AF-associated coronary embolism itself, but in the diagnostic uncertainty encountered when clinical and angiographic criteria support an embolic mechanism despite the absence of definitive pathological or intracoronary confirmation.
The diagnostic workup of suspected coronary embolism should integrate angiographic findings with a search for an embolic source and for extracoronary embolization. Aspiration thrombectomy may serve not only as a reperfusion strategy but also as a diagnostic tool, because histopathological examination of aspirated thrombotic material may help determine the nature and origin of the embolus.3 If thrombus aspiration restores coronary flow and the underlying vessel appears angiographically normal, intravascular ultrasound or optical coherence tomography may be considered to evaluate for plaque erosion and to help distinguish an embolic from a plaque-mediated mechanism.4 Transthoracic and transesophageal echocardiography are useful for detecting left ventricular thrombus, left atrial appendage thrombus, valvular lesions, or intracardiac shunts.8 Cardiac magnetic resonance imaging may be particularly useful when coronary angiography is nondiagnostic or when myocardial infarction with nonobstructive coronary arteries is under consideration.9 Concomitant extracoronary systemic embolization may provide an additional diagnostic clue and has been reported in approximately 23% of CE-related MI cases, most commonly as cerebral infarction, followed by acute limb ischemia and renal or splenic infarction.1
In the acute setting, management of coronary embolism generally follows the standard STEMI pathway, with early administration of antiplatelet therapy, high-intensity statin therapy, and urgent coronary angiography with the intent to achieve reperfusion, because the diagnosis is seldom established before catheterization.3 Once an embolic mechanism is suspected, however, treatment becomes more individualized according to the underlying etiology. Long-term oral anticoagulation is central to secondary prevention, particularly in AF-related CE.3,4 Recognition of coronary embolism is important because outcomes appear worse than those of atherosclerotic myocardial infarction. In the Shibata cohort, recurrent thromboembolism occurred in 10.4% of patients during follow-up, and the 5-year rate of major adverse cardiac and cerebrovascular events was 27.1%.1 More recent data in STEMI patients with atrial fibrillation also demonstrated excess early mortality in CE, with an adjusted 45-day mortality of 18% vs 5% in patients without AF or CE.10
Several limitations should be acknowledged. Although the clinical and angiographic findings fulfilled the Shibata criteria for definite coronary embolism, this represents a criteria-based clinical classification rather than pathological confirmation of the embolic mechanism. No thrombotic material was available for histopathological examination, and intracoronary imaging with intravascular ultrasound or optical coherence tomography was not performed to evaluate for underlying plaque rupture or erosion. Transthoracic echocardiography showed no left ventricular thrombus, and transesophageal echocardiography was not performed; therefore, a definite intracardiac embolic source was not demonstrated. Alternative mechanisms, including plaque erosion or in situ coronary thrombosis, cannot be completely excluded. In addition, unsuccessful balloon angioplasty and mechanical thrombectomy are not specific evidence of an embolic mechanism. Finally, this is a single-patient case with follow-up limited to one month, restricting assessment of recurrent thromboembolic events and longer-term outcomes.
Conclusions
Coronary embolism should be considered in patients presenting with STEMI and atrial fibrillation when coronary angiography demonstrates an abrupt distal occlusion with minimal underlying atherosclerotic disease. In this case, the clinical and angiographic findings and fulfillment of the Shibata criteria supported a suspected coronary embolic mechanism, although histopathological or intracoronary imaging confirmation was unavailable. Management should be individualized according to the myocardial territory at risk, procedural feasibility, and the patient’s underlying thromboembolic risk. Evaluation for potential embolic sources and appropriate guideline-based thromboembolic prevention in patients with atrial fibrillation remain important for secondary prevention.
Data Sharing Statement
All data supporting the findings of this case report are included within the article. No additional datasets were generated or analyzed.
Ethics Approval
Institutional review board approval was not required for this single-patient case report in accordance with local institutional policy.
Consent for Publication
Written informed consent was obtained from the patient for publication of this case report and accompanying images.
Author Contributions
All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.
Funding
No funding was received for this study.
Disclosure
The authors report no conflicts of interest in this work.
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