Paradoxical Coronary Artery Embolism Through a Patent Foramen Ovale in a Young Adult

Abstract

We describe the case of a 26-year-old man who presented with acute chest pain and was found to have single-vessel coronary occlusion most consistent with probable paradoxical embolism. Coronary angiography demonstrated complete occlusion of the ramus intermedius artery. Aspiration thrombectomy restored flow without stent implantation. Intravascular ultrasound showed no plaque rupture, atherosclerosis, or coronary dissection, supporting but not definitively confirming an embolic etiology. Transthoracic and transesophageal echocardiography subsequently identified a large patent foramen ovale with bidirectional shunting. Lower-extremity Doppler studies and an extensive hypercoagulable evaluation were negative. The patient later underwent successful percutaneous closure of the patent foramen ovale. This case highlights probable paradoxical coronary embolism as a rare cause of acute myocardial infarction in a young patient without significant atherosclerotic disease and underscores the value of multimodality imaging in supporting the diagnosis and guiding management.

1. Introduction

Paradoxical embolism refers to the passage of thrombotic material from the venous to the arterial circulation through a right-to-left shunt. The most common anatomical substrate is a patent foramen ovale (PFO), which is present in roughly one quarter of adults [1,2]. Although PFO is usually clinically silent, transient increases in right-sided cardiac pressure may permit embolic material to cross the interatrial septum and enter the systemic circulation.

Paradoxical embolism is most commonly discussed in the setting of cryptogenic stroke, but systemic arterial embolization may also affect peripheral arteries, visceral vessels, and, rarely, the coronary circulation [3,4,5,6]. Coronary embolism accounts for a small proportion of acute myocardial infarction cases and may be under-recognized, particularly in younger patients without significant atherosclerotic risk factors or angiographic evidence of coronary artery disease [7,8]. In such cases, identification of an embolic source has important implications for secondary prevention.

Multimodality imaging is central to diagnosis. Coronary angiography identifies the culprit vessel and pattern of occlusion, while intravascular imaging such as intravascular ultrasound (IVUS) can help exclude plaque rupture, plaque erosion, and spontaneous coronary artery dissection [9,10]. Echocardiography, particularly transesophageal echocardiography (TEE), is essential for identifying a PFO or other intracardiac shunt and for excluding alternative cardiac sources of embolism [11,12].

We report a case of acute myocardial infarction in a young adult most consistent with probable paradoxical coronary embolism through a large PFO. The case illustrates how angiography, IVUS, transthoracic echocardiography, and TEE can be integrated to establish the diagnosis and guide definitive management.

2. Case Description

A 26-year-old man with a history of tobacco use presented to the emergency department with sudden onset substernal chest pain radiating to the left arm. The pain was severe, pressure-like, and associated with palpitations and nausea. He denied exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, prior episodes of exertional chest pain, syncope, recent surgery, prolonged immobility, or known thromboembolic disease. He had no known cardiovascular history and denied illicit drug use. Family history was notable for premature myocardial infarction in his father, but there was no known family history of thrombophilia, venous thromboembolism, spontaneous coronary artery dissection, or inherited cardiac disease.

On presentation he was hemodynamically stable, with a blood pressure of 132/99 mmHg, a heart rate of 66 beats per minute, and an oxygen saturation of 92% on room air. Cardiac examination revealed normal heart sounds without murmurs, rubs, or gallops. Lungs were clear bilaterally. Peripheral pulses were intact and symmetric, and there was no lower-extremity edema or calf tenderness.

Initial laboratory testing showed elevated high-sensitivity cardiac troponin of 152 pg/mL, which later peaked at 615 pg/mL. Electrocardiography demonstrated T-wave inversions in leads V1–V4, consistent with ischemia (Figure 1). Given persistent symptoms and rising biomarkers, emergent coronary angiography was performed.

Angiography demonstrated complete occlusion of the ramus intermedius artery. Aspiration thrombectomy was performed with restoration of coronary flow and without need for stent placement. Post-thrombectomy angiography confirmed brisk restoration of flow (Figure 2A). IVUS of the culprit segment showed no plaque rupture, no evidence of underlying atherosclerotic disease, and no coronary dissection, findings that supported, but did not definitively confirm, an embolic mechanism rather than primary atherothrombotic myocardial infarction (Figure 2B).

Additional evaluation was undertaken to identify the embolic source. Lower-extremity Doppler ultrasound studies were negative for deep vein thrombosis. Transthoracic echocardiography demonstrated mildly reduced left ventricular systolic function with estimated ejection fraction 45–49% and global hypokinesis. Bubble study demonstrated interatrial shunting. Transesophageal echocardiography confirmed a large patent foramen ovale with bidirectional shunting across the interatrial septum and no evidence of left atrial appendage thrombus or intracardiac mass (Figure 3).

Given the patient’s age, absence of coronary atherosclerosis on IVUS, and presence of a large PFO with bidirectional shunting, probable paradoxical coronary embolism was considered the most likely mechanism of myocardial infarction. A hematologic evaluation performed during hospitalization was unrevealing and included antiphospholipid antibodies, antinuclear antibodies, protein S antigen, and antithrombin III. It is recognized that hypercoagulable testing performed during the acute phase may have limitations and does not exclude all transient or inherited prothrombotic states. The patient remained clinically stable after thrombectomy and was discharged on antithrombotic therapy and guideline-directed medical therapy. During hospitalization, the diagnostic evaluation proceeded chronologically from coronary angiography and IVUS to transthoracic echocardiography, transesophageal echocardiography, lower-extremity Doppler studies, and hematologic testing. Four weeks later, he underwent successful percutaneous closure of the PFO using a 30 mm Amplatzer Talisman device PFO Occluder (Abbott, Abbott Park, IL, USA). He remained asymptomatic without recurrent thromboembolic events.

3. Discussion

Coronary embolism is an uncommon cause of acute myocardial infarction and is typically considered after more common etiologies, such as plaque rupture, have been excluded [7,8,13,14,15]. In the present case, several features support a non-atherothrombotic mechanism: the patient was young with minimal conventional cardiovascular risk factors, angiography demonstrated an isolated abrupt occlusion of the ramus intermedius artery, and intravascular ultrasound (IVUS) revealed no evidence of plaque rupture, underlying atherosclerosis, or coronary dissection. Taken together, these findings are most consistent with a probable paradoxical coronary embolism.

The mechanism of paradoxical embolism involves the passage of thrombotic material from the venous to the arterial circulation through a right-to-left shunt, most commonly a patent foramen ovale (PFO) [1,2,3]. Favorable hemodynamic conditions for this process include transient increases in right atrial pressure exceeding left atrial pressure, such as during Valsalva maneuver, coughing, or physical exertion, which facilitate right-to-left shunting across the interatrial septum. Once in the arterial circulation, embolic material may lodge in end organs, including the coronary arteries.

Coronary embolism is less frequently observed than cerebral embolism, likely due to differences in vascular anatomy and flow dynamics. The cerebral circulation receives a greater proportion of cardiac output, and emboli preferentially travel along direct flow paths from the aortic arch to the cerebral vessels. In contrast, the coronary arteries arise at acute angles from the aortic root and are primarily perfused during diastole, which may reduce the likelihood of embolic entry and lodging within the coronary circulation.

Multimodality imaging was central to establishing the diagnosis in this case. Coronary angiography identified the culprit lesion and pattern of occlusion, while IVUS excluded plaque rupture, erosion, and dissection, thereby reducing the likelihood of a primary atherothrombotic event [9,10,16]. Echocardiographic evaluation further supported an embolic mechanism. Transthoracic echocardiography with bubble study demonstrated interatrial shunting, and transesophageal echocardiography confirmed the presence of a large PFO with bidirectional flow, providing a plausible anatomical route for paradoxical embolization [11,12,17].

A structured differential diagnosis for myocardial infarction with non-obstructive coronary arteries (MINOCA) was considered. Coronary vasospasm was deemed less likely given the presence of a fixed occlusion requiring thrombectomy rather than transient vasoconstriction. Spontaneous coronary artery dissection was excluded based on IVUS findings demonstrating no dissection or intramural hematoma. In situ coronary thrombosis without plaque rupture remains a possible alternative; however, the absence of underlying atherosclerosis and the presence of a large right-to-left shunt favor an embolic mechanism. Other potential embolic sources were not identified despite evaluation.

Although the findings strongly support an embolic etiology, definitive proof of paradoxical coronary embolism remains challenging. No venous thrombus was identified on lower-extremity Doppler imaging, and the hypercoagulable evaluation was unrevealing. Additionally, extended venous imaging and prolonged rhythm monitoring to exclude paroxysmal atrial fibrillation were not performed. Therefore, the diagnosis should be considered presumptive but highly likely, based on the integration of clinical presentation, imaging findings, and exclusion of alternative etiologies as described in prior case reports and observational studies [18,19,20,21,22].

Management of paradoxical coronary embolism requires both treatment of the acute coronary event and strategies to reduce the risk of recurrence [23,24]. In this case, aspiration thrombectomy successfully restored coronary flow without the need for stent implantation, which was appropriate given the absence of underlying coronary artery disease. The role of PFO closure in non-neurologic paradoxical embolism is less well defined than in cryptogenic stroke because the condition is rare and no randomized trial has specifically addressed coronary events. However, available data and guideline statements support closure in carefully selected patients when a causal relationship is strongly suspected [25,26,27,28,29,30,31,32]. In our patient, the presence of a large PFO, absence of competing mechanisms, and young age supported percutaneous closure as a reasonable strategy to reduce the risk of recurrent embolic events.

Failure to recognize paradoxical coronary embolism may lead to unnecessary stent placement and missed opportunities to address the underlying embolic source. This case highlights the importance of maintaining a high index of suspicion for embolic mechanisms in young patients presenting with acute coronary syndromes without clear evidence of atherosclerotic disease and demonstrates the value of integrating coronary and structural imaging to guide diagnosis and management.

4. Conclusions

Probable paradoxical coronary embolism is an uncommon but important cause of acute myocardial infarction, particularly in younger patients without significant atherosclerotic disease. This case underscores the need to consider embolic etiologies when coronary imaging does not support plaque rupture and demonstrates the value of combining angiography, IVUS, transthoracic echocardiography, and TEE to support the diagnosis. Recognition of the likely underlying mechanism allowed for targeted treatment with aspiration thrombectomy followed by percutaneous PFO closure to reduce the risk of recurrent embolic events.

5. Case Report Limitations

This report is subject to the inherent limitations of a single case. A formal CARE checklist timeline figure was not included, although the clinical course is described chronologically. In addition, patient perspective was not available. Despite these limitations, the case provides a clear diagnostic pathway supported by multimodality imaging and highlights important considerations in the evaluation of suspected embolic myocardial infarction.