Paradoxical Coronary Embolism Leading to ST-segment Elevation Myocardial Infarction in a Patient with Caval Thrombosis

Abstract

We present a case of a 48-year-old man with an atypical type 2 myocardial infarction (MI)/myocardial infarction with nonobstructive coronary arteries, caused by a coronary embolism originating from the inferior vena cava and passing through a patent foramen ovale (PFO). The patient presented to the emergency department with oppressive retrosternal chest pain. His medical history included papillary renal cell carcinoma and seminoma with recent abdominal lymph node recurrence. The electrocardiogram indicated an inferolateral ST-segment elevation (STE), prompting emergency coronary angiography, that revealed distal occlusion of the circumflex artery and the obtuse marginal branch, suggesting an embolic etiology. Stent placement was deferred, and the management approach involved thromboaspiration and unfractionated heparin infusion. Abdominal imaging identified a thrombotic formation in the inferior vena cava and a transesophageal echocardiogram revealed a PFO with a right-to-left shunt, supporting the diagnosis of a paradoxical embolism. Follow-up coronary angiography showed vessel patency, and the patient was then treated with low-molecular-weight heparin. This case underscores the importance of considering alternative etiologies for STE myocardial infarction beyond acute plaque rupture, highlighting the need for individualized management strategies, particularly in patients with complex medical histories, and given the lack of standardized treatment guidelines for coronary embolism.

INTRODUCTION

Chest pain is a common symptom that can result from a variety of conditions, some of which are severe and rapidly evolving, such as acute coronary syndromes.[1] Among the acute coronary syndromes, ST-segment elevation myocardial infarction (STEMI) is particularly critical, as it requires prompt, time-sensitive decision-making by the treating physician.[2] While the initial evaluation in the emergency department (ED) is often brief, obtaining detailed patient history and description of symptoms remains crucial in guiding both instrumental and laboratory investigations. The most frequent cause of STEMI is the rupture of an atherosclerotic coronary plaque, classified as a type 1 myocardial infarction (MI).[3] However, interventional cardiologists should remain aware of the broader spectrum of coronary occlusion etiologies, as stent placement is not always the most appropriate intervention.[4] Type 1 MI, which is most prevalent, is the primary focus of guidelines for acute coronary syndrome management. However, there is less evidence-based guidance on the treatment of other MI subtypes, as outlined in the fourth universal definition of MI.[3] Type 2 MI results from an imbalance between increased oxygen demand (e.g., arterial hypertension and hypertrophic cardiomyopathy) and/or reduced oxygen supply (e.g., coronary spasm, embolism, severe anemia, hypotension, and arrhythmias). The management of type 2 MI differs from type 1, emphasizing the resolution of the underlying cause of ischemia rather than addressing coronary artery pathology directly.[5] MI caused by coronary embolism also falls under the definition of myocardial infarction with nonobstructive coronary arteries (MINOCA).

CASE REPORT

A 48-year-old man presented to the ED with oppressive retrosternal chest pain that had persisted for approximately 2 h. His medical history was unremarkable for significant cardiological conditions or cardiovascular risk factors. However, 10 years earlier, following a car accident, he had developed a deep vein thrombosis in his left upper limb, which was treated with a 6-month course of warfarin. He also had a history of rheumatoid arthritis, for which he had been previously treated with methotrexate. The patient’s oncological history was significant. Six years prior, he had undergone a left renal tumorectomy for papillary renal cell carcinoma. He also had a history of seminoma and was treated with right orchifunicolectomy. Two months before his presentation to the ED, he was diagnosed with a recurrence of seminoma in an abdominal lymph node, and chemotherapy was initiated using the PEB regimen (cisplatin [platinum], etoposide, bleomycin).

Upon arrival at the ED, the patient underwent an electrocardiogram (ECG), which revealed normal sinus rhythm but also ventricular repolarization abnormalities indicative of an inferolateral STEMI [Figure 1]. Physical examination showed hypertensive circulation, without signs of hypoperfusion (Killip class I). The patient was promptly treated with intravenous acetylsalicylic acid (250 mg) and intravenous unfractionated heparin (UFH) 6.000 IU, leading to a partial improvement of his symptoms.

Figure 1.

The electrocardiogram performed at the emergency department, showing inferior and lateral ST-elevation

An emergency coronary angiography was then performed, revealing distal occlusion of the circumflex artery and mid-distal occlusion of the obtuse marginal branch without other significant lesions, particularly in the circumflex artery. The angiographic appearance suggested an embolic etiology [Figure 2]. After wiring the occluded vessel, manual thromboaspiration was performed and partial recanalization was observed, as shown in Figure 3. Stent placement was deferred and continuous UFH infusion was planned. The patient was then admitted to the cardiac intensive care unit and remained asymptomatic. A transthoracic echocardiogram revealed a nondilated left ventricle with localized akinesia of the inferolateral wall and an ejection fraction at the lower limit of normal. There were not significant valvular abnormalities, and the inferior vena cava was normal. Over the next few days, the ECG showed a progressive resolution of the STE, along with evidence of limited inferior necrosis and inferior-lateral ischemia [Figure 4]. In blood tests, a moderate increase in troponin was observed with a time curve compatible with MI. Improvement in the patient’s wall motion abnormalities was also observed, with an increase in ejection fraction. Given the suspicion of an embolic cause for the STEMI, further diagnostic testing was pursued. Doppler ultrasound of the lower and upper limbs was negative for thrombosis, but an abdominal ultrasound revealed a likely thrombotic formation in the inferior vena cava, confirmed by computed tomography. A transesophageal echocardiogram was then performed, revealing a patent foramen ovale (PFO) with a significant right-to-left shunt during the Valsalva maneuver [Figure 5], suggesting a paradoxical embolism event, and excluding left-sided thrombi. To complete the diagnosis, a thoracic computed tomography and brain magnetic resonance imaging were performed, negative for embolic events. Five days later, a follow-up coronary angiography showed patency of the previously occluded vessels [Figure 6]. In addition, intravascular imaging with ultrasound (IVUS) did not reveal intimal alterations along the circumflex artery axis. The patient was treated with subcutaneous low-molecular-weight heparin, along with cardioactive therapy, including ACE inhibitors and beta-blockers. He was then transferred to the oncology department for ongoing management. A timetable is available to clarify the events.

Figure 2.

The first coronary angiography performed, which showed distal occlusion of the circumflex artery and mid-distal occlusion of the obtuse marginal branch

Figure 3.

First coronary angiography: after thromboaspiration and passage of coronary guidewires, a partial recanalization was observed

Figure 4.

The electrocardiogram performed on the day of transfer to the oncological department, showing limited inferior necrosis and inferior-lateral ischemia

Figure 5.

Examinations from transesophageal echocardiography, showing a positive bubble test during Valsalva maneuver, suggestive of permeable foramen ovale

Figure 6.

The second coronary angiography performed, showing patency of previous occluded coronary arteries

DISCUSSION

This case represents an atypical type 2 MI and MINOCA caused by coronary embolism, originating from the inferior vena cava, with a paradoxical embolism through a PFO. It highlights that not all coronary occlusions during acute STEMI are due to acute plaque rupture or destabilization events. Even in acute scenarios, interventional cardiologists should remain attentive to the patient’s clinical history and consider alternative etiologies for MI, especially in cases that deviate from the typical presentations. More the patient presents a PFO that is a common condition that affects between 20% and 30% of healthy individuals. While it is usually benign and asymptomatic, in some cases, it can allow a paradoxical embolus to pass from the venous to the arterial circulation, potentially leading to systemic embolization. About the possibility of a PFO percutaneous closure, the decision was postponed once the overall prognosis was assessed. In this case, a conservative management strategy about coronary artery disease was chosen, avoiding stent placement. This decision was critical, as it prevented the initiation of dual antiplatelet therapy, which, in conjunction with anticoagulation for the inferior vena cava thrombosis, would have resulted in triple antithrombotic therapy. Such an approach could have complicated future surgical interventions related to the patient’s oncological condition in the short-to-medium term. Currently, there are not standardized treatment guidelines for managing coronary embolism, leaving treatment decisions to the physician’s discretion.[6,7,8] A thorough understanding of the unique pathogenesis of coronary embolism is essential, as it differs significantly from the mechanisms of plaque rupture and thrombus formation observed in type 1 MI.[4] In this case, the use of Intravascular imaging with ultrasound (IVUS) was instrumental in excluding an acute plaque event, thereby justifying the conservative management approach and supporting the decision to favor medical therapy.[9] In fact, traditional angiography has limitations in visualizing the vessel as a three-dimensional structure. Intracoronary imaging techniques, and optical coherence tomography in particular, allow an accurate study of the endothelium and help to understand pathophysiology. This is advantageous for choosing and guiding the best therapy, medical or interventional, even during acute coronary syndrome. With this in mind, these techniques are particularly useful during a MINOCA, when no epicardial coronary lesions are evident on angiography and several etiologies may be involved.[10]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.