Acute Myocardial Infarction Revealing a Patent Foramen Ovale in a 37-Year-Old with a History of Unexplored Transient Ischemic Attack: A Case Report

Acute Myocardial Infarction Revealing a Patent Foramen Ovale in a 37-Year-Old with a History of Unexplored Transient Ischemic Attack: A Case Report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Acute Myocardial Infarction Revealing a Patent Foramen Ovale in a 37-Year-Old with a History of Unexplored Transient Ischemic Attack: A Case Report Saleh muhammed Obeidat, Khlid Elkerrami, Ann-Iris Lemaitre, Yazid Himeur This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-5968164/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Introduction A patent foramen ovale (PFO) is a common congenital anomaly that can lead to severe complications through paradoxical embolism, particularly in young patients with no classical cardiovascular risk factors. Myocardial infarction with non-obstructive coronary arteries (MINOCA) represents a minority of acute coronary syndrome cases but is clinically significant due to its heterogeneous and often unclear etiologies. Among these, PFO-related paradoxical embolism is a rare but critical cause requiring prompt recognition and management. Case Presentation We report the case of a 37-year-old man with no cardiovascular risk factors, presenting with acute chest pain and dyspnea. His medical history revealed a transient ischemic attack (TIA) at age 25, which had remained unexplored. At presentation, the patient exhibited signs of an acute myocardial infarction (ST-elevation in inferior leads and elevated troponin). Coronary angiography revealed non-obstructive coronary lesions, confirming MINOCA. Echocardiographic evaluation identified a PFO with a right-to-left shunt, while cardiac MRI findings were consistent with ischemia in the infero-basal myocardium. The diagnosis of MINOCA secondary to paradoxical embolism through the PFO was established. The patient was treated with anticoagulation (Rivaroxaban) and underwent successful percutaneous PFO closure. Discussion MINOCA is a multifactorial clinical entity requiring advanced diagnostic tools to uncover its etiology. In this case, the detection of a PFO linked the myocardial infarction to the patient’s prior unexplained TIA, supporting a paradoxical embolic mechanism. Cardiac magnetic resonance imaging played a pivotal role in confirming the ischemic nature of the event, while intracoronary OCT ruled out significant plaque instability. Percutaneous closure of the PFO was performed to prevent recurrent embolic events. Although commonly indicated for cryptogenic strokes, PFO closure in MINOCA patients remains less established and highlights the need for further research to guide management. Conclusion The discovery of a PFO in the context of myocardial infarction in a young patient without pre-existing coronary disease highlights the need for thorough evaluation of underlying causes. Management includes pharmacological treatment and close monitoring, with PFO closure as a potential option to prevent future thromboembolic events. Myocardial Infarction Patent Foramen Ovale Transient Ischemic Attack Paradoxical Embolism Case Report Figures Figure 1 Figure 2 Figure 3 Figure 4 INTRODUCTION A patent foramen ovale (PFO) is a common congenital anomaly, present in approximately 20–25% of the general population and up to 40–50% of individuals who experience a cryptogenic stroke or transient ischemic attack (TIA) without an identified etiology( 1 ). In most cases, PFO remains asymptomatic and is incidentally discovered during an echocardiographic examination. However, it can become pathological under specific circumstances, particularly through paradoxical embolism mechanisms. These embolisms occur when a thrombus or gas embolus travels from the venous to the systemic circulation via a right-to-left shunt, leading to severe complications such as cerebral, systemic, or even coronary embolism ( 2 ). Myocardial infarction (MI) in young adults without classical cardiovascular risk factors accounts for a minority of acute coronary syndrome cases (approximately 5–10% of MIs)( 3 ). Among these, 10–15% are classified as myocardial infarction with non-obstructive coronary arteries (MINOCA), a clinical entity characterized by the absence of significant coronary stenosis on angiography (< 50%). The underlying causes of MINOCA are heterogeneous and include spontaneous coronary artery dissection, vasospasm, myocarditis, and, more rarely, paradoxical embolism—a phenomenon in which a PFO may play a central role ( 4 ) ( 5 ). Recent data indicate that up to 20% of MIs classified as MINOCA can be attributed to embolic events( 6 ). Among these, PFO is identified as a contributing factor in a significant subset. However, the precise relationship between PFO and coronary events remains underexplored, despite plausible pathophysiological mechanisms, such as the paradoxical migration of venous thrombi to coronary arteries. We present the case of a 37-year-old man, initially admitted for a myocardial infarction, in whom the discovery of a patent foramen ovale (PFO) allowed the connection of this event to a transient ischemic attack (TIA) that occurred 12 years earlier but remained unexplained. This case not only highlights the importance of a thorough investigation of underlying causes of thromboembolic events in young patients, but also underscores the key role of screening and management of PFO in preventing recurrences. CASE PRESENTATION We present the clinical case of a 37-year-old man with no significant medical history, who presents with acute chest pain and progressive dyspnea. His clinical history is marked by a transient ischemic attack (TIA) at the age of 25, which occurred suddenly, with transient facial paralysis and dysarthria. However, the TIA was poorly documented and had not been further investigated at the time. It was considered an isolated event, with no additional investigations, and the underlying cause was not identified. He has no classic cardiovascular risk factors, such as hypertension, diabetes, smoking, or hyperlipidemia, and is physically active with regular exercise. There is no family history of premature cardiovascular diseases or strokes. The patient presents to the emergency department with a constrictive chest pain, described as a "tightness," that began approximately 2 hours ago, associated with moderate dyspnea and a general sense of malaise. The pain intensity is rated 8/10 on the visual analog scale, radiating slightly to the left arm. Upon physical examination at admission, vital signs are stable: blood pressure is 130/85 mmHg, heart rate is 88 bpm, and oxygen saturation is normal at 97%. Cardiac auscultation reveals no murmurs, and heart sounds are regular. The neurological examination is normal, with no focal signs or motor or sensory deficits. The patient shows no signs of heart failure, and the initial electrocardiogram shows mild abnormalities consistent with acute coronary syndrome, including a transient ST-segment elevation in the inferior leads. The admission ECG shows typical abnormalities of a myocardial infarction, with ST-segment elevation in leads II, III, and aVF, indicating acute ischemia in the inferior region of the heart. The results show a significant elevation in cardiac biomarkers (troponin I elevated to 1.2 ng/mL, normal threshold 0.01 ng/mL), confirming a myocardial infarction. Other laboratory parameters are within normal limits, except for creatinine, which is at 1.2 mg/dL, without signs of acute renal failure. A coronary angiography was promptly performed due to the symptoms of myocardial infarction, revealing a non-significant lesion of the mid-left anterior descending artery involving the origin of the first diagonal branch (bifurcation lesion). Optical coherence tomography (OCT) revealed the appearance of a non-stenosing fibrous plaque with a white thrombus on its surface. This finding confirmed the diagnosis of myocardial infarction with non-obstructive coronary arteries (MINOCA). The transthoracic echocardiogram shows preserved left ventricular systolic function with an ejection fraction of 62%, without valvular abnormalities and no signs of pulmonary hypertension. The interatrial septum appears floppy, with a maximum excursion measured at 15 mm on subcostal view, and the bubble test is positive after the second cycle. A transesophageal echocardiogram (TEE) is performed to assess the possibility of an intracardiac shunt. The TEE reveals a patent foramen ovale (PFO) measuring 14.9 x 3.5 mm. A cardiac MRI was performed, revealing findings consistent with MINOCA involving the junction of the infero-basal and infero-septo-basal segments. Based on the clinical and paraclinical data, the diagnosis was concluded to be a MINOCA due to coronary plaque rupture or an embolic mechanism via the patent foramen ovale. The patient was treated with curative anticoagulation using Rivaroxaban 20 mg per day and Atorvastatin 10 mg per day. The patient is placed under continuous monitoring in the cardiac intensive care unit, with regular troponin checks and ECGs to track clinical progression and detect any signs of complications, such as recurrent infarction or arrhythmias. Given the presence of PFO and the history of unexplored TIA, the patient was referred for multidisciplinary evaluation. The Heart Team recommended percutaneous PFO closure to prevent future embolic events. The procedure was performed successfully two weeks later without complications. DISCUSSION Myocardial infarction without significant coronary obstruction (MINOCA) is defined as a myocardial infarction with typical clinical and biological signs (chest pain, elevated troponin, etc.), but without significant obstruction of the coronary arteries on angiography ( 7 ). The underlying mechanisms can include plaque rupture without major stenosis ( 8 ) ( 9 ), coronary vasospasm ( 10 ) ( 11 ), microemboli, endothelial dysfunction, or infarction related to paradoxical embolism through a patent foramen ovale (PFO) ( 12 ) ( 13 ). In this case, the absence of significant coronary stenosis and the discovery of a PFO suggest that the paradoxical embolic mechanism could be the cause of the infarction. A PFO is a congenital anomaly that results in a communication between the right and left atria. In the absence of this communication, blood returning from the body (via the vena cava) normally passes through the right atrium before being pumped into the lungs. However, in the presence of a PFO, a right-to-left shunt can allow clots formed in the venous circulation to pass directly into the systemic circulation, increasing the risk of paradoxical embolism. This pathophysiology is often the cause of strokes in young patients, but it can also lead to cardiac manifestations, as seen in this case of myocardial infarction. ( 14 ) The patent foramen ovale (PFO) is often an overlooked risk factor in cases of myocardial infarction, but it can be involved in paradoxical embolism. In young patients without classic risk factors, evaluating a PFO becomes essential to identify non-obstructive causes of infarction ( 15 ). In this patient's case, the history of a transient ischemic attack (TIA) at the age of 25, although forgotten in the past, takes on significant meaning with the discovery of a PFO, which could explain the migration of clots and their passage into the systemic circulation, leading to the infarction. The role of the PFO in thromboembolic events is now well documented. Recent studies have shown that a PFO is associated with an increased risk of thromboembolic diseases, especially in young patients with a history of vascular disorders ( 16 ). The connection between an unexplored TIA and a myocardial infarction in this context suggests a common embolic etiology, potentially induced by the presence of the PFO. Cardiac magnetic resonance imaging (CMR) plays a crucial role in uncovering the underlying etiology of myocardial infarction with non-obstructive coronary arteries (MINOCA), especially in cases where the cause remains unclear. This advanced imaging modality allows for detailed myocardial tissue characterization, enabling clinicians to differentiate between ischemic and non-ischemic causes. In cases of suspected paradoxical coronary embolism, CMR can identify late gadolinium enhancement patterns indicative of embolic myocardial injury, thereby supporting the diagnostic process. Furthermore, CMR serves as a complementary tool to other diagnostic techniques by excluding alternative causes such as myocarditis or Takotsubo cardiomyopathy in patients with MINOCA ( 17 ). Intracoronary OCT can contribute to understanding the mechanisms involved in paradoxical embolism by providing a detailed assessment of associated intravascular lesions. Although paradoxical embolism is primarily linked to the presence of a right-to-left shunt, such as a patent foramen ovale, OCT can identify secondary complications within the coronary circulation, such as intravascular emboli or areas of obstructed microvasculature. It also allows for the evaluation of coronary artery status in cases of suspected concomitant atherosclerosis, clarifying whether unstable plaques or thrombi play a contributory role ( 18 ). This diagnostic precision aids in differentiating the causes of embolic events and informs therapeutic decisions, such as foramen ovale closure or antithrombotic management. The management of MINOCA primarily relies on a pharmacological approach. Treatment with anticoagulants and antiplatelet agents is crucial for preventing the progression of the infarction and minimizing the risks of systemic embolism. The use of dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 receptor inhibitor, such as clopidogrel, ticagrelor or prasugrel, is standard in this context, although the effectiveness of this approach in MINOCA patients is still debated ( 19 ). In the case of our patient, the initiation of anticoagulation is particularly relevant due to the presence of a PFO. The use of anticoagulants, such as direct oral anticoagulants (DOACs), may play a preventive role in avoiding the formation of new thrombi that could pass through the PFO and cause paradoxical embolism ( 20 ). Percutaneous closure of the PFO, though increasingly common in cases of cryptogenic stroke, is considered here as a preventive measure, even in the absence of recent acute neurological episodes. The benefits of this procedure are well-established in the context of stroke, but its effectiveness in preventing myocardial infarction remains a subject of discussion. Current guidelines recommend closure of the PFO in patients who have had a stroke or TIA with a PFO, but the decision to proceed with closure should be made after evaluating the risks, including the risk of embolism and procedure-related complications ( 20 ). Long-term follow-up of the patient will be essential to prevent potential recurrence of cardiovascular events. The follow-up will include regular consultations with cardiology and neurology to monitor the patient's clinical status, as well as echocardiographic exams to assess the patency of the PFO and heart function. The cessation of cardiovascular risk factors, although absent in this patient, should be encouraged, particularly with regard to stress management and the adoption of appropriate preventive measures ( 21 ). Furthermore, management of the PFO will involve long-term medication options, especially to prevent thromboembolic events. Long-term anticoagulation therapy, with ongoing assessment of the benefit-risk ratio, will be discussed with the patient ( 22 ). Percutaneous closure of the PFO is well established in the context of cryptogenic ischemic strokes, but its role in MINOCA requires further study. Pharmacological management, including anticoagulation and secondary prevention, remains an evolving field. One of the major challenges is identifying patients with PFO who would benefit most from closure. Additionally, while direct oral anticoagulants have demonstrated effectiveness in preventing strokes, their role in preventing myocardial infarctions is still under investigation. Further research is needed to better understand the relationship between PFO and myocardial infarctions, as well as to optimize management strategies. CONCLUSION This case highlights the importance of a comprehensive diagnostic approach, especially in young patients with no history of coronary artery disease. The discovery of a PFO in a patient with a myocardial infarction and an unexplored history of TIA helps to better understand the underlying mechanisms of cardiovascular and thromboembolic events. Advances in pharmacological treatments and percutaneous interventions open new avenues for the management of these patients, but careful risk assessment is essential to ensure optimal care. Abbreviations PFO: Patent Foramen Ovale MINOCA: Myocardial Infarction with Non-Obstructive Coronary Arteries TIA: Transient Ischemic Attack ECG: Electrocardiogram OCT: Optical Coherence Tomography CMR: Cardiac Magnetic Resonance Imaging DOACs: Direct Oral Anticoagulants DAPT: Dual Antiplatelet Therapy Declarations Consent As per international standards or university standards, patient(s) written consent has been collected and preserved by the author(s). Ethical declarations This article was published after obtaining the patient’s consent and the patient’s personal information was not mentioned so the case report was published anonymously. Disclaimer (Artificial intelligence) Author(s) hereby declare that NO generative AI technologies such as Large Language Models (ChatGPT, COPILOT, etc.) and text-to-image generators have been used during the writing or editing of this manuscript. Funding None Author Contribution Obeidat Saleh wrote the main manuscript test. All authors reviewed the manuscript. Acknowledgement Not applicable. References Mojadidi MK, Zaman MO, Elgendy IY, Mahmoud AN, Patel NK, Agarwal N, et al. Cryptogenic Stroke and Patent Foramen Ovale. J Am Coll Cardiol. 6 mars 2018;71(9):1035–43. Paradoxical Embolism | Journal of the American College of Cardiology [Internet]. [cité 22 janv 2025]. Disponible sur: https://www.jacc.org/doi/ 10.1016/j.jacc.2014.04.063 Gulati R, Behfar A, Narula J, Kanwar A, Lerman A, Cooper L, et al. Acute Myocardial Infarction in Young Individuals. Mayo Clin Proc. janv 2020;95(1):136–56. Sucato V, Comparato F, Ortello A, Galassi AR. Myocardical Infarction with Non-Obstructive Coronary Arteries (MINOCA): pathogenesis, diagnosis and treatment. Curr Probl Cardiol. 1 juill 2024;49(7):102583. Ceasovschih A, Mantzouranis E, Dimitriadis K, Sorodoc V, Vlachakis PK, Karanikola AE, et al. Coronary artery thromboembolism as a cause of myocardial infarction with non-obstructive coronary arteries (MINOCA). 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Borzillo I, De Filippo O, Manai R, Bruno F, Ravetti E, Galanti AA, et al. Role of Intracoronary Imaging in Myocardial Infarction with Non-Obstructive Coronary Disease (MINOCA): A Review. J Clin Med. 8 mars 2023;12(6):2129. Chen W, Jiang Y, Chen T, Zhou Y. Antiplatelet therapy in patients with myocardial infarction with non-obstructive coronary arteries: A clinical perspective. Front Cardiovasc Med. 9 janv 2023; 9:1081934. Kavinsky CJ, Szerlip M, Goldsweig AM, Amin Z, Boudoulas KD, Carroll JD, et al. SCAI Guidelines for the Management of Patent Foramen Ovale. J Soc Cardiovasc Angiogr Interv [Internet]. 1 juill 2022 [cité 22 janv 2025];1(4). Disponible sur: https://www.jscai.org/article/S2772-9303( 22)00023-0/fulltext Wintzer-Wehekind J, Alperi A, Houde C, Côté JM, Asmarats L, Côté M, et al. Long-Term Follow-Up After Closure of Patent Foramen Ovale in Patients With Cryptogenic Embolism. J Am Coll Cardiol. 29 janv 2019;73(3):278–87. European position paper on the management of patients with patent foramen ovale. General approach and left circulation thromboembolism | EuroIntervention [Internet]. [cité 23 janv 2025]. Disponible sur: https://eurointervention.pcronline.com/article/european-position-paper-on-the-management-of-patients-with-patent-foramen-ovale-general-approach-and-left-circulation-thromboembolism Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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approximately 20\u0026ndash;25% of the general population and up to 40\u0026ndash;50% of individuals who experience a cryptogenic stroke or transient ischemic attack (TIA) without an identified etiology(\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). In most cases, PFO remains asymptomatic and is incidentally discovered during an echocardiographic examination. However, it can become pathological under specific circumstances, particularly through paradoxical embolism mechanisms. These embolisms occur when a thrombus or gas embolus travels from the venous to the systemic circulation via a right-to-left shunt, leading to severe complications such as cerebral, systemic, or even coronary embolism (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eMyocardial infarction (MI) in young adults without classical cardiovascular risk factors accounts for a minority of acute coronary syndrome cases (approximately 5\u0026ndash;10% of MIs)(\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). Among these, 10\u0026ndash;15% are classified as myocardial infarction with non-obstructive coronary arteries (MINOCA), a clinical entity characterized by the absence of significant coronary stenosis on angiography (\u0026lt;\u0026thinsp;50%). The underlying causes of MINOCA are heterogeneous and include spontaneous coronary artery dissection, vasospasm, myocarditis, and, more rarely, paradoxical embolism\u0026mdash;a phenomenon in which a PFO may play a central role (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e) (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eRecent data indicate that up to 20% of MIs classified as MINOCA can be attributed to embolic events(\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). Among these, PFO is identified as a contributing factor in a significant subset. However, the precise relationship between PFO and coronary events remains underexplored, despite plausible pathophysiological mechanisms, such as the paradoxical migration of venous thrombi to coronary arteries.\u003c/p\u003e \u003cp\u003eWe present the case of a 37-year-old man, initially admitted for a myocardial infarction, in whom the discovery of a patent foramen ovale (PFO) allowed the connection of this event to a transient ischemic attack (TIA) that occurred 12 years earlier but remained unexplained. This case not only highlights the importance of a thorough investigation of underlying causes of thromboembolic events in young patients, but also underscores the key role of screening and management of PFO in preventing recurrences.\u003c/p\u003e"},{"header":"CASE PRESENTATION","content":"\u003cp\u003eWe present the clinical case of a 37-year-old man with no significant medical history, who presents with acute chest pain and progressive dyspnea. His clinical history is marked by a transient ischemic attack (TIA) at the age of 25, which occurred suddenly, with transient facial paralysis and dysarthria. However, the TIA was poorly documented and had not been further investigated at the time. It was considered an isolated event, with no additional investigations, and the underlying cause was not identified.\u003c/p\u003e \u003cp\u003eHe has no classic cardiovascular risk factors, such as hypertension, diabetes, smoking, or hyperlipidemia, and is physically active with regular exercise. There is no family history of premature cardiovascular diseases or strokes.\u003c/p\u003e \u003cp\u003eThe patient presents to the emergency department with a constrictive chest pain, described as a \"tightness,\" that began approximately 2 hours ago, associated with moderate dyspnea and a general sense of malaise. The pain intensity is rated 8/10 on the visual analog scale, radiating slightly to the left arm. Upon physical examination at admission, vital signs are stable: blood pressure is 130/85 mmHg, heart rate is 88 bpm, and oxygen saturation is normal at 97%. Cardiac auscultation reveals no murmurs, and heart sounds are regular.\u003c/p\u003e \u003cp\u003eThe neurological examination is normal, with no focal signs or motor or sensory deficits. The patient shows no signs of heart failure, and the initial electrocardiogram shows mild abnormalities consistent with acute coronary syndrome, including a transient ST-segment elevation in the inferior leads.\u003c/p\u003e \u003cp\u003eThe admission ECG shows typical abnormalities of a myocardial infarction, with ST-segment elevation in leads II, III, and aVF, indicating acute ischemia in the inferior region of the heart. The results show a significant elevation in cardiac biomarkers (troponin I elevated to 1.2 ng/mL, normal threshold 0.01 ng/mL), confirming a myocardial infarction. Other laboratory parameters are within normal limits, except for creatinine, which is at 1.2 mg/dL, without signs of acute renal failure.\u003c/p\u003e \u003cp\u003eA coronary angiography was promptly performed due to the symptoms of myocardial infarction, revealing a non-significant lesion of the mid-left anterior descending artery involving the origin of the first diagonal branch (bifurcation lesion). Optical coherence tomography (OCT) revealed the appearance of a non-stenosing fibrous plaque with a white thrombus on its surface.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eThis finding confirmed the diagnosis of myocardial infarction with non-obstructive coronary arteries (MINOCA).\u003c/p\u003e \u003cp\u003eThe transthoracic echocardiogram shows preserved left ventricular systolic function with an ejection fraction of 62%, without valvular abnormalities and no signs of pulmonary hypertension. The interatrial septum appears floppy, with a maximum excursion measured at 15 mm on subcostal view, and the bubble test is positive after the second cycle.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eA transesophageal echocardiogram (TEE) is performed to assess the possibility of an intracardiac shunt. The TEE reveals a patent foramen ovale (PFO) measuring 14.9 x 3.5 mm.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eA cardiac MRI was performed, revealing findings consistent with MINOCA involving the junction of the infero-basal and infero-septo-basal segments.\u003c/p\u003e \u003cp\u003eBased on the clinical and paraclinical data, the diagnosis was concluded to be a MINOCA due to coronary plaque rupture or an embolic mechanism via the patent foramen ovale.\u003c/p\u003e \u003cp\u003eThe patient was treated with curative anticoagulation using Rivaroxaban 20 mg per day and Atorvastatin 10 mg per day.\u003c/p\u003e \u003cp\u003eThe patient is placed under continuous monitoring in the cardiac intensive care unit, with regular troponin checks and ECGs to track clinical progression and detect any signs of complications, such as recurrent infarction or arrhythmias.\u003c/p\u003e \u003cp\u003eGiven the presence of PFO and the history of unexplored TIA, the patient was referred for multidisciplinary evaluation. The Heart Team recommended percutaneous PFO closure to prevent future embolic events. The procedure was performed successfully two weeks later without complications.\u003c/p\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eMyocardial infarction without significant coronary obstruction (MINOCA) is defined as a myocardial infarction with typical clinical and biological signs (chest pain, elevated troponin, etc.), but without significant obstruction of the coronary arteries on angiography (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). The underlying mechanisms can include plaque rupture without major stenosis (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e) (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e), coronary vasospasm (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e) (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e), microemboli, endothelial dysfunction, or infarction related to paradoxical embolism through a patent foramen ovale (PFO) (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e) (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). In this case, the absence of significant coronary stenosis and the discovery of a PFO suggest that the paradoxical embolic mechanism could be the cause of the infarction.\u003c/p\u003e \u003cp\u003eA PFO is a congenital anomaly that results in a communication between the right and left atria. In the absence of this communication, blood returning from the body (via the vena cava) normally passes through the right atrium before being pumped into the lungs. However, in the presence of a PFO, a right-to-left shunt can allow clots formed in the venous circulation to pass directly into the systemic circulation, increasing the risk of paradoxical embolism. This pathophysiology is often the cause of strokes in young patients, but it can also lead to cardiac manifestations, as seen in this case of myocardial infarction. (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e)\u003c/p\u003e \u003cp\u003eThe patent foramen ovale (PFO) is often an overlooked risk factor in cases of myocardial infarction, but it can be involved in paradoxical embolism. In young patients without classic risk factors, evaluating a PFO becomes essential to identify non-obstructive causes of infarction (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). In this patient's case, the history of a transient ischemic attack (TIA) at the age of 25, although forgotten in the past, takes on significant meaning with the discovery of a PFO, which could explain the migration of clots and their passage into the systemic circulation, leading to the infarction.\u003c/p\u003e \u003cp\u003eThe role of the PFO in thromboembolic events is now well documented. Recent studies have shown that a PFO is associated with an increased risk of thromboembolic diseases, especially in young patients with a history of vascular disorders (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e). The connection between an unexplored TIA and a myocardial infarction in this context suggests a common embolic etiology, potentially induced by the presence of the PFO.\u003c/p\u003e \u003cp\u003eCardiac magnetic resonance imaging (CMR) plays a crucial role in uncovering the underlying etiology of myocardial infarction with non-obstructive coronary arteries (MINOCA), especially in cases where the cause remains unclear. This advanced imaging modality allows for detailed myocardial tissue characterization, enabling clinicians to differentiate between ischemic and non-ischemic causes. In cases of suspected paradoxical coronary embolism, CMR can identify late gadolinium enhancement patterns indicative of embolic myocardial injury, thereby supporting the diagnostic process. Furthermore, CMR serves as a complementary tool to other diagnostic techniques by excluding alternative causes such as myocarditis or Takotsubo cardiomyopathy in patients with MINOCA (\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIntracoronary OCT can contribute to understanding the mechanisms involved in paradoxical embolism by providing a detailed assessment of associated intravascular lesions. Although paradoxical embolism is primarily linked to the presence of a right-to-left shunt, such as a patent foramen ovale, OCT can identify secondary complications within the coronary circulation, such as intravascular emboli or areas of obstructed microvasculature. It also allows for the evaluation of coronary artery status in cases of suspected concomitant atherosclerosis, clarifying whether unstable plaques or thrombi play a contributory role (\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). This diagnostic precision aids in differentiating the causes of embolic events and informs therapeutic decisions, such as foramen ovale closure or antithrombotic management.\u003c/p\u003e \u003cp\u003eThe management of MINOCA primarily relies on a pharmacological approach. Treatment with anticoagulants and antiplatelet agents is crucial for preventing the progression of the infarction and minimizing the risks of systemic embolism. The use of dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 receptor inhibitor, such as clopidogrel, ticagrelor or prasugrel, is standard in this context, although the effectiveness of this approach in MINOCA patients is still debated (\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn the case of our patient, the initiation of anticoagulation is particularly relevant due to the presence of a PFO. The use of anticoagulants, such as direct oral anticoagulants (DOACs), may play a preventive role in avoiding the formation of new thrombi that could pass through the PFO and cause paradoxical embolism (\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e).\u003c/p\u003e \u003cp\u003ePercutaneous closure of the PFO, though increasingly common in cases of cryptogenic stroke, is considered here as a preventive measure, even in the absence of recent acute neurological episodes. The benefits of this procedure are well-established in the context of stroke, but its effectiveness in preventing myocardial infarction remains a subject of discussion. Current guidelines recommend closure of the PFO in patients who have had a stroke or TIA with a PFO, but the decision to proceed with closure should be made after evaluating the risks, including the risk of embolism and procedure-related complications (\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eLong-term follow-up of the patient will be essential to prevent potential recurrence of cardiovascular events. The follow-up will include regular consultations with cardiology and neurology to monitor the patient's clinical status, as well as echocardiographic exams to assess the patency of the PFO and heart function. The cessation of cardiovascular risk factors, although absent in this patient, should be encouraged, particularly with regard to stress management and the adoption of appropriate preventive measures (\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eFurthermore, management of the PFO will involve long-term medication options, especially to prevent thromboembolic events. Long-term anticoagulation therapy, with ongoing assessment of the benefit-risk ratio, will be discussed with the patient (\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e).\u003c/p\u003e \u003cp\u003ePercutaneous closure of the PFO is well established in the context of cryptogenic ischemic strokes, but its role in MINOCA requires further study. Pharmacological management, including anticoagulation and secondary prevention, remains an evolving field.\u003c/p\u003e \u003cp\u003eOne of the major challenges is identifying patients with PFO who would benefit most from closure. Additionally, while direct oral anticoagulants have demonstrated effectiveness in preventing strokes, their role in preventing myocardial infarctions is still under investigation. Further research is needed to better understand the relationship between PFO and myocardial infarctions, as well as to optimize management strategies.\u003c/p\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eThis case highlights the importance of a comprehensive diagnostic approach, especially in young patients with no history of coronary artery disease. The discovery of a PFO in a patient with a myocardial infarction and an unexplored history of TIA helps to better understand the underlying mechanisms of cardiovascular and thromboembolic events. Advances in pharmacological treatments and percutaneous interventions open new avenues for the management of these patients, but careful risk assessment is essential to ensure optimal care.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003ePFO: Patent Foramen Ovale\u003c/p\u003e\n\u003cp\u003eMINOCA: Myocardial Infarction with Non-Obstructive Coronary Arteries\u003c/p\u003e\n\u003cp\u003eTIA: Transient Ischemic Attack\u003c/p\u003e\n\u003cp\u003eECG: Electrocardiogram\u003c/p\u003e\n\u003cp\u003eOCT: Optical Coherence Tomography\u003c/p\u003e\n\u003cp\u003eCMR: Cardiac Magnetic Resonance Imaging\u003c/p\u003e\n\u003cp\u003eDOACs: Direct Oral Anticoagulants\u003c/p\u003e\n\u003cp\u003eDAPT: Dual Antiplatelet Therapy\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e \u003ch2\u003eConsent\u003c/h2\u003e \u003cp\u003eAs per international standards or university standards, patient(s) written consent has been collected and preserved by the author(s).\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eEthical declarations\u003c/strong\u003e \u003cp\u003eThis article was published after obtaining the patient\u0026rsquo;s consent and the patient\u0026rsquo;s personal information was not mentioned so the case report was published anonymously.\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eDisclaimer (Artificial intelligence)\u003c/strong\u003e \u003cp\u003eAuthor(s) hereby declare that NO generative AI technologies such as Large Language Models (ChatGPT, COPILOT, etc.) and text-to-image generators have been used during the writing or editing of this manuscript.\u003c/p\u003e \u003c/p\u003e\u003ch2\u003eFunding\u003c/h2\u003e \u003cp\u003eNone\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eObeidat Saleh wrote the main manuscript test. All authors reviewed the manuscript.\u003c/p\u003e\u003ch2\u003eAcknowledgement\u003c/h2\u003e\u003cp\u003eNot applicable.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eMojadidi MK, Zaman MO, Elgendy IY, Mahmoud AN, Patel NK, Agarwal N, et al. Cryptogenic Stroke and Patent Foramen Ovale. J Am Coll Cardiol. 6 mars 2018;71(9):1035\u0026ndash;43.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eParadoxical Embolism | Journal of the American College of Cardiology [Internet]. [cit\u0026eacute; 22 janv 2025]. 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J Clin Med. 8 mars 2023;12(6):2129.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eChen W, Jiang Y, Chen T, Zhou Y. Antiplatelet therapy in patients with myocardial infarction with non-obstructive coronary arteries: A clinical perspective. Front Cardiovasc Med. 9 janv 2023; 9:1081934.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKavinsky CJ, Szerlip M, Goldsweig AM, Amin Z, Boudoulas KD, Carroll JD, et al. SCAI Guidelines for the Management of Patent Foramen Ovale. J Soc Cardiovasc Angiogr Interv [Internet]. 1 juill 2022 [cit\u0026eacute; 22 janv 2025];1(4). Disponible sur: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.jscai.org/article/S2772-9303(\u003c/span\u003e\u003cspan address=\"https://www.jscai.org/article/S2772-9303(\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e22)00023-0/fulltext\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWintzer-Wehekind J, Alperi A, Houde C, C\u0026ocirc;t\u0026eacute; JM, Asmarats L, C\u0026ocirc;t\u0026eacute; M, et al. Long-Term Follow-Up After Closure of Patent Foramen Ovale in Patients With Cryptogenic Embolism. J Am Coll Cardiol. 29 janv 2019;73(3):278\u0026ndash;87.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eEuropean position paper on the management of patients with patent foramen ovale. General approach and left circulation thromboembolism | EuroIntervention [Internet]. [cit\u0026eacute; 23 janv 2025]. Disponible sur: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://eurointervention.pcronline.com/article/european-position-paper-on-the-management-of-patients-with-patent-foramen-ovale-general-approach-and-left-circulation-thromboembolism\u003c/span\u003e\u003cspan address=\"https://eurointervention.pcronline.com/article/european-position-paper-on-the-management-of-patients-with-patent-foramen-ovale-general-approach-and-left-circulation-thromboembolism\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Myocardial Infarction, Patent Foramen Ovale, Transient Ischemic Attack, Paradoxical Embolism, Case Report","lastPublishedDoi":"10.21203/rs.3.rs-5968164/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-5968164/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eIntroduction\u003c/h2\u003e \u003cp\u003eA patent foramen ovale (PFO) is a common congenital anomaly that can lead to severe complications through paradoxical embolism, particularly in young patients with no classical cardiovascular risk factors. Myocardial infarction with non-obstructive coronary arteries (MINOCA) represents a minority of acute coronary syndrome cases but is clinically significant due to its heterogeneous and often unclear etiologies. Among these, PFO-related paradoxical embolism is a rare but critical cause requiring prompt recognition and management.\u003c/p\u003e\u003ch2\u003eCase Presentation\u003c/h2\u003e \u003cp\u003eWe report the case of a 37-year-old man with no cardiovascular risk factors, presenting with acute chest pain and dyspnea. His medical history revealed a transient ischemic attack (TIA) at age 25, which had remained unexplored. At presentation, the patient exhibited signs of an acute myocardial infarction (ST-elevation in inferior leads and elevated troponin). Coronary angiography revealed non-obstructive coronary lesions, confirming MINOCA. Echocardiographic evaluation identified a PFO with a right-to-left shunt, while cardiac MRI findings were consistent with ischemia in the infero-basal myocardium. The diagnosis of MINOCA secondary to paradoxical embolism through the PFO was established. The patient was treated with anticoagulation (Rivaroxaban) and underwent successful percutaneous PFO closure.\u003c/p\u003e\u003ch2\u003eDiscussion\u003c/h2\u003e \u003cp\u003eMINOCA is a multifactorial clinical entity requiring advanced diagnostic tools to uncover its etiology. In this case, the detection of a PFO linked the myocardial infarction to the patient\u0026rsquo;s prior unexplained TIA, supporting a paradoxical embolic mechanism. Cardiac magnetic resonance imaging played a pivotal role in confirming the ischemic nature of the event, while intracoronary OCT ruled out significant plaque instability. Percutaneous closure of the PFO was performed to prevent recurrent embolic events. Although commonly indicated for cryptogenic strokes, PFO closure in MINOCA patients remains less established and highlights the need for further research to guide management.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThe discovery of a PFO in the context of myocardial infarction in a young patient without pre-existing coronary disease highlights the need for thorough evaluation of underlying causes. Management includes pharmacological treatment and close monitoring, with PFO closure as a potential option to prevent future thromboembolic events.\u003c/p\u003e","manuscriptTitle":"Acute Myocardial Infarction Revealing a Patent Foramen Ovale in a 37-Year-Old with a History of Unexplored Transient Ischemic Attack: A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-02-11 12:04:54","doi":"10.21203/rs.3.rs-5968164/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"948b5e47-d8cc-46d5-98a8-db4eba997576","owner":[],"postedDate":"February 11th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-01-27T00:39:00+00:00","versionOfRecord":[],"versionCreatedAt":"2025-02-11 12:04:54","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-5968164","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-5968164","identity":"rs-5968164","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}