Ridhava Singh*, Rajkumar Usdadia, Arjun Mohandas, Abel Paul Leslie
Pravara Institute of Medical Sciences, Loni -413736, India.
*Corresponding Author: Ridhava Singh, Pravara Institute of Medical Sciences, Loni -413736, India.
Received: January 07, 2025
Accepted: January 11, 2025
Published: January 15, 2025
Citation: Singh R, Usdadia R, Mohandas A, Abel P Leslie. (2025) “Case Report : Inferior Wall Myocardial Infarction in a Patient with Patent Foramen Ovale and Hyperhomocysteinemia.” J Clinical Cardiology Interventions, 5(1); DOI: 10.61148/2836-077X/JCCI/051
Copyright: © 2025 Ridhava Singh. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Inferior wall myocardial infarction (MI) is most commonly caused by thrombotic occlusion of the right coronary artery or its branches due to underlying atherosclerotic plaque rupture.1 However, in the absence of significant coronary artery disease, alternative mechanisms such as paradoxical embolism must be considered.2 Paradoxical embolism occurs when a venous thrombus bypasses the pulmonary circulation and enters systemic circulation through a right-to-left shunt, such as a patent foramen ovale (PFO).3 Hyperhomocysteinemia, a prothrombotic state, further exacerbates this risk.4 This case highlights the rare but significant association of paradoxical embolism facilitated by PFO and hyperhomocysteinemia, leading to inferior wall MI in a young patient.5 Early recognition and targeted management strategies are essential to improve outcomes.6
paradoxical embolism; inferior wall myocardial infarction; patent foramen ovale hyperhomocysteinemia; thromboembolism; young mi
Introduction
We present the case of a 19-year-old male who presented with sudden onset chest pain and was diagnosed with inferior wall myocardial infarction (MI). Investigations revealed a patent foramen ovale (PFO) with right-to-left shunting, elevated homocysteine levels consistent with hyperhomocysteinemia, and a venous thrombus in the left lower limb. The thrombus is believed to have traveled through the PFO into the systemic circulation, resulting in embolic occlusion of the right coronary artery (RCA). This case highlights the rare but significant association of paradoxical embolism facilitated by PFO and hyperhomocysteinemia as a cause of myocardial infarction in a young patient.
Case Presentation
History of Presenting Illness
A 19-year-old male presented to the emergency department with acute retrosternal chest pain that began 2 hours prior to admission. The pain was severe, sharp, and radiated to the left shoulder and arm. It was associated with nausea, profuse sweating, and a sense of unease. He denied any history of exertional chest pain, palpitations, or breathlessness.
The patient had no known history of cardiovascular disease, diabetes, hypertension, or smoking. However, he reported a lower limb fracture 4 weeks ago that required prolonged immobilization. He described intermittent swelling and mild pain in his left calf over the past 2 weeks. There was no family history of thromboembolic disorders, coronary artery disease, or sudden cardiac death.
General and Systemic Examination
Investigations
Investigation |
Result |
Haemoglobin (g/dL) |
13.6 |
Total WBC Count (/µL) |
9,500 |
Neutrophils (%) |
68 |
Lymphocytes (%) |
28 |
Fasting Blood Sugar (mg/dL) |
102 |
Blood Urea (mg/dL) |
22 |
Serum Sodium (mEq/L) |
139 |
Serum Potassium (mEq/L) |
4.2 |
Homocysteine (µmol/L) |
35↑ |
Protein S (%) |
78 |
Protein C (%) |
65 |
Troponin I (ng/mL) |
6.8↑ |
CRP (mg/dL) |
— |
Electrocardiogram (ECG) |
ST-elevation in leads II, III, aVF, Inverted T wave in v4,v5,v6 |
Echocardiography |
Inferior wall hypokinesia; PFO with right-to-left shunt |
Lower Limb Venous Doppler |
Left popliteal vein thrombus |
Coronary Angiography |
RCA thrombotic occlusion, no CAD |
Diagnosis - The patient was diagnosed with inferior wall myocardial infarction (MI), complicated by paradoxical embolism through a patent foramen ovale (PFO), which led to thrombotic occlusion of the right coronary artery (RCA). Contributing factors include hyperhomocysteinemia, identified as a possible risk for thrombosis and paradoxical embolism.
Immediate Management
- Antiplatelet Therapy: Aspirin 300 mg, clopidogrel 600 mg.
- Anticoagulation: Low molecular weight heparin (LMWH) for thromboembolism.
- Pain Control: Morphine and nitroglycerin.
- Oxygen therapy: 2L/min via nasal cannula.
Percutaneous Coronary Intervention (PCI)
- Successful stenting of the RCA post-thrombotic occlusion.
PFO Closure Surgery
- Day 2: Successful closure of PFO to prevent further paradoxical embolism.
Long-term Management
- Oral anticoagulation with warfarin for at least 6 months.
- Homocysteine-lowering therapy with folic acid, vitamin B6, and vitamin B12.
- Dual antiplatelet therapy (DAPT) with aspirin and clopidogrel for 1 year post-PCI.
Investigation |
Day 2 Result |
Day 3 Result |
Haemoglobin (g/dL) |
13.4 |
12.8 |
Total WBC Count (/µL) |
8,900 |
11,000↑ |
Neutrophils (%) |
65 |
72↑ |
Lymphocytes (%) |
30 |
24↓ |
Fasting Blood Sugar (mg/dL) |
98 |
110 |
Blood Urea (mg/dL) |
24 |
28↑ |
Serum Sodium (mEq/L) |
138 |
137 |
Serum Potassium (mEq/L) |
4.1 |
4.0 |
Homocysteine (µmol/L) |
34↑ |
30↑ |
Troponin I (ng/mL) |
4.5↑ |
2.1↑ |
CRP (mg/dL) |
12↑ |
16↑ |
Electrocardiogram (ECG) |
ST changes resolving |
Non-specific T-wave inversions |
Echocardiography |
Pre-op: PFO with right-to-left shunt |
Post-op: PFO successfully closed; mild hypokinesia persists |
Lower Limb Venous Doppler |
— |
No extension of thrombus |
Coronary Angiography |
— |
Post-PCI: Patent RCA stent |
Outcome and Disposition:
After timely intervention with percutaneous coronary intervention (PCI) and successful closure of the patent foramen ovale (PFO), the patient’s condition stabilized. He was closely monitored in the cardiology unit, and once stable, he was discharged with instructions for follow-up care. The patient was started on dual antiplatelet therapy (DAPT), oral anticoagulation, and vitamin supplementation to manage his hyperhomocysteinemia. A multidisciplinary approach was employed for long-term management to reduce the risk of recurrent thromboembolic events.
Discussion:
Pathophysiology:
The case presents a rare but concerning occurrence of inferior wall myocardial infarction (MI) in a young patient with a patent foramen ovale (PFO) and hyperhomocysteinemia.7,8 Paradoxical embolism through the PFO caused a venous thrombus to traverse into the left atrium, subsequently entering the coronary circulation and occluding the right coronary artery (RCA), leading to the MI.9
Clinical Implications:
This case underscores the need for heightened awareness of paradoxical embolism as a cause of MI in young patients with unexplained ischemic events.20 In individuals with a PFO and additional risk factors like hyperhomocysteinemia, clinicians should maintain a high index of suspicion for embolic events.21 Additionally, it demonstrates the importance of early intervention, including both PCI for coronary revascularization and PFO closure to prevent future embolic events.22 Long-term management must address the underlying hypercoagulable state, in this case, through the use of anticoagulation and homocysteine-lowering therapy.
Conclusion:
This case highlights the complex interplay between congenital anatomical abnormalities (PFO), hypercoagulable states (hyperhomocysteinemia), and thromboembolic events, leading to a rare and life-threatening presentation of myocardial infarction. Early recognition and intervention are essential to prevent recurrence and improve outcomes in such patients. A multidisciplinary approach, including the use of PCI, PFO closure, and long-term anticoagulation therapy, is crucial to managing these complex cases effectively.
Contributions
RS: conceptualization, write-up and manuscript preparation; AM: review of literature and manuscript preparation; RU: review of literature and manuscript preparation APL: review of literature.
Ethics declarations
Ethics approval and consent to participate.
Not applicable.
Consent for publication.
Written informed consent was obtained from the patient’s father for publication of this case report and any accompanying image.
Competing interests
The authors declare that they have no competing interests.
Conclusion
This case highlights the interplay between congenital anomalies and acquired prothrombotic states, necessitating early recognition and a multidisciplinary approach to management.