Inferior Wall Myocardial Infarction in a Patient with Patent Foramen Ovale and Hyperhomocysteinemia

Authors

Ridhava Singh*, Rajkumar Usdadia, Arjun Mohandas, Abel Paul Leslie

Pravara Institute of Medical Sciences, Loni -413736, India.

Article Information

*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.

Abstract

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

Keywords

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

  • General Condition: The patient appeared anxious but was hemodynamically stable.
  • Vital Signs: Blood pressure: 122/78 mmHg, heart rate: 88 bpm (regular), respiratory rate: 18/min, oxygen saturation: 98% on room air.
  • Cardiovascular Examination: Heart sounds were normal with no murmurs. Peripheral pulses were palpable and symmetrical.
  • Respiratory Examination: Normal breath sounds bilaterally.
  • Abdomen: Soft, non-tender with no palpable organomegaly.
  • Lower Limb Examination: Mild swelling and tenderness were noted in the left calf without erythema or warmth.
  • Neurological Examination: Normal, with no focal deficits.

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

 

A close-up of a graphDescription automatically generated

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

  1. Patent Foramen Ovale (PFO): A PFO is a common congenital cardiac anomaly that is often asymptomatic.10 However, in the presence of other risk factors, such as hypercoagulable states, it can lead to paradoxical embolism.11 In this case, the venous thrombus passed through the PFO, which is a critical pathway that allowed the clot to reach the coronary circulation and precipitate the MI.12
  2. Hyperhomocysteinemia: Elevated homocysteine levels are a known risk factor for thrombosis and endothelial dysfunction.13 Hyperhomocysteinemia can increase the propensity for thromboembolic events by promoting endothelial damage, decreasing nitric oxide bioavailability, and enhancing platelet aggregation.14 In this patient, it likely played a crucial role in the formation of the thrombus, which was then able to cross through the PFO and reach the coronary artery.15
  3. Thromboembolism and Myocardial Infarction: The thrombus, once lodged in the RCA, led to myocardial ischemia and infarction.16 The presence of a PFO compounded the risk, creating an ideal scenario for paradoxical embolism—a phenomenon in which venous thrombi bypass the pulmonary circulation and enter the systemic circulation.17
  4. Venous Thrombus and Systemic Embolization: The venous thrombus in this patient originated in the lower extremities and, due to the PFO, was able to migrate to the left atrium, the aorta, and eventually the coronary artery.18 This case highlights the importance of screening for paradoxical embolism in patients with unexplained myocardial infarction, particularly in the young population.19

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.

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