Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02180-w

Myocardial infarction with non-obstructive coronary arteries (MINOCA) by supposed coronary thromboembolism by patent foramen ovale (PFO). Should the PFO be closed ?
M. Haj Abdo1, H. Housen1, K. S. Zistler1, M. Holly1, K. Seidl1
1Medizinische Klinik I, Klinikum Ingolstadt GmbH, Ingolstadt;

Case report ( History/clinical examination):

A 47-year-old female presented to our Emergency Department (ED) because of typical chest pain, the patient has never  this pain, at admission day was the first time. This patient has no previous history of DM or hypertention.

An electrocardiogram was performed, which showed sinus rhythm with a ST elevation in II, III and AVF ( Figure 1 ). This Patient has a hs-TNI at 7ng/dl at hour 0 (normal 2.3-11.6 ng/l), , 4 hours after the admission was hs-TNI at 600 ng/dl.

Coronary angiogram was without a significant epicardial coronary artery disease. For further evaluation we measured the microcirculatory resistance (IMR=15) and coronary flow reverse (CFR =3,7) which were not pathologic.

An arterial blood gas showed the following results: pH 7.4 (normal 7.35-7.45), pO2 118 (normal 71-104 mmHg) pCO2 29 (normal 37-43 mmHg), bicarbonate 25.9 (normal 22-26 mmol/L), lactate 1.4 (normal 0.5-2.5 mmol/L), sodium 133 (normal 134-144 mmol/L), potassium 2.7 (normal: 3.5-5.5 mmol/L).The patient sufferd form hyperventilation by the stress.





Figure 1

Using  cardiac-MRI showed a suspected intramural scar in the inferior wall of the heart, Myocarditis and takutsubo cardiomyopathie were excluded.(Figure3)

In the next day we have done transesophageal echocardiographie (TEE), which showed  a patent foramen ovale (PFO). There was no event for left atrial appendage thrombosis, valvular vegetations or Myoxome. (Figure2)




Figure 2



The Echocardiographic showed a good systolic ejection fraction of left and right  ventricle .

Due to the presentation of acute coronary thrombosis and the absence of plaque or vasospasm, a paradoxical embolism or hypercoagulable state was suspected. An autoimmune and thrombophilia screen was conducted and showed no evidence of hypercoagulability.




 Figure 3

Discussion:

PFO is common abnormality affecting between 20 % and 35 % of the people. The most of people are asyptomatic, but in some, PFO can enable a paradoxical embolus and cause a thromboemolisation .

The majority of paradoxical coronary artery embolism occurrences are missed clinically and remain undiagnosed. High clinical suspicion is required to make the diagnosis. It is an important diagnosis to make as it has an impact on management and prognosis.

The case was discussed at a heart team meeting and the decision was made to offer the patient percutaneous closure of the PFO. Successful PFO closure was performed using an 18 mm Amplatzer occluder with no acute complications.

 

Conclusion:

Paradoxical coronary embolism is a rare cause of acute coronary syndrome. Once suspected, careful imaging including TEE is important for a presumptive diagnosis. In addition to acute management of acute coronary syndrome, PFO closure to prevent recurrent thromboembolism should be considered.

 


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