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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Paradoxical Coronary Embolism Leading to ST-segment Elevation Myocardial Infarction in a Patient with Caval
Davide Restelli1, Riccardo Molinari2, Silvia Massaro3
1Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
Insights
A rare case of myocardial infarction (MI) was caused by a blood clot traveling from the inferior vena cava through a patent foramen ovale (PFO). This paradoxical embolism highlights the need for diverse diagnostic approaches in ST-segment elevation MI.
Area of Science:
- Cardiology
- Vascular Medicine
- Oncology
Background:
- Type 2 myocardial infarction (MI) with nonobstructive coronary arteries presents diagnostic challenges.
- Coronary embolism is an uncommon cause of ST-segment elevation (STE) MI.
- Patients with a history of malignancy require comprehensive evaluation for thromboembolic events.
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.
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