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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Sequential development of cardiac tamponade and subacute stent thrombosis after primary percutaneous coronary
Sung Soo Kim1, Myung Ho Jeong1, Doo Sun Sim1
1The Heart Research Center of Chonnam National University Hospital, 8 Hakdong Dongku, Gwangju, South Korea.
Insights
Subacute stent thrombosis after percutaneous coronary intervention (PCI) can cause serious complications like pericardial effusion. Early diagnosis and treatment with balloon angioplasty are crucial for successful outcomes in ST-elevation myocardial infarction patients.
Area of Science:
- Cardiology
- Interventional Cardiology
Background:
- ST-elevation myocardial infarction (STEMI) requires prompt revascularization.
- Drug-eluting stents (DES) are commonly used in percutaneous coronary intervention (PCI).
- Glycoprotein IIb/IIIa inhibitors are used peri-procedurally.
Observation:
- A patient developed hemodynamic instability and cardiac tamponade hours after successful PCI with DES.
- Initial coronary angiography ruled out acute stent thrombosis or coronary perforation.
- Recurrent hypotension and ECG changes 7 days later indicated subacute stent thrombosis.
Findings:
- Subacute stent thrombosis of the left anterior descending artery (LAD) was diagnosed via repeat coronary angiography.
- Pericardial effusion was drained, temporarily stabilizing the patient.
- Successful treatment with balloon angioplasty and dual anti-platelet therapy was achieved.
Implications:
- This case highlights the potential for delayed stent thrombosis even after initial procedural success.
- Prompt recognition and emergent re-intervention are vital for managing complications of PCI.
- Long-term dual anti-platelet therapy is essential for preventing stent thrombosis.
Abstract:
A 42-year-old male suffered from ST elevation myocardial infarction and underwent successful percutaneous coronary intervention (PCI) of the left anterior descending coronary artery (LAD) with drug-eluting stent using intravenous glycoprotein IIB/IIIa inhibitor (Clotinab®, Isu Abxis). Five hours after PCI, the patient developed cold sweating and went into a stupor. Urgent 2D-echocardiography showed a large amount of pericardial effusion and akinesia in the LAD territory. A repeat emergent angiography (CAG) was done to ascertain whether acute stent thrombosis or coronary perforation had occurred after PCI. The CAG showed, however, no leakage of dye or thrombus in any coronary arteries with a patent stent in the middle LAD. Approximately 200 cm3 of bloody pericardial effusion was drained, and his blood pressure returned to normal immediately after pericardiocentesis. Seven days later, he again developed sudden hypotension, bradycardia, and loss of consciousness. The ECG showed ST elevation in V1-V6 and 2D-echocardiography showed scanty pericardial effusion. Emergent CAG showed total occlusion of the LAD due to subacute stent thrombosis. He was successfully treated with balloon angioplasty and was discharged with dual anti-platelet therapy. A follow-up CAG after 9 months showed good flow without residual stenosis across the stented segment.
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