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Published on: May 28, 2019
A Rare Case of Persistent ST-Elevation Myocardial Infarction Post-Tissue Plasminogen Activator With White Clot
Syed S Fatmi1, Paramjit Kaur1, Emmanuel Tangco2
1Internal Medicine, Southeast Health Medical Center, Dothan, USA.
Insights
This case report details a persistent ST-elevation myocardial infarction (STEMI) in a patient who formed a white clot, unresponsive to recombinant tissue plasminogen activator (rTPA). This highlights potential limitations of rTPA in treating white clot STEMIs.
Area of Science:
- Cardiology
- Thrombosis Research
Background:
- ST-elevation myocardial infarction (STEMI) is typically associated with red clots, while NSTEMI involves white clots.
- Recent research indicates a subset of STEMIs result from white clot formation, often at coronary artery bifurcations.
Observation:
- A case of persistent STEMI post-recombinant tissue plasminogen activator (rTPA) administration is presented.
- The patient, using depot contraception, formed a white clot unresponsive to rTPA, requiring thrombectomy.
Findings:
- This is the first reported case of a white clot STEMI occurring after rTPA administration.
- Limited data exists on rTPA's efficacy in lysing white clots, raising questions about its effectiveness.
Implications:
- This case underscores the need for further investigation into the efficacy of rTPA for white clot lysis.
- Understanding and managing white clot STEMIs, especially in patients with specific risk factors like depot contraceptive use, is crucial for improving treatment strategies.
Abstract:
ST-elevation myocardial infarction (STEMI) occurs when vulnerable intravascular plaques rupture and produce eventual occlusion of the coronary circulation. With the increased prevalence of coronary artery disease, STEMIs and NSTEMIs are very well-studied and have generally been known to be caused by red and white thrombi, respectively. STEMIs have been more commonly associated with red clots, while NSTEMIs tend to be caused by white clots. Recent studies have also shown that a third of STEMIs are due to white clot formation, resulting in transmural infarction, most commonly seen at the coronary artery bifurcation. However, no cases of white clot STEMIs post-recombinant tissue plasminogen activator (rTPA) administration have been described in the literature. The data regarding the utility of rTPA in lysing white clots is limited, questioning the overall efficacy of rTPA with white clot lysis. This case report presents a patient on depot contraceptive who had a persistent STEMI despite rTPA administration and was found to have formed a white clot, which was extracted on thrombectomy. As this unique presentation and its associated risk factors are explored in the future, we hope that this case report contributes to the body of knowledge in the detection and management of white clot MIs in the context of rTPA efficacy.
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