Key result
Tenecteplase for stroke triggers an embolic posterolateral STEMI despite complete neurological recovery.
Why the study?
While tenecteplase for acute ischemic stroke carries a known bleeding risk, subsequent major thrombotic events such as acute myocardial infarction are less commonly described.
Case Report (n=1)
No
This case report demonstrates that acute myocardial infarction can occur rapidly following tenecteplase administration for acute ischemic stroke due to coronary embolization of mixed thrombus and calcified atherosclerotic plaque fragments, highlighting the need for close cardiovascular monitoring and individualized revascularization strategies post-thrombolysis.
Warrants vigilance for acute MI after tenecteplase in stroke; single case leaves open causality and incidence.
Introduction: Acute ischemic stroke is a leading cause of morbidity and mortality, with tenecteplase being a cornerstone of acute management. While tenecteplase carries a known risk of bleeding, major thrombotic events such as acute myocardial infarction (AMI) after stroke reperfusion are less commonly described. Case Report: We present the case of a 67-year-old man who presented with acute stroke symptoms. After ruling out intracranial hemorrhage and managing blood pressure, he received tenecteplase, and all neurological deficits resolved. Soon after, he developed acute chest pain, and his repeat electrocardiogram confirmed a ST-elevation myocardial infarction. He underwent emergent cardiac catheterization, revealing 100% occlusion of the left circumflex artery, which was successfully revascularized with thrombectomy and angioplasty. Intravascular ultrasound further supported the presence of embolic phenomenon. Pathology of the retrieved material identified thrombus alongside atherosclerotic plaque fragments. The patient experienced complete symptom resolution and was discharged after a short hospitalization.This case highlights the complexities encountered when a patient with acute ischemic stroke who is treated with tenecteplase subsequently develops an AMI. Potential mechanisms include a coincidental plaque rupture, possibly exacerbated by the stress of the acute stroke, a rare paradoxical prothrombotic effect of thrombolysis, or a combination thereof. The pathological finding of mixed thrombus and atherosclerotic plaque underscores the underlying disease contributing to this event. Conclusion: This case accentuates the importance of maintaining a high index of suspicion for new cardiovascular events in post-thrombolysis patients, especially those with significant cardiovascular risk factors. Rapid and judicious diagnostic evaluation is crucial for timely management of these complex, life-threatening complications.
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Howell et al. (2026) conducted a case report in Acute ischemic stroke complicated by ST-elevation myocardial infarction (n=1). Tenecteplase followed by aspiration thrombectomy and balloon angioplasty was evaluated on Neurological recovery (NIHSS score) and coronary revascularization following acute posterolateral STEMI. Tenecteplase (0.25 mg/kg) resolved acute stroke deficits (NIHSS 10 to 0) within 15 minutes, but was followed at 30 minutes by an embolic posterolateral STEMI with 100% left circumflex occlusion.
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