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Published on: April 1, 2019
Multiple gene polymorphisms predisposing to the prothrombotic state in an adolescent with acute myocardial infarction
1Department of Cardiology, Medical School, Suleyman Demirel University, Isparta, Turkey. adogan35@hotmail.com
Insights
This study highlights a rare case of acute myocardial infarction with ST-segment elevation in an adolescent. Multiple prothrombotic gene variations were identified, suggesting a potential genetic link in adolescent STEMI.
Area of Science:
- Cardiology
- Genetics
- Thrombosis
Background:
- Acute myocardial infarction with ST-segment elevation (STEMI) is uncommon in adolescents.
- The underlying causes of STEMI in this age group are not well understood.
- A prothrombotic state is increasingly linked to acute STEMI.
Observation:
- A case of adolescent STEMI with normal coronary arteries is presented.
- The patient exhibited catheter-induced coronary artery spasm.
- Multiple prothrombotic genetic polymorphisms were identified.
Findings:
- The adolescent patient possessed polymorphisms in beta fibrinogen, methylenetetrahydrofolate reductase, and cholesteryl ester transfer protein genes.
- Genotypes for plasminogen activator inhibitor-1 and human platelet antigen type-1 were also noted.
- These genetic factors may contribute to a prothrombotic state.
Implications:
- Prothrombotic genetic factors may play a role in the pathogenesis of adolescent STEMI.
- Understanding these genetic predispositions could inform future risk assessment and prevention strategies.
- Treatment involved a calcium antagonist and aspirin for catheter-induced spasm.
Abstract:
Acute myocardial infarction with ST-segment elevation (STEMI) is rare in adolescents and its pathogenesis is unclear. Growing evidence shows an association between the prothrombotic state and acute STEMI. Prothrombotic genetic factors may be involved in the pathogenesis of STEMI. We present a case of an adolescent with acute STEMI who had multiple prothrombotic gene polymorphisms: in the beta fibrinogen, methylenetetrahydrofolate reductase and cholesteryl ester transfer protein genes, as well as genotypes in plasminogen activator inhibitor-1 and human platelet antigen type-1. He had normal coronary arteries with catheterinduced spasm and was treated with a calcium antagonist and aspirin.
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