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[Coronary spasm-induced acute myocardial infarction associated with intracoronary thrombosis]
A Hasegawa1, M Horimoto, T Takenaka
1Division of Cardiology, National Sapporo Hospital.
Insights
Coronary artery spasm can trigger thrombus formation and acute myocardial infarction. This case highlights the crucial role of coronary spasm in the development of myocardial infarction.
Area of Science:
- Cardiology
- Vascular Biology
Background:
- Acute myocardial infarction (AMI) is a leading cause of mortality worldwide.
- The pathogenesis of AMI is complex, involving atherosclerosis, thrombosis, and potentially vasospasm.
Observation:
- A 63-year-old man presented with acute anteroseptal myocardial infarction due to severe left anterior descending (LAD) artery stenosis.
- Initial angiography revealed significant LAD stenosis with intraluminal thrombus.
- Treatment with isosorbide dinitrate and urokinase improved blood flow and reduced thrombus burden.
Findings:
- Chronic phase angiography showed persistent LAD stenosis.
- Intracoronary acetylcholine administration provoked coronary spasm at the stenotic site, inducing chest pain and ST-segment elevation.
- This suggests a dynamic interplay between fixed stenosis and vasospasm in causing acute coronary events.
Implications:
- Coronary artery spasm is a significant factor in the pathogenesis of acute myocardial infarction.
- Understanding the role of spasm in thrombosis may lead to novel therapeutic strategies for AMI.
- This case underscores the importance of considering dynamic vasospasm in patients with acute coronary syndromes.
Abstract:
A 63-year-old man was admitted with an acute anteroseptal myocardial infarction. Coronary angiography performed 3 hours after the onset of chest pain revealed 99% stenosis of the proximal left anterior descending coronary artery (LAD) with delayed filling and intraluminal thrombus distal to the stenosis. After the intracoronary injection of isosorbide dinitrate, the delayed filling disappeared and a subsequent intracoronary urokinase partially dissolved the thrombus. Repeat coronary angiography in the chronic phase disclosed 75% stenosis of the LAD and disappearance of the thrombus. Intracoronary acetylcholine provoked a coronary spasm at the stenotic site of the LAD, concomitantly with chest pain and ST-segment elevation in the anterior leads. The present case demonstrated that coronary spasm plays an important role in thrombus formation and acute myocardial infarction. To date, the concept has been postulated that a dynamic interaction between atherosclerosis, platelet aggregation and spasm may work to cause coronary thrombosis and subsequently lead to acute myocardial infarction. Our report shed light on the importance of coronary spasm in the pathogenesis of myocardial infarction.