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Acetylcholine Re-Challenge After Intracoronary Nitroglycerine Administration
Published on: April 4, 2022
[Acute coronary syndrome after diclofenac induced coronary spasm]
A Wieckhorst1, A Tiroke, M Lins
1Universitätsklinikum Schleswig Holstein, Campus Kiel, Med. Klinik, Klinik für Kardiologie, Schittenhelmstrasse 12, 24105 Kiel, Germany. Wieckh.@gmx.de
Insights
Diclofenac, a nonsteroidal anti-inflammatory drug, can provoke coronary vasospasm, leading to acute myocardial infarction. This case highlights the potential risks of NSAIDs in patients with coronary artery disease.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Acute coronary syndrome (ACS) requires prompt diagnosis and management.
- Percutaneous coronary intervention (PCI) is a standard treatment for obstructive coronary artery disease.
Observation:
- A 67-year-old man presented with ACS due to a left anterior descending thrombus, treated with PCI.
- Post-PCI, the patient developed podagra, treated with colchicine and diclofenac.
- Following diclofenac administration, the patient experienced severe angina and signs of myocardial infarction.
Findings:
- Coronary angiography revealed extensive right coronary artery vasospasm.
- Intracoronary verapamil and nitroglycerin successfully resolved the vasospasm.
- The patient self-reported diclofenac use prior to symptom onset.
Implications:
- Oral diclofenac can precipitate coronary vasospasm, even in patients without significant coronary artery disease.
- Clinicians should exercise caution when prescribing NSAIDs to patients with or at risk for coronary artery disease.
- This case underscores the importance of a thorough medication history in managing cardiovascular events.
Abstract:
We report about a 67-year old man, who was submitted to our clinic with acute coronary syndrome. The cardiac catheterization showed a proximal thrombus in the left anterior descending (LAD). The other coronary arteries did not have significant lesions. After percutaneous transluminal coronary angioplasty with stent-implantation into the proximal LAD the patient remained clinically stable. Cardiac enzymes confirmed no myocardial necrosis. Three days after the acute coronary syndrome the patient developed a podagra, which was treated with colchicinum, diclofenac and local cooling. Five hours after initial therapy the patient developed severe symptoms of angina pectoris and electrocardiographical signs of an acute posterior and anterior myocardial infarction. Immediate coronary angiography demonstrated extended vasospasm of the right coronary artery. Intracoronary application of verapamil and nitroglycerin resolved the coronary spasm. The patient reported about a self-indicated application of diclofenac six hours before hospital admission. This case demonstrates that oral application of diclofenac can provoke coronary vasospasm.
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