Related Experiment Video
Updated: Jul 5, 2026

06:39
Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
Published on: August 18, 2016
Multifocal spasm with acetylcholine in Prinzmetal angina
1Department of Cardiology Catharina Hospital, Eindhoven, the Netherlands.
Summary
Prinzmetal angina can cause vasospasm in normal coronary arteries, not just blocked ones. This case highlights the importance of provocative testing to guide treatment and avoid unnecessary interventions for coronary artery disease.
Area of Science:
- Cardiology
- Interventional Cardiology
- Pharmacology
Background:
- Prinzmetal angina, a condition characterized by coronary artery vasospasm, can present atypically.
- Distinguishing vasospasm from fixed obstructive lesions is crucial for appropriate patient management.
- Percutaneous coronary intervention (PCI) is typically considered for significant coronary obstructions.
Purpose of the Study:
- To investigate the diagnostic utility of acetylcholine provocative testing in a patient with suspected Prinzmetal angina and a non-critical coronary obstruction.
- To determine the appropriate management strategy for coronary artery vasospasm identified during diagnostic angiography.
Main Methods:
- Coronary angiography was performed in a 60-year-old female patient with Prinzmetal angina.
- Provocative testing using incremental doses of acetylcholine was administered to assess coronary artery reactivity.
- The response of coronary segments, including the site of a non-critical obstruction, was evaluated.
Main Results:
- Acetylcholine infusion induced diffuse mild vasoconstriction and multifocal hyperreactive vasoconstriction in apparently normal coronary segments.
- No significant hyperreactivity was observed at the site of the non-critical (<50%) right coronary artery obstruction.
- These findings indicated vasospasm in non-obstructed segments, characteristic of Prinzmetal angina.
Conclusions:
- Percutaneous coronary intervention was deemed inappropriate given the absence of significant obstructive disease and the presence of vasospasm in normal segments.
- Management focused on medical therapy, including nitrates and calcium antagonists, and avoidance of beta-blockade.
- Acetylcholine provocative testing is valuable in diagnosing Prinzmetal angina and guiding therapeutic decisions, preventing unnecessary interventions.
Related Concept Videos
Angina II: Classification
Angina, also known as angina pectoris, is a chest pain resulting from diminished blood flow to the heart muscle and is often a symptom of coronary artery disease. Angina presents several variants with distinctive attributes, etiologies, and therapeutic approaches. The main types of angina include stable, unstable, variant (Prinzmetal's), microvascular, intractable, and silent ischemia.Stable angina is caused by atherosclerosis, which leads to the formation of plaques that narrow the coronary...
Angina I: Introduction
Definition and Symptoms: Angina (angina pectoris) is chest pain or discomfort caused by myocardial ischemia, which occurs when the heart muscle receives insufficient oxygen-rich blood. It typically manifests as pressing, squeezing, or crushing sensations in the chest and may radiate to the shoulders, arms, neck, jaw, or back.Primary Cause: In a healthy state, the coronary arteries can dilate (widen) to increase blood flow and meet the increased oxygen demand during physical activity or...
Angina III: Clinical Manifestations and Assessment
Angina manifests as chest pain, tightness, or squeezing discomfort typically located behind the breastbone. It can radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, most commonly the left arm. Patients may experience shortness of breath, fatigue, profuse sweating, dizziness, indigestion, heartburn, palpitations, anxiety, and vomiting as accompanying symptoms. This pain often lasts a few minutes and is triggered by physical exertion, emotional stress, heavy meals, or cold...
Cholinergic Receptors: Muscarinic
The pharmacological actions of acetylcholine are elicited via its binding to two families of cholinergic receptors or cholinoceptors, namely, muscarinic and nicotinic receptors. Muscarinic receptors are G protein-coupled receptors and have five subtypes, M1–M5. All mAChR subtypes are activated by acetylcholine and blocked by the antagonist, atropine.
The subtypes M1, M3, and M5 couple with the Gq subunit and activate the phospholipase C (PLC) activity, mobilizing intracellular Ca2+. Activation...
The subtypes M1, M3, and M5 couple with the Gq subunit and activate the phospholipase C (PLC) activity, mobilizing intracellular Ca2+. Activation...
Chemical Synapses
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

