ECG criteria
- Transient ST-segment elevation during a pain episode, roughly ≥1 mm (0.1 mV) in two or more contiguous leads, serves as a reference point for assessing ischemic ST elevation rather than a standalone diagnostic criterion for vasospastic angina itself
- Transient ST depression ≥1 mm (0.1 mV) or other transient ST-T changes during the attack are also possible — the distribution depends on the territory of the spastic artery
- ST elevation or depression is localized in leads corresponding to the territory of the spastic artery (most commonly the right coronary or left anterior descending artery, with the circumflex artery also possible)
- ST changes usually rapidly regress after the pain subsides or a nitrate is administered; the response to nitrates supports the diagnosis but does not confirm it by itself, and reversibility may be incomplete
- Between attacks, the ECG may be completely normal
- Reciprocal ST changes in opposite leads may occur during the episode
- At the peak of ischemia, transient rhythm disturbances are possible: ventricular extrasystoles, ventricular tachycardia, AV block (especially during right coronary artery spasm)
- The T wave may temporarily increase in amplitude (hyperacute) synchronously with ST elevation
What it looks like on ECG
During the attack, ST-segment elevation occurs, morphologically resembling STEMI — dome-shaped (coved) or upwardly convex; transient ST depression is also possible. The localization corresponds to the spastic artery's territory, but the match is not strictly fixed: during right coronary artery spasm, changes are most often in II, III, aVF; during left anterior descending spasm — in V1–V4; during circumflex artery spasm, the distribution is variable and may include lateral leads I, aVL, V5–V6, inferior II, III, aVF, and/or posterior V7–V9 — if posterior ischemia is suspected, these should be recorded separately. Unlike true infarction, a pathological Q wave usually does not form, and ST changes typically regress rapidly after pain relief (nitroglycerin, spontaneous resolution of spasm), although complete reversibility is not mandatory — residual T-wave changes or, in prolonged spasm, permanent injury are possible.
Reciprocal ST depression in opposite leads is possible. At the height of the episode, the T wave may temporarily increase and merge with the elevated ST, resembling hyperacute T waves. Frequently, it is precisely at the peak of ischemia that ventricular extrasystoles, runs of ventricular tachycardia, or even ventricular fibrillation are recorded — the ECG at this moment is critically important for diagnosis.
| Phase | ECG pattern |
|---|---|
| Attack | ST elevation (less commonly depression) in the spasm zone, ± reciprocal changes |
| After relief | ST usually regresses; the T wave may normalize, temporarily invert, or retain residual changes |
| Interictal period | ECG frequently without abnormalities |
Holter monitoring or an ECG recorded directly during the pain episode is best suited for documenting the episode.
Mechanism
The underlying mechanism is focal, intense smooth muscle spasm of an epicardial coronary artery, which sharply reduces the vessel lumen up to complete occlusion for a brief period. This causes transmural myocardial ischemia in the affected territory — ST elevation reflects transmural (rather than just subendocardial) injury, similar to the mechanism in STEMI, but without atherosclerotic plaque rupture. The spasm is associated with endothelial dysfunction and increased reactivity of the vascular wall smooth muscle cells; it can occur both in intact arteries and in segments with non-stenosing atherosclerosis, and can also be triggered by exertion when combined with stable atherosclerotic disease or pronounced vasomotor reactivity. After the spasm resolves, blood flow is restored, and the ECG usually normalizes.
Causes
Established risk factors:
- Coronary artery endothelial dysfunction
- Smoking — one of the main risk factors
- Use of cocaine and other vasoconstrictive substances
Potential triggers and associations (role is ambiguous or less fully studied):
- Autonomic imbalance and fluctuations in vascular smooth muscle tone (attacks are frequent at night and early morning, but can also occur with exertion)
- Migraine and Raynaud's phenomenon (associated vascular reactivity)
- Hypomagnesemia as a potential trigger
- Cold, hyperventilation, emotional stress
Differential diagnosis
- STEMI due to plaque rupture: without reperfusion, ST elevation usually persists or progresses, troponin rises; however, spontaneous reperfusion, intermittent occlusion, and early spontaneous resolution of ST elevation are possible, and troponin may still be normal initially — the transient nature of changes does not rule out acute coronary occlusion or MINOCA, decisions are made based on clinical presentation, serial ECGs, troponin, and risk, rather than ST reversibility alone. In Prinzmetal angina, ST elevation is transient and usually resolves spontaneously or after nitrates
- Takotsubo syndrome: ST elevation is diffuse, often following emotional stress, but the dynamics are slower and apical akinesia on echocardiography is typical
- Early repolarization: ST elevation is stable, does not change over time, and has no relation to pain
- Pericarditis: diffuse, usually concave ST elevation with PR depression, reciprocal changes predominantly in aVR (sometimes V1), without local attachment to a coronary territory and in conjunction with clinical presentation and dynamics
- Brugada pattern: ST elevation in V1–V2 of 'saddleback' or 'coved' type, unrelated to anginal attacks and not changing synchronously with anginal pain
Clinical significance and management
The main danger is not the ST elevation itself, but ventricular arrhythmias at the peak of ischemia, which can lead to sudden cardiac death; less commonly, the spasm is prolonged enough to cause a true myocardial infarction.
In the presence of persistent ST elevation, ongoing pain, hemodynamic instability, or life-threatening arrhythmias, the initial contact management does not differ from suspected STEMI: immediate evaluation and emergency coronary angiography to rule out thrombotic occlusion (bearing in mind that the temporary disappearance of ST elevation does not rule out the occlusion itself). If the attack has already completely resolved and there is no ongoing ischemia, ST elevation alone does not automatically dictate emergency angiography — urgent ACS risk stratification is performed: serial ECG and troponin, clinical assessment, and early coronary angiography according to indications.
Diagnosis of vasospastic angina (VSA) is conventionally described according to the criteria of the international COVADIS study group, dividing it into definite and suspected forms. Definite VSA is nitrate-responsive typical anginal pain (usually at rest, often at night or early morning, although exertion-induced attacks are also possible) combined with documented transient ischemic ECG changes during a spontaneous episode and/or angiographically confirmed coronary artery spasm — transient lumen narrowing usually greater than 90% with reproduction of symptoms and ischemic ECG changes during a provocation test. If the set of features is incomplete (e.g., typical clinical presentation without documented ECG changes or spasm of such degree), it is termed suspected VSA. The absence of significant stenosis on angiography and pain relief alone do not confirm the diagnosis — vasospasm may coexist with atherosclerotic lesions, and symptom resolution does not rule out MINOCA or another cause of ACS.
Provocative testing is performed only in an experienced center under continuous ECG monitoring and with readiness to immediately relieve the spasm: the preferred method is the intracoronary acetylcholine test during coronary angiography, and ergonovine is also used according to local protocol; hyperventilation has lower diagnostic value and is not equivalent to invasive provocation.
Basic therapy (at the physician's tactical level): calcium channel blockers as first-line drugs for seizure prevention, with long-acting nitrates added if necessary; mandatory elimination of triggers (smoking, vasoconstrictors, cold). Non-selective and general β-blockers without a specific indication are undesirable—they can exacerbate coronary spasm and are not a treatment for VSA. In cardiac arrest due to spasm, indications for cardioverter-defibrillator implantation are evaluated based on the risk of recurrence. Repeat Holter monitoring helps establish the link between attacks and a specific time of day and identify concurrent arrhythmias.
Common interpretation errors
- Interpreting transient ST elevation as definitive STEMI without correlating the ECG with pain dynamics
- Failing to repeat the ECG after pain relief, thereby missing the key sign: the reversibility of changes
- Ignoring ventricular arrhythmias occurring synchronously with ST elevation as an incidental finding
- Confusing with early repolarization due to the visual similarity of ST elevation without considering clinical dynamics
- Considering complete resolution of an attack without ongoing ischemia as an indication for immediate angiography in every case, forgetting about risk stratification
- Ruling out Prinzmetal's angina solely on the grounds that the attack occurred during exertion
1. Which ECG sign is characteristic of Prinzmetal's angina during an attack?
The main sign is a reversible ST elevation temporally associated with a pain episode and coronary artery spasm.
2. Which complication is most dangerous at the peak of ischemia in Prinzmetal's angina?
Transmural ischemia due to spasm creates myocardial electrical instability and can provoke life-threatening ventricular arrhythmias.
3. How does ST elevation in Prinzmetal's angina differ from STEMI caused by plaque rupture?
The key difference is the transient nature of the changes: the spasm resolves, and the ST segment typically returns to the baseline without the formation of a Q wave and without marked troponin elevation.
Frequently asked questions
How does Prinzmetal's angina differ from regular angina pectoris?
Prinzmetal's angina typically occurs at rest, often at night or early in the morning, but attacks can also occur during physical exertion, especially when combined with atherosclerotic coronary artery disease. Classically, it is accompanied by transient ST elevation, but ST depression and other transient changes are also possible. In stable angina pectoris, ischemia is usually related to exertion and more commonly presents with ST depression.
Is Prinzmetal's angina dangerous?
Yes, during an episode of spasm, ventricular arrhythmias up to ventricular fibrillation and sudden cardiac death can occur, and prolonged spasm can lead to myocardial infarction.
How is the diagnosis confirmed if there are no changes on a routine ECG?
Holter monitoring is used to record episodes, and in a specialized hospital setting, provocative testing—preferably with acetylcholine during coronary angiography (or ergonovine according to protocol)—is performed under continuous ECG monitoring.
Is emergency coronary angiography necessary for ST elevation during an attack?
If ST elevation or pain persists, hemodynamic instability or life-threatening arrhythmias are present, the approach is the same as for suspected STEMI: immediate angiography to rule out thrombotic occlusion. If the attack has already completely resolved without ongoing ischemia, urgent ACS risk stratification is performed, and invasive assessment is carried out according to clinical indications.
Why does the Q wave usually not form in Prinzmetal's angina?
Ischemia is caused by brief spasm rather than permanent occlusion, so the myocardium usually does not have time to necrose, and a pathological Q wave generally does not form.
ECG Course
Interpretation from basics to myocardial infarction — learn to read any ECG using a systematic algorithm.
- Video lessons and theory for every topic
- Simulator case studies under every lesson
- Unlimited ECG simulator practice
- Study guide: "All ECGs in 25 minutes"
ECG Strip Simulator
ECG, radiology, histology, pathomorphology, pharmacology — thousands of flashcards with detailed explanations.
- Real ECG strips, not textbook drawings
- Instant answers and explanations
- Streaks and progress tracking in your dashboard
Related terms
More in the section "Ischemia and Myocardial Infarction"
Sources
- Hampton J.R. The ECG in Practice
- Surawicz B., Knilans T.K. Chou's Electrocardiography in Clinical Practice
- Orlov V.N. Guide to Electrocardiography
- ESC Guidelines for the management of acute coronary syndromes, 2023
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.