Vasospastic Angina
Vasospastic angina, also known as Prinzmetal's angina or variant angina, is a type of chest pain caused by transient coronary artery spasm, which reduces blood flow to the heart (myocardial ischemia). Unlike typical angina, which is usually triggered by physical exertion or stress, vasospastic angina occurs at rest and is associated with spontaneous coronary vasoconstriction.
1. Mechanism:
- Vasospastic angina occurs due to coronary artery spasm, a temporary narrowing of the coronary arteries caused by smooth muscle constriction, leading to reduced oxygen supply to the heart muscle.
- The spasm can occur in arteries that may or may not have atherosclerotic plaques. Thus, it may happen in both normal and diseased coronary arteries.
2. Clinical Presentation:
- Chest pain at rest: The pain typically occurs at rest, often during the night or early in the morning (circadian variation).
- The pain is often described as tightness or pressure in the chest, similar to other forms of angina.
- The episodes are usually brief, lasting about 5 to 15 minutes.
- The pain may be associated with ST-segment elevation on an electrocardiogram (ECG) during the episode, which resolves once the spasm subsides.
3. Triggers:
- While vasospastic angina can occur spontaneously, some common triggers include:
- Cold exposure.
- Stress.
- Hyperventilation.
- Smoking.
- Use of stimulants (e.g., cocaine, amphetamines).
4. Electrocardiogram (ECG) Findings:
- During an episode, transient ST-segment elevation may be seen, mimicking an acute myocardial infarction (heart attack).
- These ECG changes reverse once the coronary spasm resolves.
- Unlike a typical heart attack, the ST-segment elevation is temporary and does not result in permanent damage to the heart muscle if the spasm is relieved quickly.
5. Pathophysiology:
- The exact cause of coronary artery spasm is not fully understood, but it may involve an imbalance between vasoconstricting and vasodilating factors in the coronary arteries.
- The role of the endothelium (lining of blood vessels) is important in regulating vascular tone. Endothelial dysfunction, where the normal production of nitric oxide (a vasodilator) is impaired, is thought to play a role in the development of coronary artery spasm.
- Additionally, an increased sensitivity of the smooth muscle of the coronary arteries to vasoconstrictors (e.g., endothelin, serotonin) may contribute to the spasm.
6. Diagnosis:
- Diagnosis is primarily based on the clinical history of chest pain at rest, often accompanied by transient ST-segment elevation on ECG.
- Coronary angiography is usually normal or may show only mild coronary artery disease. In some cases, provocative testing with agents like ergonovine or acetylcholine is used to induce coronary spasm during the procedure.
7. Management:
- Calcium channel blockers (CCBs): These are the mainstay of treatment for vasospastic angina. They work by inhibiting the contraction of smooth muscle in the coronary arteries, reducing the likelihood of spasm.
- Examples include diltiazem, verapamil, and amlodipine.
- Nitrates: These medications, such as nitroglycerin, are also effective because they directly dilate the coronary arteries and relieve the spasm.
- Avoidance of Triggers: Stopping smoking, managing stress, and avoiding stimulant drugs are important lifestyle modifications.
- Beta-blockers: These are not typically used in vasospastic angina, as they can potentially exacerbate coronary artery spasm by allowing unopposed alpha-adrenergic stimulation.
8. Prognosis:
- With appropriate treatment, the prognosis of vasospastic angina is generally good, although it can be associated with serious complications like arrhythmias or myocardial infarction if left untreated.
Vasospastic angina is caused by transient coronary artery spasms, leading to chest pain primarily at rest, often during the night or early morning. It is diagnosed through episodes of chest pain with transient ST-segment elevation on ECG, but without permanent damage to the heart muscle. Treatment involves calcium channel blockers, nitrates, and lifestyle modifications to reduce triggers.
- Lanza, G.A., et al. Coronary artery spasm: a 2021 update. Eur Heart J. 2021.
- Prinzmetal, M., et al. Angina pectoris I: A variant form of angina pectoris. JAMA. 1959.
Vasospastic angina, also known as Prinzmetal's angina or variant angina, is a type of chest pain caused by transient coronary artery spasm, which reduces blood flow to the heart (myocardial ischemia). Unlike typical angina, which is usually triggered by physical exertion or stress, vasospastic angina occurs at rest and is associated with spontaneous coronary vasoconstriction.
1. Mechanism:
- Vasospastic angina occurs due to coronary artery spasm, a temporary narrowing of the coronary arteries caused by smooth muscle constriction, leading to reduced oxygen supply to the heart muscle.
- The spasm can occur in arteries that may or may not have atherosclerotic plaques. Thus, it may happen in both normal and diseased coronary arteries.
2. Clinical Presentation:
- Chest pain at rest: The pain typically occurs at rest, often during the night or early in the morning (circadian variation).
- The pain is often described as tightness or pressure in the chest, similar to other forms of angina.
- The episodes are usually brief, lasting about 5 to 15 minutes.
- The pain may be associated with ST-segment elevation on an electrocardiogram (ECG) during the episode, which resolves once the spasm subsides.
3. Triggers:
- While vasospastic angina can occur spontaneously, some common triggers include:
- Cold exposure.
- Stress.
- Hyperventilation.
- Smoking.
- Use of stimulants (e.g., cocaine, amphetamines).
4. Electrocardiogram (ECG) Findings:
- During an episode, transient ST-segment elevation may be seen, mimicking an acute myocardial infarction (heart attack).
- These ECG changes reverse once the coronary spasm resolves.
- Unlike a typical heart attack, the ST-segment elevation is temporary and does not result in permanent damage to the heart muscle if the spasm is relieved quickly.
5. Pathophysiology:
- The exact cause of coronary artery spasm is not fully understood, but it may involve an imbalance between vasoconstricting and vasodilating factors in the coronary arteries.
- The role of the endothelium (lining of blood vessels) is important in regulating vascular tone. Endothelial dysfunction, where the normal production of nitric oxide (a vasodilator) is impaired, is thought to play a role in the development of coronary artery spasm.
- Additionally, an increased sensitivity of the smooth muscle of the coronary arteries to vasoconstrictors (e.g., endothelin, serotonin) may contribute to the spasm.
6. Diagnosis:
- Diagnosis is primarily based on the clinical history of chest pain at rest, often accompanied by transient ST-segment elevation on ECG.
- Coronary angiography is usually normal or may show only mild coronary artery disease. In some cases, provocative testing with agents like ergonovine or acetylcholine is used to induce coronary spasm during the procedure.
7. Management:
- Calcium channel blockers (CCBs): These are the mainstay of treatment for vasospastic angina. They work by inhibiting the contraction of smooth muscle in the coronary arteries, reducing the likelihood of spasm.
- Examples include diltiazem, verapamil, and amlodipine.
- Nitrates: These medications, such as nitroglycerin, are also effective because they directly dilate the coronary arteries and relieve the spasm.
- Avoidance of Triggers: Stopping smoking, managing stress, and avoiding stimulant drugs are important lifestyle modifications.
- Beta-blockers: These are not typically used in vasospastic angina, as they can potentially exacerbate coronary artery spasm by allowing unopposed alpha-adrenergic stimulation.
8. Prognosis:
- With appropriate treatment, the prognosis of vasospastic angina is generally good, although it can be associated with serious complications like arrhythmias or myocardial infarction if left untreated.
Vasospastic angina is caused by transient coronary artery spasms, leading to chest pain primarily at rest, often during the night or early morning. It is diagnosed through episodes of chest pain with transient ST-segment elevation on ECG, but without permanent damage to the heart muscle. Treatment involves calcium channel blockers, nitrates, and lifestyle modifications to reduce triggers.
- Lanza, G.A., et al. Coronary artery spasm: a 2021 update. Eur Heart J. 2021.
- Prinzmetal, M., et al. Angina pectoris I: A variant form of angina pectoris. JAMA. 1959.