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The mystery of coronary artery spasm: How does it cause angina?
Coronary artery spasm is a sudden complete or partial temporary obstruction of the coronary arteries. As early as 1959, Prinzmetal et al first described this chest pain and called it variant angina. This type of angina has since become known in the literature as Prinzmetal angina. Later studies further differentiated this type of angina from traditional angina through cardiac catheterization and found that patients with Prinzmetal angina did not show atherosclerotic plaques in their coronary arteries during examination, which was exactly the opposite of the typical findings of traditional angina. .
When coronary artery spasm occurs, the temporary blockage can lead to ischemia, which can result in a wide range of symptoms and may even lead to myocardial infarction and sudden cardiac death.
Signs and symptoms
Coronary artery spasm often produces chest pain in a static state, which is called variant angina (or vasospastic angina). This type of chest pain is usually more common at certain times of the day (usually night to early morning). Patients may experience symptoms such as nausea, vomiting, cold sweats, and fainting at the same time. Fatigue, shortness of breath, and heart palpitations may also be primary symptoms, but these conditions may also occur along with chest pain. Notably, some patients with coronary artery spasm do not even have any symptoms, leading to silent myocardial ischemia.
Complications
Different lengths of coronary artery obstruction may cause different symptoms of myocardial ischemia. Shorter obstructions may result in silent myocardial ischemia, whereas longer obstructions may cause stable or unstable angina, myocardial infarction, or even sudden cardiac death.
Risk factors
Unlike traditional angina, coronary artery spasm is not significantly affected by traditional cardiovascular risk factors, with the only exception being smoking, which is considered a modifiable risk factor for vasospastic angina. A variety of factors are thought to trigger the onset of coronary artery spasm, often by affecting the autonomic nervous system. For example, coca use can trigger coronary artery spasm through its effects on adrenergic receptors, while exercise, cold weather, mental stress, and hyperventilation are also possible triggers.
Pathophysiology
The exact pathomechanism of coronary artery spasm has not been fully elucidated, but multiple factors have been proposed as possible contributors. Among them, certain abnormalities in the coronary arteries can cause them to overreact to vasoconstrictive stimuli, which can lead to complete or temporary obstruction of blood flow, resulting in ischemia.
Diagnosis
There are currently no clear criteria for diagnosing coronary artery spasm. A detailed medical history can help confirm the diagnosis, especially identifying the characteristics of chest pain. Additionally, an electrocardiogram (EKG) can be used for diagnosis in some cases. However, due to the transient nature of coronary artery spasm, EKG sometimes fails to capture these episodes, so coronary catheterization can be used to induce spasm for closure testing. Such tests use agonists to induce spasm of the coronary arteries, but are not routinely used clinically because of the serious side effects of these drugs.
EKG Discovery
When coronary artery spasm results in complete obstruction, the electrocardiogram may show ST-segment elevation in the territory supplied by that artery. In cases of subtotal obstruction, transient ST-segment depression may occur. Sometimes, arrhythmias caused by ischemia will also appear on the electrocardiogram, including premature ventricular contraction, ventricular pulsation, and ventricular fibrillation.
History
Since chest pain due to coronary artery spasm was first described in 1959 by Prinzmetal et al., this phenomenon has been given its name, and subsequent studies have helped to better define the process and its treatment.
Coronary artery spasm is a complex phenomenon, and there are still many unknowns about its specific induction and pathological mechanisms. So, will understanding these unknown factors have a profound impact on future medical treatment?
