A heart spasm, medically known as a coronary artery spasm (CAS) or Prinzmetal Angina, is a sudden, temporary, and intense tightening of the muscular wall of one of the coronary arteries. These arteries supply oxygen-rich blood to the heart muscle, and the spasm causes a severe, transient reduction in blood flow, leading to chest pain, or angina. Unlike the more common form of angina caused by fixed blockages from plaque, Prinzmetal Angina typically occurs at rest, often in the early morning hours. This temporary occlusion can be serious, potentially leading to heart attack or life-threatening arrhythmias.
The Physiological Mechanism of Spasm
The physical event of a heart spasm is rooted in the abnormal behavior of the coronary artery wall’s inner lining, called the endothelium, and the surrounding layer of smooth muscle cells. The endothelium normally regulates the artery’s diameter by releasing substances that cause relaxation, most notably nitric oxide (NO). This potent vasodilator ensures the artery remains open and responsive to the heart’s needs.
In individuals susceptible to spasms, the production or bioavailability of nitric oxide is impaired, a condition known as endothelial dysfunction. This deficit removes the natural brake on the artery’s muscular layer, making the vessel hyper-reactive to constricting signals. The smooth muscle cells also exhibit an increased sensitivity to constrictive stimuli, often due to an imbalance in intracellular calcium handling. This hyper-contractility, combined with the lack of sufficient nitric oxide, results in the sudden and severe constriction that characterizes the spasm.
Acute External Triggers
While the underlying predisposition for a spasm is chronic, the event itself is often initiated by an immediate, external trigger. Exposure to cold temperatures can provoke a spasm by activating the body’s sympathetic nervous system, causing generalized vasoconstriction in an already susceptible coronary artery. Similarly, intense emotional stress elevates the sympathetic nervous system activity, which can precipitate a spasm through the release of constricting hormones.
Certain substances and medications can directly trigger the hyper-reactive smooth muscle cells. Recreational drugs such as cocaine and amphetamines are potent vasoconstrictors and are well-known spasm inducers. Prescription drugs, including specific migraine medications and decongestants containing pseudoephedrine, can cause a spasm in sensitive individuals due to their effect on blood vessel constriction. Hyperventilation can also serve as an acute trigger by altering the blood’s acid-base balance, further promoting constriction.
Chronic Predisposing Factors
The most significant and independent chronic factor predisposing an individual to coronary artery spasms is heavy cigarette smoking. The toxins in tobacco smoke cause direct and cumulative damage to the delicate endothelial lining, leading to severe endothelial dysfunction and reduced nitric oxide availability. This damage establishes the baseline hyper-reactivity of the coronary arteries.
Genetic factors also play a substantial role in determining susceptibility in certain populations. For instance, a polymorphism in the aldehyde dehydrogenase 2 (ALDH22) gene is a strong risk factor, especially prevalent among East Asian populations. This genetic variation impairs the body’s ability to detoxify harmful aldehydes, which are byproducts of alcohol metabolism and tobacco smoke, thereby increasing oxidative stress and vascular damage.
Low-grade systemic inflammation, indicated by elevated levels of C-reactive protein, is frequently observed in patients with CAS and contributes to the ongoing endothelial impairment. Furthermore, a deficiency in magnesium can increase the smooth muscle cell’s contractility. While traditional risk factors like hypertension and high cholesterol are less consistently linked to CAS than to typical coronary artery disease, they still contribute to overall vascular stress and dysfunction.
Identifying a Coronary Artery Spasm
Diagnosing a coronary artery spasm can be challenging due to its transient nature; the artery returns to normal once the spasm resolves. The initial suspicion often arises from a patient reporting chest pain that occurs at rest or wakes them from sleep. During an episode, an electrocardiogram (ECG) typically shows a temporary elevation in the ST-segment, which signifies a complete lack of blood flow to a portion of the heart muscle.
The definitive diagnostic method is often an invasive procedure called coronary angiography. During this test, a small catheter is inserted into the coronary artery, and a pharmacological agent, such as acetylcholine or ergonovine, is administered to intentionally provoke a spasm. A positive diagnosis is confirmed if the artery narrows by 90% or more, accompanied by the patient’s typical symptoms and corresponding ECG changes.