What are coronary spasms?
Spasm of the coronary arteries, also known as vasospastic angina, is thought to occur from hypersensitivity and hyperreactivity of the smooth muscle within the coronary arteries that impact constriction and dilation. In the case of vasospastic angina, the arteries constrict, leading to reduced flow and lower perfusion of heart muscle. The result is cardiac chest pain (angina).
The smooth muscle of the coronary arteries is under the influence of the autonomic nervous system (ANS), part of the homeostasis of circulation in general. In the ANS, sympathetic stimulation causes constriction and parasympathetic stimulation causes relaxation, and an imbalance in this regulation can result in vasospasm; alternately, an overstimulation from both increased sympathetic tone and vagal tone (parasympathetic) can provoke it. Other contributions to vasospasm of the coronary arteries include endothelial (inner arterial lining) abnormalities and inflammation.
The major risk factor for coronary vasospasm is cigarette smoking. Exercise does not usually provoke it, but other triggers include:
- Changes in activity of the ANS
- Toxicity of drugs, including ephedrine-based products, cocaine, marijuana, alcohol, and amphetamines
- Botulism (food/ingestion of botulinum toxin)
- Hypomagnesemia (magnesium deficiency)
- Interventional coronary angioplasty
- Allergies that evoke inflammatory mediators
Signs and Symptoms
Recurrent chest pain (angina) in vasospastic angina is indistinguishable from classic angina, except that
- It occurs primarily at rest, frequently from mid-night to morning
- Pain lasts from 5-15 minutes or longer
Like classic angina, vasospastic angina’s similarities include:
- pain that is a vague discomfort rather than overt pain
- episodes are gradual in onset and resolution
- position or respiration do not affect it
- pain is poorly localized
- there may be nausea, sweating, palpitations, dyspnea, or dizziness