Coronary Spasm: Symptoms, Types, Causes and Treatment

Coronary spasm, also known as coronary artery spasm or vasospastic angina, is a transient and often dramatic narrowing of the coronary arteries that can lead to chest pain, arrhythmias, myocardial infarction, or even sudden cardiac death. Unlike classic coronary artery disease caused by fixed atherosclerotic blockages, coronary spasm is characterized by temporary constriction of either large (epicardial) arteries or the smaller microvasculature, often in patients with otherwise normal or near-normal coronary arteries. Understanding its symptoms, types, causes, and treatments is crucial for accurate diagnosis and effective management.

Symptoms of Coronary Spasm

The symptoms of coronary spasm can be subtle or severe, mimicking other forms of heart disease. Recognizing these symptoms is critical for timely intervention and prevention of complications.

Symptom	Description	Severity/Occurrence	Source(s)
Chest Pain	Often at rest, can be severe	Frequent, especially at night/early morning	2 4 10 11 12
Arrhythmias	Irregular heartbeats, may be lethal	May cause syncope or sudden death	2 5 10
ECG Changes	ST elevation/depression, U wave	During attacks	2 4 10 12
Syncope	Temporary loss of consciousness	During severe attacks	2 5 10 11

Table 1: Key Symptoms

Chest Pain: The Hallmark Symptom

Chest pain due to coronary spasm is unique. It most often occurs at rest, frequently between midnight and early morning hours, and is not usually triggered by exertion—unlike classic angina. The pain can be intense and may last from a few minutes to over half an hour. Some patients describe it as squeezing or pressure-like discomfort, sometimes radiating to the arms, neck, or jaw 2 4 10 11 12.

Arrhythmias and Syncope

A significant aspect of coronary spasm is its potential to provoke dangerous arrhythmias. These may include ventricular tachycardia, ventricular fibrillation, and advanced heart block, all of which can cause syncope (fainting) and, in severe cases, sudden cardiac death. Multi-vessel coronary spasm especially increases this risk 2 5 10 11.

Electrocardiogram (ECG) Changes

During an episode, ECG typically reveals transient ST-segment elevation or depression, and sometimes negative U waves. These changes help distinguish coronary spasm from other types of chest pain. Obtaining an ECG during an episode is vital for accurate diagnosis 2 4 10 12.

Other Associated Symptoms

• Shortness of breath (dyspnea)
• Palpitations
• Nausea

These symptoms may sometimes accompany or precede chest pain, especially in women or patients with microvascular spasm 8.

Types of Coronary Spasm

Coronary spasm is not a one-size-fits-all phenomenon. It can affect different segments of the coronary circulation, leading to various clinical presentations and implications.

Type	Location Affected	Key Features	Source(s)
Epicardial	Large surface arteries	Classic vasospastic angina, ST changes	1 4 6 7 8 13
Microvascular	Small intramyocardial vessels	Angina with normal arteries, ischemia	1 6 7 8 13
Focal	Specific artery segment	Localized, site-specific spasm	3 5 13
Diffuse	Multiple/many segments	Widespread constriction	3 5 13

Table 2: Types of Coronary Spasm

Epicardial Spasm

Epicardial spasm involves the large, visible coronary arteries running on the heart's surface. It's the classic form, frequently causing chest pain at rest and ST-segment elevation on ECG (variant or Prinzmetal angina). It can occur even in the absence of significant coronary artery disease and is often triggered by acetylcholine or ergonovine during diagnostic testing 1 4 6 7 8 13.

Microvascular Spasm

Microvascular spasm affects the tiny vessels within the heart muscle, invisible on standard coronary angiograms. Patients often present with angina and evidence of ischemia, but their coronary arteries appear normal or minimally diseased. Microvascular spasm is more common in women and is often associated with diastolic dysfunction 1 6 7 8 13.

Focal vs. Diffuse Spasm

• Focal Spasm: Localized narrowing at a specific artery segment, often reproducible at the same site with provocative testing 3 5 13.
• Diffuse Spasm: Involves multiple or long segments of coronary arteries, sometimes leading to widespread myocardial ischemia 3 5 13.

Overlap and Coexisting Types

It's not uncommon for patients to have both epicardial and microvascular spasm simultaneously, and recognition of this overlap can guide more tailored therapies 13.

Causes of Coronary Spasm

The causes of coronary spasm are multifactorial, involving both intrinsic and extrinsic factors that heighten the reactivity of coronary vessels.

Cause/Risk Factor	Mechanism	Notes/Impact	Source(s)
Smoking	Endothelial dysfunction, NO loss	Major risk factor	10 11
Genetic Factors	eNOS polymorphisms, familial risk	Population differences	10 11
Inflammation	Low-grade, chronic	hsCRP, P-selectin elevated	10
Hyperreactive Vessels	Enhanced smooth muscle contraction	↑Ca2+, RhoA/ROCK pathway	9 10
Triggers	Drugs, stress, cold, hyperventilation	Circadian variation	12

Table 3: Major Causes and Risk Factors

Vascular Hyperreactivity and Smooth Muscle Contraction

The fundamental abnormality is a hyperreactivity of the vascular smooth muscle, resulting in exaggerated contraction. This is primarily mediated by increased intracellular calcium and heightened Ca2+ sensitivity, often through the RhoA/ROCK signaling pathway. Endothelial dysfunction—especially reduced nitric oxide (NO) activity—amplifies this effect 9 10.

Endothelial Dysfunction and Inflammation

Patients with coronary spasm exhibit impaired endothelial NO production, leading to less vasodilation and more susceptibility to constriction. Chronic low-grade inflammation, reflected in increased hsCRP and P-selectin, is also commonly observed 10.

Smoking and Genetic Predisposition

Cigarette smoking is the single most significant modifiable risk factor. Genetic predispositions, especially polymorphisms affecting endothelial NO synthase (eNOS), explain higher prevalence in certain populations (e.g., Japanese, Korean) 10 11.

Triggers and Circadian Variation

Attacks frequently occur at rest, especially at night or early morning, likely due to circadian changes in vascular tone and autonomic activity. Other triggers include:

• Emotional stress
• Exposure to cold
• Certain medications (e.g., vasoconstrictors)
• Hyperventilation (which alters calcium handling in vessels) 12

Association with Other Heart Conditions

Coronary spasm can occur on a background of normal arteries or superimposed on atherosclerotic plaques, potentially precipitating myocardial infarction or unstable angina 5 10 11.

Treatment of Coronary Spasm

Management aims to relieve acute attacks, prevent recurrences, and reduce the risk of complications such as arrhythmias and myocardial infarction.

Treatment	Mechanism/Goal	Effectiveness/Notes	Source(s)
Nitrates	Vasodilation (NO donor)	Rapid relief of spasm	2 13 14 15
Calcium Channel Blockers	↓Ca2+ entry, relaxation	Mainstay for prevention	2 10 12
RhoA/ROCK Inhibitors	↓Smooth muscle sensitivity	Emerging therapy	9 10
Lifestyle Modification	Smoking cessation, avoid triggers	Reduces risk	10 11
Surgery (rare/select cases)	Bypass or denervation	Limited role, mixed results	2 14

Table 4: Treatment Approaches

Acute Attack: Immediate Relief

• Sublingual/intravascular nitrates quickly relieve spasm and restore blood flow, with improvement in symptoms and ECG changes often within minutes 2 13 14 15.
• During cardiac procedures or postoperative episodes, intracoronary nitrate or calcium channel blockers may be required for prompt reversal 15.

Long-Term Prevention

• Calcium channel blockers (CCBs) (e.g., diltiazem, nifedipine, verapamil) are the cornerstone of prevention. They inhibit calcium influx into smooth muscle, reducing contractility and preventing new episodes 2 10 12.
• Long-acting nitrates may be added for persistent symptoms, especially in patients with both epicardial and microvascular spasm 13.
• RhoA/ROCK pathway inhibitors are a novel therapeutic class showing promise in preclinical models and select clinical contexts, especially for patients resistant to standard therapy 9 10.

Lifestyle and Risk Factor Management

• Smoking cessation is critical.
• Managing emotional stress and avoiding known triggers can reduce attack frequency 10 11.

Surgical Approaches

• Surgical interventions such as cardiac denervation or bypass are reserved for refractory cases and have shown limited and often unpredictable benefit. Most patients respond well to medical therapy 2 14.

Tailored Treatment: Recognizing Overlap

Recent studies support a tailored approach, as some patients have mixed epicardial and microvascular spasm. In such cases, therapy may need to be adjusted based on detailed provocative testing (e.g., acetylcholine rechallenge) and individual response to medications 13.

Conclusion

Coronary spasm is a complex, under-recognized cause of angina, arrhythmias, and myocardial infarction. Key points include:

• Symptoms are often dramatic, with chest pain at rest, arrhythmias, and characteristic ECG changes, but may mimic other heart conditions.
• Types include epicardial and microvascular spasm, each with unique features and clinical implications.
• Causes involve vascular smooth muscle hyperreactivity, endothelial dysfunction, inflammation, genetic risk, and environmental triggers (especially smoking).
• Treatment focuses on rapid relief with nitrates, long-term prevention with calcium channel blockers, lifestyle modification, and—in select cases—emerging therapies or surgical options.
• Early diagnosis and tailored therapy are critical for preventing serious complications and improving quality of life.

In summary:

• Chest pain at rest, especially at night/early morning, is a red flag for coronary spasm.
• Both large (epicardial) and small (microvascular) vessels can be affected.
• Smoking and genetic factors are key drivers.
• Nitrates and calcium channel blockers are the mainstays of therapy.
• Recognizing overlapping spasm types allows for more precise, effective treatment.

If you or someone you know has unexplained chest pain, especially at rest, seek medical evaluation—coronary spasm is treatable, but timely diagnosis is essential.