Can microvascular spasm trigger cardiac arrest in patients with a history of microvascular spasm and underlying cardiovascular disease or risk factors?

Can Microvascular Spasm Trigger Cardiac Arrest?

Yes, microvascular spasm can trigger cardiac arrest through polymorphic ventricular tachycardia or ventricular fibrillation, though this mechanism is less common than epicardial coronary spasm. 1

Mechanism and Evidence

Coronary artery spasm—both epicardial and microvascular—is an established cause of life-threatening ventricular arrhythmias and sudden cardiac death. 1 The key distinction is:

• Epicardial spasm causes transient ischemia that can precipitate polymorphic VT or VF, particularly when associated with ST-segment elevation or depression during the spasm episode 1
• Microvascular spasm is diagnosed when acetylcholine provocation testing produces symptoms and ischemic ECG changes with <90% epicardial lumen reduction, indicating the spasm occurs at the arteriolar level 1

The 2006 ACC/AHA/ESC guidelines explicitly state: "Transient ischemia resulting from coronary artery spasm may cause polymorphic VT or VF. In such cases, treatment of coronary spasm may be sufficient to prevent recurrent arrhythmia. Coronary artery spasm may increase the risk of ventricular arrhythmias and SCD." 1

Clinical Recognition and Diagnostic Approach

High-Risk Features Suggesting Spasm-Related Arrest

• Cardiac arrest survivors without obstructive coronary disease on angiography should undergo acetylcholine provocation testing to identify vasospastic mechanisms 1
• Women, younger patients (<50 years), and habitual smokers have higher rates of spasm-related cardiac events 2
• Rest angina or nocturnal symptoms suggest vasospastic angina rather than fixed obstructive disease 3

Diagnostic Protocol

The 2024 ESC guidelines recommend the following acetylcholine-based protocol for patients with suspected vasospastic disease: 1

• Perform testing after ≥24 hours washout from calcium channel blockers and nitrates 1
• Administer incremental intracoronary acetylcholine doses (2 μg → 20 μg → 100 μg → 200 μg) with continuous ECG and symptom monitoring 1
• Microvascular spasm diagnosis: Symptoms + ischemic ECG changes + <90% epicardial lumen reduction 1
• Epicardial spasm diagnosis: Symptoms + ischemic ECG changes + ≥90% epicardial lumen reduction 1

The safety of this protocol has been repeatedly demonstrated, even in patients with recent acute coronary syndrome. 1

Treatment Strategy to Prevent Recurrent Arrest

For Confirmed Vasospastic Cardiac Arrest

Calcium channel blockers are the cornerstone of therapy and can prevent recurrent cardiac arrest in spasm-related cases. 1, 2

• Titrate calcium channel blocker dose (diltiazem, verapamil, nifedipine, or amlodipine) until repeat provocation testing is negative 2
• In a study of seven cardiac arrest survivors with isolated coronary spasm, six remained event-free over 58 months on calcium channel blockers; the one recurrence occurred in a patient who continued smoking 2
• Beta-blockers are absolutely contraindicated when a vasospastic component is present, as they may worsen spasm 4

Role of ICD Therapy

The evidence regarding ICD implantation for spasm-related cardiac arrest remains uncertain: 3

• No randomized trials have evaluated ICD versus medical therapy alone in this population 3
• The 2006 guidelines note that "treatment of coronary spasm may be sufficient to prevent recurrent arrhythmia" in patients with normal ventricular function and no history of MI 1
• However, if ventricular function is abnormal, cardiac arrest should not be attributed solely to spasm, and evaluation should proceed as for other cardiac arrest survivors 1

Algorithm for Management

1. Confirm spasm mechanism with acetylcholine provocation testing 1
2. Assess ventricular function with echocardiography or cardiac MRI 1
3. If normal ventricular function + no prior MI: Initiate calcium channel blocker therapy and titrate to negative provocation test 1, 2
4. If abnormal ventricular function: Consider ICD in addition to calcium channel blockers, as spasm may not be the sole mechanism 1
5. Mandatory smoking cessation and aggressive risk factor modification 2
6. Repeat provocation testing after medication optimization to confirm spasm suppression 2

Critical Pitfalls to Avoid

• Assuming normal epicardial arteries exclude a cardiac cause of arrest—microvascular spasm can cause life-threatening arrhythmias without visible epicardial disease 1, 5
• Prescribing beta-blockers without excluding vasospasm—this can precipitate unopposed alpha-adrenergic vasoconstriction and worsen spasm 4
• Failing to perform provocation testing in cardiac arrest survivors with non-obstructive coronary arteries—this misses a treatable cause 1, 2
• Attributing arrest solely to "reversible causes" without long-term therapy—even with spasm treatment, mortality remains elevated without appropriate medical therapy 1
• Inadequate smoking cessation counseling—the one recurrent arrest in the landmark study occurred in the patient who continued smoking 2

Prognosis with Appropriate Treatment

When coronary spasm is identified and treated appropriately with calcium channel blockers, long-term outcomes are favorable. 2 In the absence of structural heart disease, medical therapy alone may be sufficient to prevent recurrent events, though close follow-up and repeat provocation testing are essential to confirm therapeutic efficacy. 2