What are the causes and management strategies for myocardial infarction (MI) associated with Schedule 2 medication use, such as opioids (e.g., fentanyl, oxycodone) and stimulants (e.g., methamphetamine, cocaine)?

Causes and Management of Schedule 2 Medication-Associated Myocardial Infarction

Schedule 2 medications, particularly cocaine and methamphetamine, can cause myocardial infarction through multiple mechanisms including coronary vasospasm, accelerated atherosclerosis, increased myocardial oxygen demand, and thrombosis. 1

Causes of Schedule 2 Medication-Induced MI

Cocaine-Related MI Causes

• Coronary artery vasospasm - cocaine causes direct vasoconstriction of coronary arteries 1
• Increased myocardial oxygen demand due to tachycardia, hypertension, and increased contractility 1
• Accelerated atherosclerosis in chronic users 1
• Enhanced platelet aggregation and thrombus formation due to increased thromboxane A2 production 1
• Reduced protein C and antithrombin III levels, favoring coronary thrombosis 1

Methamphetamine-Related MI Causes

• Similar pathophysiology to cocaine, including coronary vasospasm 1
• Increased myocardial oxygen demand through tachycardia and hypertension 2
• Potential for direct myocardial toxicity 1
• Can occur with both acute and chronic use 3

Risk Factors for Schedule 2 Medication-Induced MI

• Young age (typically under 40 years) 1
• Male gender 1
• Cigarette smoking 1
• Concomitant use of alcohol and/or cigarettes 1
• Can occur with any route of administration 1
• Can occur with small or large doses 1

Management of Schedule 2 Medication-Induced MI

Initial Assessment

• Obtain ECG immediately to evaluate for ischemia, ST-segment elevation/depression 2
• Check cardiac biomarkers (troponin preferred over CK-MB due to higher specificity) 1
• Assess for contraindications to standard MI therapies (hypertension, seizures, aortic dissection) 1

Acute Management of Cocaine/Methamphetamine-Induced MI

For Patients with ST-Elevation MI:

1. Administer sublingual nitroglycerin or calcium channel blockers (e.g., diltiazem 20 mg IV) as first-line therapy 1
2. If no response to nitrates/calcium channel blockers, proceed to immediate coronary angiography 1
3. Percutaneous coronary intervention (PCI) is preferred over fibrinolytic therapy 1
4. If PCI is unavailable and no contraindications exist, administer fibrinolytic therapy 1
5. Avoid beta-blockers in the acute phase as they may worsen coronary vasospasm 1, 2
6. For patients receiving stents, prefer bare-metal stents over drug-eluting stents due to concerns about medication adherence 1

For Patients without ST-Elevation:

1. Administer sublingual nitroglycerin or oral calcium channel blockers 1
2. Observe in a monitored setting 1
3. Draw cardiac biomarkers at 6-hour intervals or at 3,6, and 9 hours 1
4. If ECG shows ST-segment changes with normal biomarkers, observe for 24 hours 1
5. Consider coronary angiography for patients with persistent ST-segment depression or T-wave changes unresponsive to nitrates and calcium channel blockers 1

Observation Period

• Patients with ECG changes and normal cardiac biomarkers should be observed in a monitored setting for 24 hours 1
• A shorter observation period of 9-12 hours with serial troponin measurements at 3,6, and 9 hours may be appropriate in select cases 1, 2
• Most complications will occur within 24 hours 1

Medications to Use and Avoid

Recommended:

• Nitrates - reverse cocaine-induced hypertension and coronary vasoconstriction 1
• Calcium channel blockers (e.g., verapamil, diltiazem) - reverse cocaine-induced vasoconstriction 1
• Aspirin - safe in cocaine-associated chest pain 1
• Heparin (unfractionated or low-molecular-weight) - for patients with confirmed MI 1

Use with Caution or Avoid:

• Beta-blockers - may worsen coronary vasospasm in acute phase 1, 2
• If beta-blockade is necessary, consider labetalol (combined alpha and beta blocker) with caution 1
• Opioids - may result in less salvageable myocardium in MI patients 1

Special Considerations

Long-term Management

• Counsel patients on cessation of substance use - cornerstone of secondary prevention 4
• Consider beta-blockers for long-term management after acute phase has resolved 4
• Dual antiplatelet therapy adherence is critical for patients who receive stents 1
• Regular cardiovascular risk assessment is important as substance users have higher rates of coronary artery disease 3

Common Pitfalls

• Misinterpreting elevated CK or CK-MB as MI when it may be due to increased motor activity or rhabdomyolysis after cocaine use - troponin is more specific 1
• Failing to recognize that MI can occur hours after cocaine or methamphetamine use, not just immediately 1
• Automatically using beta-blockers as would be standard in non-drug-induced MI 1, 2
• Overlooking the possibility of aortic or coronary artery dissection as complications 1