Why does cocaine intoxication present with ST inversions on an electrocardiogram (ECG) without elevated creatine kinase-muscle band (CKMB) enzymes, and does this indicate a non-ST elevation myocardial infarction (NSTEMI)?

Cocaine-Induced ST Inversions Without Elevated Cardiac Enzymes

Cocaine-induced ST inversions without elevated CK-MB do not necessarily indicate NSTEMI, but rather represent coronary vasospasm that can cause transient myocardial ischemia without actual infarction. 1

Pathophysiology of Cocaine-Induced ECG Changes

Cocaine affects the cardiovascular system through several mechanisms:

1. Coronary Artery Spasm:

   • Cocaine blocks presynaptic reuptake of neurotransmitters like norepinephrine and dopamine, leading to excess concentrations at postsynaptic receptors 2
   • This causes sympathetic activation and direct contractile effects on vascular smooth muscle 2
   • Coronary vasospasm can occur with normal or minimally obstructive coronary arteries 2

2. Discrepancy Between ECG Changes and Enzyme Elevations:

   • ST inversions can occur due to transient ischemia from vasospasm without actual myocardial necrosis 1
   • Only about 6% of patients presenting with cocaine-associated chest pain actually develop MI 1
   • Troponin I and T are more specific markers for myocardial injury than CK-MB in cocaine users 2

Differential Diagnosis

• Transient ischemia without infarction: ST inversions without enzyme elevation typically represent vasospasm-induced ischemia without actual cell death 1
• Early presentation: Cardiac biomarkers may not be elevated if presentation is very early after symptom onset
• NSTEMI: True NSTEMI would typically show troponin elevation within 3-6 hours
• Takotsubo cardiomyopathy: Cocaine can trigger stress cardiomyopathy with ECG changes and minimal enzyme elevation 3

Diagnostic Approach

1. Cardiac Biomarkers:

   • Troponin I or T should be preferred over CK-MB 1
   • Draw cardiac markers at presentation and at 6-hour intervals 2
   • CK-MB can be elevated due to skeletal muscle injury and rhabdomyolysis from cocaine use, even without MI 2

2. ECG Monitoring:

   • Monitor for dynamic ECG changes, as cocaine users can have frequent episodes of ST-segment changes 2
   • ST inversions may resolve with appropriate treatment 4

3. Imaging:

   • If ECG shows persistent changes and clinical suspicion is high, coronary angiography may be indicated 2
   • Coronary CT angiography may be useful in low-risk patients to rule out significant stenosis 5

Management Implications

1. Initial Treatment:

   • Sublingual nitroglycerin or intravenous calcium channel blockers (e.g., diltiazem 20 mg IV) are first-line treatments 1
   • Both nitroglycerin and calcium channel blockers can reverse cocaine-induced coronary vasospasm 2
   • Avoid beta-blockers in the acute phase due to risk of unopposed alpha-adrenergic stimulation 2

2. Observation Period:

   • If ECG shows ST changes but cardiac biomarkers remain normal, observe in a monitored bed for 9-24 hours 1
   • Serial troponin measurements at 3,6, and 9 hours can be used for a shorter observation protocol 2

3. Interventional Management:

   • If ST changes persist despite medical therapy, coronary angiography is indicated 2
   • If occlusive thrombus is found, PCI is recommended, preferably with bare-metal stents due to concerns about adherence to dual antiplatelet therapy 1, 6

Clinical Pearls and Pitfalls

• Pearl: ST inversions that resolve with nitroglycerin or calcium channel blockers strongly suggest vasospasm rather than fixed coronary obstruction 4
• Pitfall: Relying solely on CK-MB can lead to false positives due to skeletal muscle injury from cocaine use 1
• Pearl: A normal ECG has a 95% negative predictive value for ACS in cocaine users with chest pain 7
• Pitfall: Discharging patients too early without adequate observation period can miss delayed presentations of true ACS

In conclusion, cocaine-induced ST inversions without elevated CK-MB typically represent transient ischemia from coronary vasospasm rather than true NSTEMI. However, careful monitoring with serial troponin measurements and appropriate treatment with vasodilators is essential to rule out actual myocardial infarction.