Methamphetamine abuse is a growing global health concern. Cardiovascular disease is the leading cause of death in methamphetamine users because of its significant effects on vasoconstriction, pulmonary hypertension, atherosclerotic plaque formation, cardiac arrhythmias, and cardiomyopathy. Stimulants like methamphetamine and cocaine are known to induce severe coronary vasospasm resulting in angina and myocardial infarction (MI), but MI secondary to methamphetamine-induced coronary thrombosis is rarely reported. A 40-year-old female with medical history of immune thrombocytopenia s/p splenectomy, NSTEMI, tobacco and substance abuse presented to the hospital via EMS in an unresponsive state. Patient was admitted to the hospital 20 days before the current episode with complaints of chest pain and was diagnosed with NSTEMI due to troponin elevation without EKG changes; Echocardiogram at that time showed a left ventricular ejection fraction (LVEF) of 55-60% without any other abnormalities. Coronary angiography at that time was unremarkable except for mild luminal irregularities of the left anterior descending (LAD) artery. The patient’s symptoms resolved and was discharged home with a diagnosis of COVID-induced MI with nonobstructive coronaries.
During the current episode, the patient started having crushing substernal chest pain radiating to left shoulder and associated with dizziness. She suffered cardiac arrest on the way to the hospital but was successfully resuscitated. EKG revealed anterior STEMI and the patient was loaded with aspirin. Emergent coronary angiography showed 100% occlusion of proximal LAD, while other coronaries were completely patent without any atherosclerotic plaque. A successful mechanical thrombectomy followed by a 4 x 28 mm drug-eluting stent was placed in the ostial-proximal LAD. TIMI-3 flow was restored and post-intervention troponin peaked at 70. Urine drug screen was positive for amphetamines and benzodiazepines. The echocardiogram showed a reduced LVEF of 30%. Patient was started on dual antiplatelet therapy with aspirin and ticagrelor, rosuvastatin, and low-dose metoprolol tartrate; further guideline-directed medical therapy could not be initiated due to patient’s low blood pressure. Hypercoagulability workup was negative for any abnormalities. As other usual causes were ruled out, the patient was deemed to have methamphetamine-induced coronary thrombosis resulting in myocardial infarction, and cardiomyopathy. Discussion Amphetamines are potent sympathomimetic agents that increase the risk of MI through various cardiovascular effects. Elevated serum catecholamines lead to increased heart rate, and blood pressure resulting in increased myocardial oxygen demand, while also inducing coronary vasospasm which can limit myocardial oxygen supply. Furthermore, in-vitro studies have shown amphetamines are prothrombotic as they can induce tissue factor (TF) expression, activate endothelial cells, and inhibit the activity of tissue factor pathway inhibitor (TFPI). They also increase the expression of plasminogen activator inhibitor-1 (PAI-1), a key fibrinolysis suppressant. In contrast to cocaine, amphetamines can induce thrombosis even in a non-inflamed endothelium, affecting even young individuals without atherosclerotic risk factors. These cumulative procoagulant effects may result in coronary artery thrombi as seen in our patient, which combined with other adrenergic effects, poses a significant risk for acute coronary events.
| Identifer | oai:union.ndltd.org:ETSU/oai:dc.etsu.edu:asrf-2054 |
| Date | 25 April 2023 |
| Creators | Sanku, Koushik, Nemalikanti, Sanskrita, Patel, Jeetendra Bhagubhai |
| Publisher | Digital Commons @ East Tennessee State University |
| Source Sets | East Tennessee State University |
| Detected Language | English |
| Type | text |
| Source | Appalachian Student Research Forum |
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