Acute cardiovascular complications of sympathomimetic recreational drug use (2026)

INTRODUCTION: Recreational drug use is rising globally, with significant cardiovascular implications. Sympathomimetic substances such as cocaine, amfetamine(amphetamine)-type stimulants and synthetic cathinones are increasingly associated with emergency department presentations and acute cardiac events. Despite this growing burden, standardized guidance for diagnosing and managing acute sympathomimetic recreational drug-related cardiovascular complications remains limited.
METHODS: A narrative review of the literature was conducted to identify acute cardiovascular complications associated with commonly used recreational drugs. A PubMed search was performed from database inception to 1 March 2024 using combinations of cardiovascular symptoms and cardiovascular complications with terms related to sympathomimetic recreational drug use.
RESULTS: These substances exert potent sympathomimetic effects through catecholamine excess, and cause receptor activation, ion channel interference, and direct myocardial toxicity. Cocaine additionally induces vasospasm and thrombosis via endothelin-1 and causes sodium channel and potassium channel blockade. Amfetamine-type stimulants and synthetic cathinones amplify catecholamine release, contributing to arrhythmia, ischemia, and myocardial injury. Acute cardiovascular manifestations include chest pain, acute coronary syndrome, arrhythmias, cardiomyopathy, and sudden cardiac death. Presentations often mimic classical cardiac syndromes but may be more severe, especially in younger patients without traditional risk factors. Diagnosis begins with detailed history-taking, although self-reported drug use is frequently unreliable. Depending on symptoms, electrocardiography, cardiac biomarkers and echocardiography may be essential for risk stratification and identifying the underlying pathology. Toxicological testing may be considered when clinically indicated and should be interpreted in conjunction with clinical findings. For cocaine associated chest pain patients, risk stratification with the HEART pathway may guide safe discharge in low-risk cases. Management should be individualized based on the specific recreational drug involved and the presenting symptoms. Sedation, antihypertensives, and dual antiplatelet therapy are foundational, with vasodilators when indicated. Beta-blockers with alpha-blocking properties may be beneficial in selected patients. Early drug counselling and referral are critical to reduce recurrence.
DISCUSSION: In most cases, evaluation and management of acute cardiovascular symptoms in patients with suspected sympathomimetic drug use should follow standard guideline-based cardiovascular care. However, specific modifications may be required, including selective use of toxicological testing when it is expected to influence clinical decision-making, early sedation to reduce sympathetic overactivity, and cautious selection of beta-blockers depending on the substance involved. Awareness of these distinctions is essential to avoid both under- and overtreatment.
CONCLUSION: Clinicians must recognize the acute cardiovascular risks of sympathomimetic recreational drugs and integrate routine drug screening, tailored management, and addiction intervention into acute care pathways to improve outcomes and reduce morbidity. [Author's abstract]