Key result
Alcohol withdrawal-driven autonomic storm unmasks Lown-Ganong-Levine pattern mimicking acute coronary syndrome.
Why the study?
Chest pain in psychiatric inpatients with alcohol use disorder can mimic acute coronary syndrome, and rare conduction abnormalities like Lown–Ganong–Levine syndrome may be unmasked during alcohol withdrawal, complicating diagnosis and management.
Case Report (n=1)
Alcohol withdrawal can unmask rare pre-existing conduction anomalies like Lown-Ganong-Levine syndrome and mimic acute coronary syndrome, underscoring the need for careful ECG interpretation to prevent misdiagnosis.
Requires ECG vigilance in alcohol withdrawal to avoid ACS misdiagnosis; leaves open LGL unmasking prevalence and mechanisms.
Introduction Chest pain in psychiatric inpatients often raises concern for acute coronary syndrome (ACS), particularly in those with alcohol use disorder, where somatic complaints and cardiological risks are common. Yet not all such pain reflects myocardial ischemia. Beyond the well-known “holiday heart syndrome,” rare conduction anomalies like Lown–Ganong–Levine (LGL) syndrome may appear with paroxysmal supraventricular tachycardia. Alcohol withdrawal, marked by autonomic overactivity, can further unmask these arrhythmias and complicate the clinical picture. Objectives To demonstrate how alcohol withdrawal can mimic acute coronary syndrome and unmask rare conduction abnormalities such as LGL syndrome, emphasizing the importance of careful ECG interpretation in psychiatric settings. Methods Clinical observation of a 49-year-old inpatient undergoing alcohol withdrawal. The patient was assessed through physical examination, continuous monitoring of vital signs, and standard 12-lead electrocardiography. Supportive care was provided within a psychiatric ward setting, with cardiological consultation available if symptoms worsened. Results Electrocardiography revealed a short PQ interval (<120 ms), narrow QRS complexes, and no delta wave, consistent with a LGL conduction pattern. The episode was interpreted as a paroxysmal supraventricular tachycardia most likely triggered by autonomic flux during withdrawal. Symptoms subsided spontaneously with supportive care, without need for acute pharmacological or invasive intervention. An electrophysiological study would be required for definitive confirmation of the LGL syndrome. This case illustrates how chest pain in psychiatric patients can easily be misinterpreted. In alcohol withdrawal, autonomic storm not only produces somatic sensations mimicking ACS but can also reveal pre-existing conduction anomalies. Misreading such ECG patterns as ischemic changes could unnecessarily prompt transfer to intensive care or invasive procedures. Previous reports in the literature have described arrhythmias unmasked by withdrawal, yet this remains under-recognized in psychiatric settings. Importantly, LGL syndrome may be overlooked because its ECG findings are subtle and may resemble normal variants. Differentiation from other pre-excitation syndromes, particularly Wolff–Parkinson–White, is essential to avoid misclassification. Careful ECG interpretation and awareness of such rare conditions can prevent misdiagnosis and reduce risk for the patient. Image 1: Image 1: Long description. Image 2: Image 2: Long description. Conclusions Even the possible presence of conduction abnormalities must be considered in psychiatric contexts, both to guide monitoring and to avoid misdiagnosis and harm. This case underscores the need for collaboration between psychiatry and cardiology in the management of alcohol withdrawal, ensuring that uncommon but clinically relevant conduction anomalies are not missed. Disclosure of Interest None Declared
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O. Plavkov (2026) conducted a case report in Alcohol withdrawal (n=1). Alcohol withdrawal was evaluated on Electrocardiography findings. Alcohol withdrawal triggered an autonomic storm that unmasked a Lown-Ganong-Levine conduction pattern with a short PQ interval (<120 ms), mimicking acute coronary syndrome.
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