Acute inferior ST-elevation myocardial infarction due to delirium tremens: a case report

Abstract Background Delirium tremens is a severe form of alcohol withdrawal syndrome. Literature documenting acute coronary events in the setting of alcohol withdrawal remains scarce. An accepted hypothesis for the underlying process is focused on the hyperadrenergic state that leads to coronary vasospasm and increased myocardial oxygen demand. Case presentation A 47-year-old Caucasian man with a past medical history of tobacco and alcohol abuse, hypertension, and anxiety presented to the emergency department for crampy epigastric abdominal pain with intractable nausea and vomiting for the past 2 days. His reported last alcoholic intake was about 10 days prior; however, outpatient records indicated otherwise. He was admitted for electrolyte replacement and fluid resuscitation secondary to gastrointestinal losses from presumed early alcohol withdrawal syndrome. The following night, he developed acute substernal chest pain with elevated cardiac enzymes. Electrocardiography showed an acute inferoposterior infarct with reciprocal changes in leads V1–V4. The patient was taken for emergent catheterization, and a drug-eluting stent was placed in the middle of the left anterior descending artery. Postcatheterization electrocardiography showed sustained inferolateral ST elevations consistent with acute injury pattern. The patient had not required any benzodiazepines until this point. On the morning of catheterization, the patient’s Clinical Institute Withdrawal Assessment for Alcohol–Revised score was 19 with a high of 25, and he was actively hallucinating. He was treated for delirium tremens and an acute coronary event along with an incidental pneumonia. He did not require any benzodiazepines during the last 4 days of admission, and he made a full recovery. Conclusions The prevalence of alcohol dependence in hospitalized patients is substantial. Although our patient was being treated with the standard protocols for alcohol withdrawal, he rapidly developed delirium tremens, which led to an acute inferior ST-elevation myocardial infarction in the setting of nonoccluded coronary vessels. This case report adds to the sparse literature documenting acute coronary events in the setting of alcohol withdrawal and suggests that our patient’s ST-elevation myocardial infarction is not fully explained by the current coronary vasospasm hypothesis, but rather was in part the result of direct catecholamine-associated myocardial injury. Further research should be conducted on prophylactic agents such as β-blockers and calcium channel blockers. </jats:sec

Low energy internal cardioversion of atrial fibrillation resistant to transthoracic shocks.

OBJECTIVE: To investigate the efficacy of internal cardioversion using low energy shocks delivered with a biatrial electrode configuration in chronic atrial fibrillation resistant to transthoracic shocks. METHODS: Low energy internal cardioversion was attempted in 11 patients who had been in atrial fibrillation for 233 (SD 193) days and had failed to cardiovert with transthoracic shocks of 360 J in both apex-base and anterior-posterior positions. Synchronised biphasic shocks of up to 400 V (approximately 6 J) were delivered, usually with intravenous sedation only, between high surface area electrodes in the right atrium and the left atrium (coronary sinus in nine, left pulmonary artery in one, left atrium via patent foramen ovale in one). RESULTS: Sinus rhythm was restored in 8/11 patients. The mean leading edge voltage of successful shocks was 363 (46) V [4.9 (1.2) J]. Higher energy shocks induced transient bradycardia [time to first R wave 1955 (218) ms]. No proarrhythmia or other acute complications were observed. CONCLUSIONS: Low energy internal cardioversion of atrial fibrillation can restore sinus rhythm in patients in whom conventional transthoracic shocks have failed