The patient was a 52-year-old man who came to the emergency department for a syncopal episode while he was watching his son's football match. Due to the infrequent aetiopathogenesis of the condition and treatment, we consider it interesting to report it.

HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
No known drug allergies.
Active smoking (3-4 cigars/day).
Chronic alcoholism.
No other cardiovascular risk factors (CVRF).
No surgical history.
In treatment with disulfiram, with no other chronic medications.

Present illness
A 52-year-old man came to the emergency department for a syncopal episode with a fall to the ground while watching a football match. The episode was preceded by facial flushing, sweating, general malaise and pallor. He had no chest pain, dyspnoea or palpitations. Eyewitnesses denied convulsive movements. Emergency medical services were contacted and he was treated on the spot.

Physical examination
Blood pressure (BP) (on arrival at the emergency department) 90/50 mmHg. Heart rate (HR) 70 bpm.
Oxygen saturation 96% on room air. Respiratory rate 16 rpm. Good general condition. Conscious and oriented. No obvious neurological focality. Afebrile. Sweating. Jugular venous pressure normal. Cardiac auscultation: rhythmic heart sounds, no murmurs. Pulmonary auscultation: preserved vesicular murmur, no extra sounds. No oedema in the lower extremities, no signs of deep vein thrombosis (DVT).


COMPLEMENTARY TESTS
Laboratory tests:
Blood count: normal.
Biochemistry: basal glucose 94 mg/dl; creatinine 0.9 mg/dl; normal ions and transaminases; total cholesterol 152 mg/dl; LDL-C 87 mg/dl. Hyperlactacidemia without acidosis, transient. Maximal serial myocardial necrosis markers: troponin T us 657 ng/l (normal < 13 ng/l).
Baseline coagulation: INR 1.13; PT 87%; aPTT ratio 1.15.

Electrocardiogram:
On arrival of the emergency medical team (image 1): sinus tachycardia at 110 bpm. Narrow QRS, axis at -15o. Embryonic R wave with flat T wave in DIII and aVF.
J-point descent of 1 mm in V1-V2. Discrete elevation (maximum 1 mm in V5) of the ST segment from V3 to V6.
At discharge: sinus rhythm at 60 bpm, with high R wave in V2 and negative T waves in inferior face.
Echocardiogram: left ventricle (LV) of normal size and thickness, preserved systolic function (EF 60%) with mild inferior hypokinesia. Left atrium (LA) and right chambers normal. No significant valvular abnormalities. No pulmonary hypertension. Aortic root of normal size. No pericardial effusion.
Interconsultation with the psychosomatic department: treatment for addiction is reinforced. Start of clomethiazole.
Coronary angiography: images of intracoronary thrombus (without complicated plaque) in proximal-medial DC. After 1 week of treatment with i.v. sodium heparin, the thrombus resolved.
Optical coherence tomography (OCT) showed an image suggestive of plaque erosion in the proximal-medial right coronary artery (RCA), which was not treated (medical treatment).
The rest of the coronary arteries showed no significant lesions.

CLINICAL EVOLUTION
On arrival of the emergency medical team, frank arterial hypotension was observed (70/40 mmHg) and an ECG was performed showing ST segment underleveling from V3 to V6, which subsequently evolved to discrete ST segment supralowing in these leads, for which reason he was transferred to the emergency department of our centre. On arrival, the ECG normalised. Despite initially denying it, he admitted alcohol intake minutes before the syncopal episode (currently under treatment with disulfiram). After documenting a significant increase in ultrasensitive troponin T in serial determinations, it was decided to admit him to the cardiology ward for study and treatment with an initial diagnosis of high-risk non-ST-segment elevation acute coronary syndrome (NSTEACS).
During his stay on the ward he remained stable and asymptomatic. The echocardiogram showed preserved LV systolic function with slight inferior hypokinesia. Early coronary angiography revealed the presence of a thrombus in the proximal and middle DC, secondary to the acetaldehyde reaction due to alcohol-disulfiram interaction, and the decision was made to maintain double antiplatelet therapy and initiate anticoagulation with i.v. sodium heparin for 1 week.

After a week of anticoagulation, coronary angiography was repeated, showing the disappearance of the thrombus in the DC, although OCT detected plaque erosion in this location, which was not considered necessary to revascularise. The need to maintain alcohol abstinence and avoid alcohol intake under treatment with disulfiram, as well as smoking cessation, is insisted upon. Treatment at discharge with double antiplatelet therapy with acetylsalicylic acid and ticagrelor, PPI (omeprazole), and treatment by the psychiatrist, maintaining disulfiram with strict control and clomethiazole.

DIAGNOSIS
Acute non-Q myocardial infarction of inferior location, secondary to acetaldehyde reaction due to alcohol-disulfiram interaction with intracoronary thrombus formation in proximal and middle DC, resolved after double antiplatelet therapy and 1 week of parenteral anticoagulation. Preserved LV systolic function with inferior hypokinesia.
