A 19-year-old man presented to the emergency department with palpitations and presyncope. He experienced three episodes of near complete loss of consciousness in the last few hours prior to presentation. Each episode had lasted for less than thirty seconds and had been accompanied by palpitations. One hour before symptom onset, the patient had smoked a joint. He had been using cannabis since 2 years, on average 2–3 joints per week. Never before had he experienced syncope or presyncope. He had no past medical history except for autism spectrum disorder diagnosed at age 11 and he was not taking any medication. Family history was negative for sudden death or pacemaker implantation.

On clinical examination, the patient appeared well. He had no fever (36.9°C), oxygen saturation at room air was 99%, respiratory rate 20/min, and blood pressure 120/70 mmHg. On initial examination, heart rate was 100 beats per minute. Heart sounds were normal without murmurs, lung auscultation was clear and the remainder of the clinical exam was unremarkable.

Initial electrocardiogram (ECG) showed intermittent sinus rhythm and junctional tachycardia up to 120 beats per minute. During observation, ECG monitoring showed several episodes of third-degree atrioventricular block, with underlying sinus rhythm but without ventricular escape. These episodes, the longest of which lasted 7.2 s (Figure 1) provoked the same symptoms as the patient had described.

Urinary 11-nor-9-carboxy-Δ⁹-tetrahydrocannabinol (THC-COOH) was 110 ng/mL (Cannabinoids II SemiQuantitative 50® Assay, run on COBAS INTEGRA® 800 Analyzer, Roche Diagnostics). Urine toxicology screen was negative for cocaine, amphetamines, opiates, neuroleptics, or antidepressants. Blood digoxin level was negative. High sensitivity troponin was 0.018 mcg/L (reference value, <0.013), with a rise to 0.027 mcg/L three hours later and gradual decline thereafter. NT-proBNP was 176 ng/L (reference value, <115). C-reactive protein was normal (0.7 mg/L, reference value, <5.0). Hemoglobin (15.6 g/dL, reference value, 14.0–18.0), white blood cell count (7.24 ^∗ 10⁹/L, reference value, 4.00–10.00), and platelets (235 ^∗ 10⁹/L, reference value, 150–450) were normal, as were creatinine (0.89 mg/dL, reference value, 0.67–1.17), electrolytes (potassium: 4.22 mmol/L, reference value, 3.45–4.45), liver, and thyroid function tests. Borrelia serology was negative and kininase II (angiotensin converting enzyme, ACE) level was normal (49 U/L, reference value, 8–52).

An isoprenaline (isoproterenol) infusion was started at 0.5 mcg/min and the patient was admitted to the coronary care unit. The isoprenaline infusion was stopped after one day without recurrence of bradycardia. The patient was observed for 4 days, without any further events. ECG at discharge was normal. Echocardiography at presentation and at discharge was normal. Chest X-ray was unremarkable. CT angiography showed no coronary anomaly or stenosis. Cardiac magnetic resonance imaging showed no structural abnormalities or areas with late gadolinium enhancement. Electrophysiological (EP) study was entirely normal and showed a normal atrioventricular conduction time.

Cannabis-induced atrioventricular block was suspected. The patient was advised to quit using cannabis. No further therapy was initiated. Follow-up 5-day ambulatory ECG monitoring, after cessation of cannabis use, showed normal sinus rhythm without atrioventricular block, apart from physiological Wenckebach phenomenon.