A 30-year-old healthy male, known to smoke marijuana on a daily basis for the last 5 years, presented with a 3-day history of palpitations. The patient recalled no associated chest pain or dizziness and had no family history of sudden cardiac death (SCD) or premature coronary artery disease. His past medical history was remarkable for unexplained sudden-onset syncope without prodrome, 5 years prior to his index admission, as well as a 5-year history of frequent episodes of palpitations occurring at the end of physical activity. At the time of presentation to our clinic his resting 12-lead electrocardiogram (ECG) was unremarkable apart from an early repolarization pattern. The QTc was normal with no epsilon wave. Blood tests confirmed normal electrolytes and thyroid hormone levels. Transthoracic echocardiogram demonstrated non-dilated ventricles with a normal, systolic left ventricular ejection fraction and no evidence of valvular heart disease. The left atrial (LA) size was normal (LA diameter 38 mm, LA area 13.8 cm², LA volume 31 mL). Pulmonary artery pressures were within normal limits. The patient underwent an exercise test, which showed no evidence of either inducible myocardial ischaemia or arrhythmias during 13 min of exercise. After 45 s of recovery, however, his ECG changed to a wide complex tachycardia, 190 b.p.m., suspected to be polymorphic ventricular tachycardia (VT), starting with an outflow tract premature ventricular contraction (Figure 1). At this point, the patient was haemodynamically stable and asymptomatic, nevertheless, following the initiation of a Valsalva manoeuver, he reverted to a regular narrow complex tachycardia of 226 b.p.m. with associated symptoms of palpitations (Figure 2). Subsequently, he developed AF before converting spontaneously to haemodynamically stable VT (Figure 3). After 5 min within the recovery stage, his VT spontaneously converted to normal sinus rhythm. A second exercise test induced similar sustained monomorphic outflow tract VT (left bundle inferior axis with transition in V2–V3 leads). Coronary angiography demonstrated normal coronary arteries. Cardiac magnetic resonance (CMR) confirmed normal LA dimensions, non-dilated ventricles, and no evidence of late gadolinium enhancement ruling out previous MI, myocarditis, cardiac sarcoidosis, or arrhythmogenic right ventricular cardiomyopathy (ARVC).

The patient was then referred for electrophysiological study. Voltage mapping using three-dimensional electroanatomical mapping, Carto^® system (Biosense Webster), showed no evidence of scar tissue within the right ventricle and its outflow tract. A subsequent VT study with aggressive ventricular programmed stimulation, with and without isoprenaline and in washout, was performed, with no induction of VT demonstrated. We were unable to reveal dual atrioventricular (AV) node physiology. During ventricular pacing, supraventricular tachycardia (SVT) was induced with concentric atrial activation (Figure 4A). It was not possible to finish the study due to incessant, differential arrhythmias. During episodes of atrial and ventricular pacing the patient developed several episodes of AF with a fast ventricular response, requiring recurrent electrical cardioversion in order to continue the study (Figure 4B). Once completed, the patient was instructed to withhold from marijuana use and was started on a non-selective beta-blocker (Propranolol SR titrated to 120 mg daily). A subsequent exercise test confirmed no evidence of inducible VT/SVT, following which he was changed to a selective beta-blocker (Bisoprolol 5 mg daily) and a repeat exercise test confirmed the absence of inducible cardiac arrhythmia, hence the decision was taken not to implant an implantable cardioverter-defibrillator. He was seen in our clinic 2 months after discharge, where a third exercise stress test was undertaken again without any abnormality at maximum workload. In addition, 24-h ambulatory ECG monitoring was unremarkable. Eighteen months after his arrhythmic presentation the patient remains well and has not smoked cannabis since.

A 30-year-old healthy male with a history of smoking tobacco/marijuana, occasional cocaine use (last reported use a week prior to his index admission) presented with a 1-day history of palpitations and chest discomfort. The symptoms were temporarily relieved by cycling and other physical activities. The following morning, in addition to the aforementioned symptoms, he recalled episodes of dizziness. He was initially assessed in his local urgent care centre, where his examination revealed normal vital signs, however, a 12-lead ECG confirmed sinus rhythm with complete AVB. A repeat ECG demonstrated Type 1, second-degree AVB (Wenckebach conduction) with a single junctional escape beat with AV conduction block (Figure 5A). A subsequent ECG showed atrial flutter with variable conduction, resulting in an urgent referral to our institution. On admission, he was haemodynamically stable with an entirely normal examination. Blood tests, including electrolytes and thyroid function tests, were within normal range. Electrocardiograms on admission showed Mobitz Type I AVB (Figure 5B) followed by atrial flutter with a ventricular rate of 140 b.p.m. after the patient had been instructed to perform squatting exercises. Transthoracic echocardiogram confirmed normal chamber dimensions with good biventricular systolic function with no evidence of valvular heart disease. During a subsequent exercise test, in which the patient achieved a heart rate of 180 b.p.m., there was no evidence of inducible ischaemia or worsening of the baseline first-degree AVB.

Three days after hospitalization the patient was discharged home, asymptomatic with a normal ECG. He was strongly advised to stop all illicit drug use and counselled accordingly. Unfortunately, following discharge he was lost to follow-up.

A healthy 24-year-old male, known to be a regular smoker of cannabis, was admitted to our arrhythmia clinic with a history of two, identical episodes of malignant syncope within the past year, both associated with head injury. On each occasion, whilst he was having his hair cut, he became symptomatic with dizziness leading to transient loss of consciousness. His past history was remarkable for asymptomatic sinus bradycardia. His baseline examination and blood tests were entirely normal. Urine toxicology was positive for cannabis but no other recreational drugs were detected. A 12-lead ECG showed inverted P-waves in leads II, III, and AVF and upright P-waves in aVR-consistent with retrograde sinoatrial node activation from an ectopic site (Figure 6).

Stand-up tilt test, carotid sinus massage, and 24-h Holter ECG monitoring were all normal. A computed tomography brain scan revealed no evidence of intracerebral haemorrhage or infarction and no cerebral masses. His echo study was entirely normal. The patient underwent further assessment with an implantable loop recorder (ILR) and was counselled with regards to smoking cessation including marijuana. During a follow-up visit he reported to smoking less marijuana (single episode per week) with no further episodes of syncope despite ongoing evidence of nocturnal and early morning sinus bradycardia, as recorded by his ILR.