In September 2017, a 21-year-old male patient was referred to our emergency room with constant substernal chest tightness, unrelated to breathing, with radiation into the left shoulder, lasting for 2 h before admission. Physical examination was unremarkable; there were no additional heart sounds on auscultation and no pulmonary rales. The heart rate was 67 b.p.m. and blood pressure 130/75 mmHg. Jugular venous pressure was not elevated and no pitting oedema was present. On electrocardiogram (ECG), sinus rhythm with ST-segment elevation in the precordial leads and in leads II, III, and aVF was noted (Figure 1A). Laboratory measurements showed elevation of the cardiac biomarkers troponin (0.239 ng/mL; upper limit of normal <0.1 ng/mL) and creatine kinase (initial 469 U/L, peak 1563 U/L; upper limit of normal <169 U/L). Treatment with aspirin 250 mg intravenously was initiated, a heparin infusion started and a loading dose of 180 mg ticagrelor administered. Subsequent coronary angiography showed thrombotic subtotal occlusion of the left anterior descending artery (LAD) at the take-off of the first diagonal branch (Figure 1B;Supplementary material online, Video S2). No other lesions were observed and the remaining coronary arteries did not show any atherosclerotic alterations (Supplementary material online, Video S1). Because coronary blood flow could not be fully re-established by thrombus aspiration (Supplementary material online, Video S3) and infusion of glycoprotein IIb/IIIa inhibitors (GPI), implantation of a drug-eluting stent (DES; 4.0 × 18 mm) was necessary after pre-dilatation of the lesion (Figure 1C and D, Supplementary material online, Videos S4 and S5). During intervention, we used a FilterWire EZ™-system (Boston Scientific, Marlborough, MA, USA) to protect the peripheral vessels from thrombotic occlusion (Supplementary material online, Videos S4 and S5, Figure 1). The culprit lesion was reopened successfully and TIMI III flow could be established (Figure 1E, Supplementary material online, Video S6). The culprit lesion was reopened successfully (Figure 1E, Supplementary material online, Video S6). No periprocedural arrhythmias occurred and the patient recovered quickly. Dual antiplatelet therapy (100 mg aspirin once daily and 90 mg ticagrelor twice daily), a betablocker (47.5 mg metoprolol once daily), and a statin (40 mg atorvastatin once daily) were prescribed. Transthoracic echocardiography revealed hypokinesia of the anterior wall resulting in overall mildly reduced left ventricular ejection fraction but no other abnormalities.

To rule out an embolic source for the thrombotic coronary occlusion in this young patient, we additionally performed transoesophageal echocardiography with echo contrast but could not find any evidence for an intracardiac shunt or any other source of cardiac embolism. Moreover, laboratory testing for thrombophilia did not show any abnormalities and testing for autoimmune diseases was negative. Blood lipid and glucose levels were within the normal range. The patient had a history of frequent cannabis abuse but denied cigarette smoking. He had no family history of CAD and did not regularly take any medication. Urine toxicology revealed elevated levels of delta-9-tetrahydrocannabinol but was negative for any other drugs. Thus, we considered cannabis abuse as the most likely cause of the MI and strictly advised the patient to avoid further cannabis consumption. The patient was discharged from the hospital in good clinical status under optimal medical treatment. However, the patient continued his cannabis abuse and suffered from three ACS relapses within 2 years, although medication was continued. The first MI occurred 8 months later and was caused by thrombotic occlusion of a diagonal branch despite optimal adaptation of the previously implanted stent in the LAD which was visualized by optical coherence tomography (Figure 2A–C). This occlusion was treated by GPI and implantation of another DES into the diagonal branch (Figure 2D–F). The second relapse was a non-ST elevation ACS in February 2019 and was due to thrombotic re-occlusion of the diagonal branch, again despite optimal stent adaptation. One month later, the patient again presented with angina at rest, this time without cardiac enzyme release, caused by thrombotic occlusion of the proximal circumflex artery. Both events were treated by GPI alone. Coronary angiography did not reveal any evidence of coronary dissection in any of the ACS relapses. Cannabis consumption was continued during the whole period. After the fourth ACS, left ventricular ejection fraction was still only mildly reduced. Since the last relapse, the patient stopped cannabis abuse and has been symptom-free for 8 months, i.e. until the last follow-up in November 2019.