A 27-year-old man of North African descent attended the emergency room of our tertiary percutaneous coronary intervention centre because of chest pain. Since 12 h, he had experienced severe retrosternal chest pain with sweating, nausea, and vomiting. Electrocardiography demonstrated ST-elevation in the anterior leads (Figure ). Detailed history revealed that in the hours prior to presentation, he had been recreationally using high amounts of N2O by inhalation from balloons. For the last 24–48 h, he had been sleep-deprived and, while sitting in a car, he had inhaled approximately 3.3 kg (or 420 balloons) of N2O and smoked 4 joints of cannabis. The patient had not experienced recent trauma, had no co-morbidities and was not under any prescription. He had never experienced chest pain before, there were no signs of acute heart failure. Besides smoking nicotine and cannabis, he did not have any other cardiovascular risk factors. There was no family history of coronary disease or sudden cardiac death. Drug screening upon presentation was positive for tetrahydrocannabinol (THC). Patient admitted to regularly smoke cannabis but denied consumption of alcohol or any other recreational drugs.\nAs per hospital protocol, he received 180 mg ticagrelor orally, 300 mg aspirin intravenously (i.v.) and 5000 EH heparin i.v. and was referred for immediate coronary angiography (CAG). This showed a normal aspect of the left main, right coronary and circumflex artery. The distal left anterior descending artery (LAD) was totally occluded, and thrombus was angiographically visible in the proximal segment, with maintained flow (TIMI 3) (Figure and ). Despite successful wire passage into the distal LAD and multiple balloon dilatations, no recanalization was achieved. Therefore, mechanical thrombectomy by means of AngioJet was attempted without distal recanalization, nor angiographical resolution of the proximal thrombus. Optical coherence tomography of the proximal LAD confirmed the presence of residual thrombus but excluded atherosclerotic media thickening. Plaque/endothelial erosion underneath the thrombus could not be excluded (Figure and ). Because of a minimal lumen area of 10.75 mm2 no further intervention was undertaken. The procedure was discontinued, and the patient received tirofiban i.v. for 48 h, on top of standard dual antiplatelet therapy (DAPT: ticagrelor and aspirin).\nThe first high-sensitive troponin T and CK-MB levels were 0.418 μg/L and 77 μg/L, peaking at 5.35 μg/L (upper limit of reference range: 0.014 μg/L) and >300 μg/L (upper limit of reference range: 7.6 μg/L). Transthoracic echocardiogram (TTE) showed a reduced (30–40%) left ventricular ejection fraction (LVEF) with apical and mid septal akinesia, a normal right ventricular function and no valvular abnormalities (). Migration of a venous thromboembolism due to intracardiac right-left shunt was excluded by using right-sided contrast. Vitamin B12 (114 pmol/L; reference range: 160–700 pmol/L), folic acid (7.7 nmol/L; 8.8–40 nmol/L), and homocysteine (205 μmol/L; <15 μmol/L) levels were measured upon admission.\nAfter 5 days, serum homocysteine levels had decreased to 86 μg/L. Additional analysis excluded the presence of a methylenetetrahydrofolate reductase (MTHFR)-gene polymorphism. To evaluate the effect of the initiated antiplatelet therapy CAG was repeated after 7 days. The size of the thrombus in the proximal LAD was slightly reduced, but the distal LAD remained occluded. (Figure and ). After initiation of heart failure medication, he was discharged with the advice to take DAPT for 1 year, discontinue drug abuse and take oral folic acid and vitamin B12 supplementation. Upon discharge persistent ST-elevation with negative T- (V2–V6) and pathological Q-waves (V2–V6) in the anterior leads was shown on the electrocardiogram (Figure ).\nAfter 3 months, a repeat TTE showed improvement of LVEF (53%), with remaining anteroseptal wall motion abnormalities (). He did not report recurrent angina or symptoms of heart failure.
A 45-year-old male with no significant past medical or psychiatric history presented with sudden onset of numbness below the umbilicus and unsteady gait. At the time of admission, the patient also had cognitive impairment with a Montreal cognitive assessment (MoCA) score of 22/30. There was no associated phonophobia or photophobia. During the hospital stay, the patient had experienced urinary retention with subsequent Foley catheterization. On physical examination, he had no vibratory sensation or proprioception in bilateral (B/L) lower extremities with cold temperature and spared pinprick. Reflexes were 2+ in B/L knees and ankle (left) with non-sustained clonus on left ankle, big toes were down going, with diminished sensation around T10, increased muscle tone in B/L lower extremities, and no obvious muscle weakness in lower extremities. He had a normal anal tone and post-void residual. Findings were suggestive of a spinal cord lesion mainly affecting the posterior column.\nAll laboratory findings were unremarkable except mean corpuscular volume of 111 fl (80-100 fl), B12 level of 311 pg/mL (160-950 pg/ml), methylmalonic acid (MMA) level of 7397 nmol/L (< 370 nmol/L), and a homocysteine level of 89.7 umol/L (< 15 umol/L). He had a recent history of abuse of nitrous oxide due to recreational usage. Magnetic resonance imaging (MRI) C spine (with and without contrast), T spine (with and without contrast), L spine (with and without contrast), and MRI brain (with and without contrast) were unremarkable. Cerebrospinal fluid (CSF) analysis revealed the presence of immunoglobulin G (IgG) oligoclonal bands. Electromyography showed left non-localizable peroneal neuropathy with a small peroneal compound muscle action potential (CMAP) and small superficial peroneal CMAP with no evidence of polyneuropathy. Based on all these findings, the final diagnosis of “myelopathy secondary to vitamin B12 deficiency induced by nitrous oxide abuse” was made.\nLater, the patient was treated with intramuscular vitamin B12 followed by oral formulation, and discharged to a rehabilitation center. Upon follow-up after 16 weeks, the patient's memory loss and confusion had improved with repeat B12 and MMA values of 1409 pg/mL and 139 nmol/L, respectively. The patient was able to ambulate without the assistance of a walking device and was able to perform all other activities of daily living. The patient's only remaining symptom was mild vibratory sensation deficits below the knees B/L, which was no longer noted at his 24-week follow-up.