When coronary spasm strikes: a case report on the dreadful association between cannabinoids and caffeine

Coronary artery spasm (CAS) is a temporary, severe narrowing of the coronary arteries typically presenting with nitrate-responsive angina at rest, transient ischaemic ECG changes, and in some cases leading to silent myocardial ischaemia, acute myocardial infarction, life threatening arrhythmias and cardiac arrest.

A 47-years-old man with a history of chronic coronary syndrome and a working diagnosis of probable pheochromocytoma was admitted to the Emergency Department after two episodes of out-of-hospital cardiac arrest successfully resuscitated. Transient ST segment elevation was observed, and emergency coronary angiography (CA) revealed no significant coronary stenosis. His history also included past alcohol abuse and ongoing cannabinoid use. A negative gallium positron emission tomography along with normal urinary metanephrines levels ruled out the diagnosis of pheochromocytoma. During the hospital stay, the patient experienced new episodes of chest pain, followed by two episodes of in-hospital cardiac arrest successfully resuscitated. The ECG showed transient ST-segment elevation in the anterior and lateral leads. Emergency CA revealed severe dynamic vasospasm at the ostium and proximal segments of the left anterior descending artery and circumflex artery, that regressed after intracoronary nitroglycerine. Therapy with both non-dihydropyridine and dihydropyridine calcium channel blockers, alongside nitrates, was initiated. Reviewing the patient’s medical history revealed that he had been consuming at least 3 L of cola daily at home. Approximately 1 h before his last two cardiac arrests, he drank another can of cola. Before discharge, he received a dual-chamber defibrillator for secondary prevention.

Life-threatening arrhythmias and recurrent cardiac arrest are rare but severe potential consequences of CAS, particularly in the presence of synergistic triggers such as caffeine and cannabinoids. Lifestyle modification and targeted pharmacotherapy in high-risk CAS patients may not be sufficient to prevent life-threatening complications.