Bead‐like coronary spasm

A 59-year-old man with a history of hypertension, mitral valve replacement and tricuspid valve annuloplasty for infective endocarditis presented with frequent episodes of chest pain and progressive dyspnoea on exertion for 6 months. He underwent cardiac catheterisation and coronary angiogram because of worsening symptoms and a positive exercise stress test. Multiple tandem concentric stenotic lesions were disclosed in the left anterior descending coronary artery and right coronary artery, implying severe double vessel coronary artery disease. (Fig. 1a,b). Because he developed symptomatic bradycardia, a temporary pacemaker was placed. He was treated with nitrates and aspirin. A subsequent coronary angiogram obtained seven days later showed normal coronary arteries (Fig. 1c,d). The diagnosis of coronary artery spasm was made. The patient’s symptoms of chest pain have been controlled with oral nitrates and a calciumchannel blocker during a follow-up of 2 years. Severe chest pain, usually unrelated to physical effort and with a concurrent ECG showing transient ST elevation, is a common finding of coronary artery spasm. The major factors in the development of coronary artery spasm include cigarette smoking, endothelial dysfunction because of reduced nitric oxide bioavailability, hypercontractility of vascular smooth muscle in spastic arteries, increased autonomic tone, increased oxidative stress, hypomagnesaemia, low-grade inflammation, and genetic susceptibility. Although the cellular and molecular mechanisms of coronary spasm are still not well understood, calcium antagonists, long-acting nitrates and