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A 50 year old woman was admitted with central crushing chest pain. She had a strong family history of ischaemic heart disease (IHD). Her cholesterol was 4.7 mmol/l. There were no other risk factors for IHD. At the time of admission she was haemodynamically stable. Her ECG showed 2–6 mm ST segment elevation in the inferior leads. She was thrombolysed with tenecteplase. The ECG showed complete resolution of the ST segment. There was no elevation of cardiac troponin. She developed further chest pain with ST segment elevation in the inferior leads, and coronary angiography showed complete occlusion of the proximal right coronary artery (upper panel, middle). A prophylactic temporary pacemaker was inserted because the patient developed severe sinus bradycardia. This lesion did not respond to intracoronary nitrates. Hence the lesion was predilated and stented (Guidant Penta 4/38) with a good result angiographically (lower panel, middle). Twenty four hours later the patient developed further chest pain and ST segment elevation in the inferior leads. Repeat coronary angiography showed the stent was widely patent but there was a severe diffuse coronary artery spasm distal to the stent (upper panel, right) which responded very well with intracoronary nitrates (lower panel, right).
We believe that the complete occlusion of the right coronary artery initially was probably caused by severe coronary artery spasm which was resistant to intracoronary nitrates. The patient was discharged on maximal dose of calcium channel blockers and nitrates. She still has recurrent chest pain and a recent angiogram showed mild spasm of the proximal coronary artery just proximal to the origin of the stent, which responded to intracoronary nitrates.
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