Focal coronary spasm is often associated with an area of mural plaque disease. This report describes a patient with recurrent severe coronary spasm unresponsive to medical treatment. Coronary arteriography and intravascular ultrasound identified a candidate area of minor coronary atheromatous disease but ergonovine provocation testing showed the spastic coronary segment to be distal to and distinct from this area. Coronary stenting of the site identified by ergonovine provocation testing was effective in relieving provoked and spontaneous spasm. P atients with severe recurrent coronary spasm unresponsive to medical treatment may respond to stenting of the spastic coronary segment. [1][2][3][4] The site of spasm is often associated with an area of mural atheromatous plaque.
5Intravascular ultrasound (IVUS) may be used to identify the site of non-stenotic mural plaque, but spasm provocation testing is necessary to identify the spastic coronary segment for stent deployment.
CASE REPORTA 54 year old woman presented to the outpatient clinic of a district general hospital with a five week history of chest pain unrelated to exertion. The pain was central and radiated to the left arm. Symptoms usually occurred in the early hours of the morning, lasting for one or two hours with spontaneous relief. The frequency of chest pain had progressed from two episodes a week to daily. She had a medical history of asthma and controlled hypertension for which she was prescribed salbutamol and fludrocortisone inhalers and enalapril 20 mg once daily. She had recently undergone endoscopy to investigate symptoms of dysphagia, with normal results.Clinical examination in the outpatient clinic was normal. Twelve lead ECG showed symmetrical T wave inversion in chest leads V2-V4 (fig 1). An exercise tolerance test was carried out in the clinic. The patient exercised for over nine minutes with no chest pain. There was pseudonormalisation of the inverted T waves on exercise but no other new ECG changes. Transthoracic echocardiography was normal. The patient was started on clopidogrel 75 mg, long acting diltiazem 200 mg, simvastatin 20 mg, and a glycerine trinitrate spray. She was referred for early outpatient coronary angiography.Eighteen days later she presented to the emergency room after an episode of more severe chest pain. The ECG showed no new changes. Troponin T was 0.2 ng/ml (laboratory range , 1.10) and myoglobin was 63 ng/ml (laboratory range , 70). Inpatient stress echocardiography showed no wall motion abnormality at dobutamine doses up to 40 mg/kg/min. In view of this finding it was felt that there was a low probability of fixed stenotic coronary artery disease. The patient was started on a proton pump inhibitor and discharged. One month later she presented again with severe chest pain. This time a 12 lead ECG undertaken by her primary care physician showed anterior ST segment elevation. This had settled by the time she was admitted to hospital. She was started on intravenous nitrate and unfractionated heparin. Despite this she ha...