A cataclasm due to spasm

Abstract

We describe a 59-year-old patient presenting with ST-elevation acute coronary syndrome. Coronary angiography with intravascular ultrasound (IVUS) showed an important nonsignificant atherosclerotic lesion in the proximal left anterior descending artery (LAD) and presence of bridging in the mid-LAD. Our hypothesis was that focal spasm at this site was the cause of transmural ischaemia; therefore, treatment was given by performing a percutaneous coronary intervention (PCI) of the lesion. The patient remained symptom-free which confirmed our conclusion. The myocardial bridging had no clinical implications at this moment.Keywords Coronary spasm . Myocardial bridging . Intravascular ultrasound A 59-year-old negroid male presented to the emergency department with chest pain. His previous medical history consisted of heterozygous alpha thalassaemia type 2, reflux disease and lumbar hernia. A coronary angiogram 6 years ago had shown only slight vessel wall abnormalities. Cardiac risk factors were hypertension, a positive family history for coronary artery disease and nicotine abuse in the past. There was no history of cocaine abuse. During the last 5 months he had been complaining of sudden chest pain occurring at rest, which radiated to the left arm and only lasted for roughly 10 min. He had never had any exerciseinduced symptoms. The pain also reacted swiftly to sublingual nitrate. An exercise test performed in the week before his admission showed no abnormalities. His current medication was acetylsalicylic acid, amlodipine, losartan, bisoprolol, proton pump inhibitor and ranitidine. Blood pressure was 129/79 mmHg with a pulse of 53 beats/min. Further physical examination revealed no abnormalities. The symptom-free electrocardiogram showed sinus rhythm and diffuse repolarisation abnormalities with T-wave inversion in leads II, III and V4 to V6. During chest discomfort, there was ST elevation in leads I, aVL, and V2 to V6 with reciprocal depression in leads III and aVF (Fig. 1). Laboratory tests showed no abnormalities and the cardiac enzymes remained normal. He was treated for an acute coronary syndrome with clopidogrel, fraxiparine and intravenous nitroglycerin. Coronary angiography showed 50 % stenosis of the proximal LAD (Fig. 2), myocardial bridging of the mid LAD, 90 % stenosis of the first and second diagonal branch and 70 % stenosis of margo obtuse and posterolateral branches. The culprit lesion appeared to be the proximal LAD as this could explain the electrographic changes. Due to the fact that this stenosis did not seem to be significant on visual assessment, an FFR measurement was performed. This showed a value of 0.96; therefore, the lesion was not considered to be haemodynamically important and PCI was not performed. Although the angiogram showed no evidence of coronary spasm the clinical evidence started to point in this direction. After discontinuing bisoprolol and under treatment with maximum doses of oral nitrate and calcium antagonist he had recurring short and sudden episodes of chest pain. ...

ST-segment elevation associated with allergic reaction to echocardiographic contrast agent administration

“…In another case report, reversible ST-segment elevation was reported after administration of Sonovue® but before starting DSE[ 13 ]. However, coronary angiography was not performed in either of these patients, while the current case report could demonstrate the absence of intra-coronary thrombus, but the presence of significant coronary spasm as a cause of the ST-segment elevation [ 14 ].…”