Intravascular ultrasound in the diagnosis of the no-reflow phenomenon after primary angioplasty for myocardial infarction.

A 73 year old man was admitted with haematemesis and was found to have a pangastritis. Three days later he developed central chest pain, and ECG changes indicated an acute anterior myocardial infarction. In view of his recent haematemesis we performed emergency coronary angiography, which showed proximal occlusion of the left anterior descending (LAD) artery (TIMI 0 flow), with normal circumflex and right coronary arteries. We proceeded to primary percutaneous transluminal coronary angioplasty (PTCA) with a 7 French left 4.5 Judkins guide, a Magnum wire (Schneider UK, Staines, Middlesex, UK), and a 3.5 mm Viva balloon (Boston Scientific Ltd, St Albans, Herts, UK). Unfractionated intravenous heparin 10 000 units was given. The lesion was crossed with Magnum wire and injections at that time showed TIMI 1 flow. The site of occlusion was dilated with the 3.5 mm balloon to 6 then 8 atm with subsequent TIMI 0 flow. Dissection was thought to be the most likely cause of the no-reflow phenomenon and a 3.5 × 34 mm mounted Bard stent (Bard Ltd, Crawley, West Sussex, UK) was deployed at 13.5 atm. Subsequent injections showed TIMI 0 flow (fig 1) and 200 μg of intracoronary nitrate was given to exclude coronary spasm as a cause of the no-reflow phenomenon, with no improvement. At this stage it was impossible to find the cause of the no-reflow phenomenon and intravascular ultrasound (IVUS) was used to examine the distal vessel with an Ultracross 3.2 F 30 MHz IVUS probe (Boston Scientific Ltd). This showed segments of severe distal disease, a satisfactory appearance to the stented lesion proximally, and normal artery between these two areas (fig 2). The most severe segment was dilated with a 2.5 mm Viva balloon at 8 atm, and perfusion then improved. A 16 mm mounted Jo stent (Jomed UK Ltd, Knutsford, Cheshire, UK) was deployed at 11 atm and further inflations were made to additional distal lesions. TIMI 3 flow was thus achieved in the epicardial artery (fig 3). After the procedure, the patient was given ticlopidine; no other antiplatelet agents or anticoagulants were used. A blood sample taken at the end of the operation showed an activated partial thromboplastin time ratio of greater than 8.0.