Value of indium-111 monoclonal antimyosin antibody for imaging in acute myocardial infarction

Abstract

In most patients with chest pain, clinical history and observed electrocardiographic and enzymatic changes are sufficient to prove or rule out an acute myocardial infarction (AMI). However, in some patients these methods fail to rule out or do not allow to localize the site of an AMI. In patients admitted several days after the acute attack of chest pain, enzyme levels may have returned to normal and the electrocardiogram may not differentiate old from recent infarction. In addition, the enzyme changes after coronary artery bypass grafting may be comparable to those seen during an AMI, but confirmation of the diagnosis and localization of the AMI on the electrocardiogram may be difficult. Localization of myocardial infarction may also be difficult in patients with a left bundle branch block or Wolff-Parkinson-White syndrome. Finally, although infarct size has been estimated by measuring enzyme levels, these values may be less reliable as a marker of infarct size after thrombolytic therapy. To overcome these problems nuclear imaging techniques have been used, particularly technetium-99m stannous pyrophosphate imaging. 1,2 However, technetium stannous pyrophosphate has disadvantages. Persistent blood pool activity and low-grade uptake in the region of the heart may be confused. In addition, uptake by overlying ribs and sternum may make interpretation of the technetium pyrophosphate scan difficult. Also, one must wait at least 24 hours, and preferably 48 to 72 hours, after the onset of chest pain. These problems may be resolved if single photon emission computed tomography and blood pool overlay techniques are used. 3 Since monoclonal antimyosin antibody labeled to indium-111 was available in our laboratory a study was undertaken to assess the value of this antibody to localize an AMI. To study the value of this technique patients were selected in whom electrocardiographic changes allowed localization of the AMI.