Imaging arterial thrombi. An elusive goal.

T he role of thrombotic processes in the conversion of a quiescent atherosclerotic plaque into a clinically active atherothrombotic le-sion has been well established over the past decade.' In coronary, cerebral, and peripheral arterial beds, atherothrombotic events underlie acute clinical vas-cular syndromes ranging from unstable angina and myocardial infarction to transient ischemic attack and stroke.2 See pp 288, 298 In the coronary circulation in particular, recognition of the role of thrombosis in acute myocardial infarction is largely responsible for the recent development and clinical application of thrombolytic therapy. Because invasive angiographic assessment is not logistically feasible or ethically acceptable before the initiation of thrombolytic therapy in most patients with evolving infarction, the diagnosis is made without firm evidence for the presence of an acute thrombotic coronary process, let alone unequivocal identification of the involved vessel: The localization of a "culprit" lesion in' acute infarction rests largely on inferential electrocardiographic, echocardio-graphic, or scintigraphic data. The lack of a simple, relatively noninvasive method for identifying an acute atherothrombotic stenosis or occlusion is a notable deficiency in current cardiovas-cular practice. Inaccurate diagnosis, ineffective therapeutic response, and reocclusion or restenosis after initially successful therapy are all potential pitfalls of current approaches to patients with suspected acute occlusive arterial syndromes; improvement in diagnosis and management would be facilitated by an efficient and specific method for defining noninva-sively and unequivocally the status of the culprit vascular lesion. The majority of studies and methods developed to image thrombi involve the use of radionuclide imaging agents. The earliest successful scintigraphic approach was that using ["'I]-fibrinogen in the diagno-The opinions expressed in this editorial comment are not necessarily those of the editors or of the American Heart Association. sis of deep vein thrombosis.3,4 This method, still currently in use, requires an actively growing throm-bus and several days of imaging for optimal diagnostic sensitivity. However, labeling the large circulating fibrinogen pool results in a low thrombus-to-blood activity ratio; this requires that imaging be deferred until adequate clearance of circulating label has occurred to provide target-to-background activity ratios sufficient for thrombus detection. The experience with ['25I]-fibrinogen in deep vein thrombosis highlights the principal problems with which one is confronted in scintigraphic imaging of thrombus. First and foremost, one must label some component of the thrombus relatively selectively; ideally, that component should not be present in the circulating blood pool. Second, the element of the thrombus that is labeled must be in …