Myocardial perfusion imaging: perspectives from a turbulent twenty-five years

It is almost twenty-five years since stress myocardial perfusion imaging was first described for the detection of ischemia. Since that time, significant refinements have occurred in the technology of making the measurements, and in the range of clinical indications to perform these measurements. In parallel with the growth of radionuclide techniques, other imaging technologies have developed substantial tools to examine the heart. Although radionuclide imaging remains unique in its ability to visualize the regional distribution of perfusion, the value of perfusion imaging is being called into question by practitioners of the competing technologies. To address these comments, every facet of the examination should be reviewed, and the examination tailored to answer the specific clinical question raised by the patients condition. Particular attention should be paid to data interpretation and the specific choice of words used to describe the images in the report. In addition, the information provided by the examination can be enriched by adding measurements of ejection fraction, regional wall motion and regional wall thickening to the procedure. This combination of additional data and a clear, clinically focussed report make the information more valuable to the referring clinician. Several new techniques are on the horizon, including 99mTc glucarate imaging, to identify acute myocardial necrosis, and direct identification of myocardial hypoxia with 99mTc labeled nitroimidazoles. Initial studies in humans with glucarate suggest that acute necrosis can be identified with one hour of onset of chest pain. Experimental studies with the nitroimidazoles suggest that they will be valuable to identify myocardial ischemia as a zone of increased uptake. Both techniques may be useful in the evaluation of patients presenting with chest pain syndromes in the emergency room. Other areas of potential promise include the possibility of detecting residual clots following thrombolytic therapy and identifying macrophages in unstable plaque.