Radionuclide assessment and diagnosis of acute myocardial infarction.

The prototype radionuclide imaging technique for detecting acute myocardial infarction is technetium-99m stannous pyrophosphate ( mTc PPi) myocardial scintigraphy. Today, this imaging assessment is commonly made with single photon emission cornputed tomography (SPEGT) that allows the detection of infarcts as small as 1 g, localization of the site of infarction, and accurate measurements of the size of the infarct. Technetium-99rn-PPI scintigraphy was developed with the hypothesis that pyrophosphate might bind to calcium deposited in irreversibly darnaged myocardial cells with myocardial infarction. Large numbers of patients have been evaluated with this technique and it has been repeatedly demonstrated that pyrophosphate administered one to four days after acute myocardial infarction, without reperfusion, identifies 85 to 90 percent of infarctions ordinarily missing only those less than 3 g in size, many of which are subendocardial in location. With thrombolytic therapy and the reestablishment of coronary blood flow soon after infarction, “Tc-PPi may be used for detection of infarction within one to two hours after the onset of symptoms suggestive of infarction. Given intravenously, Tc-PPi and SPEGT imaging within one to two hours of successful thrombolytic therapy allow accurate detection of small infarctions and the sizing of these lesions. Previous clinicopathologic correlates have established that pyrophosphate is incorporated into areas of irreversible cellular damage with some persistent coronary blood flow and that pyrophosphate complexes with calcium deposited in soluble and insoluble form in the injured myocardial cells. Some ofthe pryophosphate uptake may also be the result of nonspecific trapping within injured cells. More than four days after myocardial infarction, approximately half the abnormal pyrophosphate scans revert to negative as the area of infarction is replaced by inflammatory tissue and a scar develops. In patients who retain “persistently abnormal” results of ’Tc-PPi myocardial scintigrams, clinicopathologic correlates have established continuing myocardial ischemia and chronic myocardial cellular injury as mechanisms for the “persistently abnormal” scintigrams.