Noninvasive quantitation of myocardial infarction with technetium 99m pyrophosphate.

Abstract

SUMMARYWe sought to quantitate infarct size using radioactive imaging techniques. Infarcts were created in closed chest dogs. Using a scintillation camera interfaced to a computer, infarct images were made in the anterior, left lateral, LAO, and RAO projections, 48 Fourteen mongrel dogs weighing 14 to 31 kg were anesthetized with intravenous sodium pentobarbital (5 mg/kg). Via a carotid approach, utilizing a modified coaxial catheter and a closed chest technique,"' we selectively embolized small occluded catheter segments to branches of the left coronary artery, creating discrete areas of myocardial infarction. The dogs were given an antiarrhythmic drug (lidocaine, 50 mg, intravenously preinfarction; 1 hour postinfarction, and as needed) and antibiotic (cephazolin, 500 mg, intravenously) prophylaxis at the time of the procedure, and allowed to recover. Standard 12 lead electrocardiograms were taken preinfarction and one and 48 hours postinfarction. Forty-eight hours following infarction the dogs were again anesthetized and injected intravenously with 15 mCi of Tc-PYP formulated in our laboratory.'4 Seventy-five to ninety minutes later, infarct images were obtained in ten animals in the anterior, lateral, LAO and RAO projections. Two normal dogs were also imaged with Tc-PYP.The dogs were sacrificed two hours following Tc-PYP injection, at which time the hearts were removed and the ventricles isolated. The right ventricle was separated from the interventricular septum anteriorly. The septum was freed from the posterior ventricular wall and the specimen laid open. A necropsy image was taken. In each experiment, using a cork bore biopsy tool, a total of 74 cylindrical, transmural specimens were taken from grossly normal, grossly infarcted, and marginal zones of both ventricles. These biopsy specimens were counted in a well counter, quick frozen in dry ice and alcohol, and then stored at

Pathophysiology of technetium-99m stannous pyrophosphate and thallium-201 scintigraphy of acute anterior myocardial infarcts in dogs.

“…Thus, the thesis that positive mTc-PYP myocardial scintigrams in subjects with acute myocardial infarcts result primarily from visualization of high levels of 9mTc-PYP in necrotic myocardium is supported by the findings in this study as well as by: (a) the close correlation between estimates of infarct size obtained from measurements of infarct area on mTc-PYP myocardial scintigrams and morphologically determined infarct size in dogs with proximal LAD occlusion (46,47); (b) the findings of Martonffy et al (48) indicating that significant 'mTc-PYP concentration occurs only after intervals of ischemia which produce myocardial necrosis in the canine left circumflex coronary occlusion model (28,38); and (c) the characteristic time course of positive "mTc-PYP myocardial scintigraphy, with positive myocardial scintigrams being observed between 12-16 h and 7-14 days after experimental LAD occlusion or clinical onset of infarction (16)(17)(18)(19)(20)35).…”

Magnetic resonance imaging (MRI) in different stages of myocardial infarction using the contrast agent gadolinium‐DTPA

“…Diagnosis of chronic infarction is not difficult (Bodenheimer et al, 1975(Bodenheimer et al, , 1976Hillis and Braunwald, 1977;Selwyn er al., 1977). Tomoscintigraphic studies have demonstrated a high degree of accuracy in estimation of the stage and size of acute and chronic myocardial infarction (Botvinick et al, 1975;Eichstaedt et al, 1980;Kronenberg et al, 1979;Momson et al, 1980;Wackers et al, 1977). Both M-mode echocardiography (Rasmussen and Corya, 1975) and two-dimensional techniques (Grube er al., 1979;Hecht et al, 1980;Parisi et al, 1981) have proved helpful in estimation of infarct size.…”

Sites and Mechanisms of Localization of Technetium-99m Phosphorus Radiopharmaceuticals in Acute Myocardial Infarcts and other Tissues

“…These findings were interpreted as supporting the proposed role of tissue calcification in concentration of the agent, but as not excluiding the possibility of other mechanisms (3)(4)(5)(6). Other reports (7)(8)(9)(10)(11)(12)(13)(14)(15)(16) have confirmed the dependence of 99mTc-P concentration on the presence of myocardial necrosis, and the importance of blood flow for modulating the level of 99mTc-P uiptake. Previous studies from our own and other laboratories, however, have not resolved certain important questions regarding 99mTc-P uptake after myocardial injury.…”