Morphologic correlates of technetium-99m stannous pyrophosphate imaging of acute myocardial infarcts in dogs.

Buja, L. Maximilian; Parkey, Robert W.; Dees, Jane H.; Stokely, Ernest M.; Harris, Ryan A.; Bonte, Frederick J.; Willerson, James T.

doi:10.1161/01.cir.52.4.596

Cited by 146 publications

(41 citation statements)

References 15 publications

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“…This is consistent with our electron microscopic observations which showed some nonmitochondrial calcium deposition in (3,(26)(27)(28)(29)(30)(31)(32)(33)(34)(35). Damaged border zone myocardium with mildly elevated calcium levels and focal mitochondrial calcification also showed significant 99mTc-P uptake, indicating that massive calcium accumulation is not required for 99mTc-P concentration.…”

Section: Concentration Of Technetium-99m Phosphorus Agents 731supporting

confidence: 91%

“…Hearts with proximal LAD occlusion had transmural anterior infarcts with histopathologically distinct central and peripheral regions as previously described (3,4).…”

Section: Methodssupporting

confidence: 52%

“…A more detailed analysis was undertaken of the distribution of 99mTc-P and calcium in infarcted myocardium. Study of corresponding histologic sections allowed assignment of samples for tissue assay to the various histopathologically defined infarct zones (3,4). Total number of infarct samples assayed for each dog ranged from 15 to 35.…”

Section: Methodsmentioning

confidence: 99%

“…Bonte and associates first showed that the 99mTc-P bone scanning agents concentrate in areas of acute myocardial infarction, and suggested that this phenomenon was related to labeling of calcium deposits in the infarcts (2). Our previous experimental studies have demonstrated that a positive 99mTc-P myocardial scintigram results from selective concentration of the agent in areas with partial to homogeneous myocardial necrosis, mtultifocal mtusele cell calcification, and residual blood flow (3)(4)(5)(6). 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).…”

mentioning

confidence: 97%

“…Our previous experimental studies have demonstrated that a positive 99mTc-P myocardial scintigram results from selective concentration of the agent in areas with partial to homogeneous myocardial necrosis, mtultifocal mtusele cell calcification, and residual blood flow (3)(4)(5)(6). 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.…”

mentioning

confidence: 99%

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

Buja¹,

Tofe²,

Kulkarni³

et al. 1977

J. Clin. Invest.

205

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A B S T R A C T This study was performed to elucidate the localization at the cellular level of technetium-99m phosphorus (991'Tc-P) radiopharmaceuticals in acute myocardial infarcts and the mechanisms responsible for 99mTc-P uptake in acute myocardial infarcts and other tissues. In 20 dogs with proximal left anterior descending coronary arterial ligation for 1-3 days, elevated calcium levels were measured at all sites of increased 99mTc-P uptake (acute myocardial infarcts, necrotic thoracotomy muscle, lactating breast, and normal bone); however, a consistent linear relationship between 99mTc-P and calcium levels was not observed. A strong correlation (r = 0.95 and 0.99, n = 2 dogs) was demonstrated between levels of 3H-diphosphonate and 99mTc-P in infarcted myocardium. Auito studies revealed major localization of both 99mTc-P and calcium in the soluble supernate and membranedebris fractions of infarcted myocardium and less than 2% of total 99mTc-P and calcium in the mitochondrial fractions; however, electron microscopic examination showed that mitochondria with calcific deposits were not preserved in the mitochondrial fractions. In vitro studies evaluating the role of serum protein binding on tissue uptake of 99mTc-P agents demonstrated that, in spite of significant complexing with serum proteins, serum 99mTc-P activity retained the ability to adsorb to calcium hydroxyapatite and amorphous calciumni phosphate. In vivo stuidies showed that concentration of human seirum albtumin (labeled with iodine-131) in infarcted myocardiutim reached a maximuiim of only 3.8 times normal after a circulation time of 96 h, whereas 99mTc-P uiptake was at least 10 times normal after a circulation time as short as 1 h. It is concluded that: (a) 99mTc-P uptake in acutely infarcted myocardium, and possibly other types of soft tissue damage, is limited to necrotic and severely injured cells; (b) concentration of 99mTc-P results from selective adsorption of 99mTc-P with various forms of tissue calcium stores, including amorphous calcium phosphate, crystalline hydroxyapatite, and calcium complexed with myofibrils and other macromolecules, possibly supplemented by calcium-independent complexing with organic macromolecules; and (c) lack of a linear relationship between 99mTc-P and tissuie calcitum levels mainly results from local differences in composition and physicochemical properties of tissuie calcium stores and from local variations in levels of blood flow f'or delivery of 99mTc-P agents.

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Section: Concentration Of Technetium-99m Phosphorus Agents 731supporting

confidence: 91%

“…Hearts with proximal LAD occlusion had transmural anterior infarcts with histopathologically distinct central and peripheral regions as previously described (3,4).…”

Section: Methodssupporting

confidence: 52%

Section: Methodsmentioning

confidence: 99%