Experimental Infarct Sizing Using Computer Processing and a Three-Dimensional Model

Lewis, Mary Ann; Buja, L. Maximilian; Saffer, Sara; Mishelevich, David J.; Stokely, Ernest M.; Lewis, Samuel E.; Parkey, Robert W.; Bonte, Frederick J.; Willerson, James T.

doi:10.1126/science.327541

Cited by 38 publications

(4 citation statements)

References 16 publications

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“…-~~~~~~~~~~~~~~, ---.1----FIGURE 5 Electron micrograph of damaged border zone muscle cell. The muscle cell exhibits intact myofibrils, some glycogen granules, vacuolated sarcoplasmic reticulum (V), numerous lipid droplets (L), and swollen mitochondria which are devoid of amorphous matrix densities but contain small, electron dense deposits of early calcification (arrows).…”

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

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: 99%

“…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.…”

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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.

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204

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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 731mentioning

confidence: 99%

mentioning

confidence: 99%

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.

Self Cite

204

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“…Others have suggested that nonspecific protein binding of technetium-99m pertechnetate within damaged myocardial cells may also be a factor (7). It also must be kept in mind that the limit of resolution of the technique is 3 g of irreversibly damaged tissue in experimental animals with myocardial infarcts; infarcts smaller than this size would not be expected to be consistently visualized with this imaging technique (10,14).…”

Section: Discussionmentioning

confidence: 99%

Technetium‐99m stannous pyrophosphate myocardial scintigraphy: Serial imaging to detect myocardial infarcts in patients

Falkoff

Parkey

Bonte

et al. 1978

Clinical Cardiology

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Summary:Typically, technetium-99m stannous pyrophosphate ~9"'Tc-PYP) myocardial scintigrams become abnormal within 10-12 h following acute myocardial infarction. Ordinarily, the 99mTc_PYP scintigrams become increasingly abnormal between 24 and 72 h follOwing the infarct and then become normal 6-7 days after the event. However, occasional patients and their 99mTc_PYP myocardial scintigrams deviate from this expected pattern by initially developing an abnormal 99mTc_PYP scintigram as late as 4-5 days following an acute myocardial infarction. Others retain "persistently abnormal" 99"'Tc_PYP myocardial scintigrams after their myocardial infarcts. The clinical importance and potential prognostic importance of these deviations from the expected patterns with 99"'Tc_PYP myocardial imaging are discussed and the need for serial myocardial imaging is emphasized.

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Is There a Need for Additional Means of Recognizing Myocardial Necrosis?

Willerson

Parkey

Buja

et al. 1977

JAMA

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Experimental Infarct Sizing Using Computer Processing and a Three-Dimensional Model

Cited by 38 publications

References 16 publications

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

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

Technetium‐99m stannous pyrophosphate myocardial scintigraphy: Serial imaging to detect myocardial infarcts in patients

Is There a Need for Additional Means of Recognizing Myocardial Necrosis?

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