Myocsrdial uptake of technetium-99m stannous pyrophosphate following direct current transthoracic countershock.

DiCola, Vincent; Freedman, Gerald S.; Downing, S. E.; Zaret, Barry L.

doi:10.1161/01.cir.54.6.980

Cited by 78 publications

(19 citation statements)

References 20 publications

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“…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.…”

mentioning

confidence: 87%

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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confidence: 87%

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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“…Defibrillation threshold at the time of implant did not significantly differ among the groups. The cumulative energy delivered in groups 1, 2, and 3 was not significantly different; however, the total energy and number of discharges delivered in patients in group 4 were significantly higher (p<0.001) than in patients in any of the other groups. Further analysis of the CPK and CPK-MB data is shown in Figure 1.…”

Section: Spontaneous Aicd Shocks In Groupmentioning

confidence: 66%

“…We conclude that 1) defibrillation efficacy testing limited to 85±29 J does not cause detectable myocardial injury; 2) spontaneous discharges of the AICD with a maximum cumulative energy of 330 J does not result in detectable myocardial injury when the rate of discharge for five rapid shocks is less than one shock per minute; 3) rapid consecutive (more than 12 at less than 1 minute apart) AICD discharges can result in a positive 9mTc pyrophosphate scan and CPK-MB release (however, electrocardiographic changes consistent with new myocardial infaretion are rare); 4) the appearance of new Q waves or persistent (after 48-72 hours) T wave changes, together with significant release of CPK isoenzymes, is probably because of myocardial infarction caused by vascular occlusion; patients is being exposed to repeated defibrillations cardiac defibrillation. [2][3][4][5] No report, however, has applied directly to the heart. Laboratory animal data specifically focused on whether defibrillators using suggest that detectable myocardial injury can occur two-patch electrode configuration, implanted over Group 2 was made up of nine patients who were evaluated at the time of initial surgery for patch placement and AICD generator implant (new AICD implants, screw-in leads plus patches).…”

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confidence: 99%

Automatic implantable cardioverter/defibrillator discharges and acute myocardial injury.

et al. 1990

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Multiple defibrillations by the automatic implantable cardioverter/defibrillator (AICD) have been reported to result in localized epicardial damage. No data exist, however, regarding whether this damage can be detected in the clinical setting or whether it interferes with the detection of true myocardial infarction. Forty-nine patients who received defibrillations by patch electrodes were studied prospectively. We attempted to document the presence of myocardial injury with the following three commonly used modalities for the detection of myocardial infarction: serial electrocardiographic changes, serial creatine phosphokinase (CPK) and CPK-MB release, and technetium 99m pyrophosphate scanning. Fifteen patients received defibrillations by AICD patches at the time of AICD generator replacement. Nine patients received defibrillations at the time of new AICD lead placement. The average total energy delivered was 85±29 J. None of these patients had detectable myocardial injury. Ten patients had defibrillations by the AICD patches at the time of bypass operation. One patient in this group developed acute myocardial infarction in the inferior wall after posterior descending coronary bypass operation, as detected by electrocardiogram, 'mTc pyrophosphate scanning, and CPK-MB analysis. Fifteen patients were evaluated for spontaneous AICD discharges. Thirteen had a maximum of five consecutive shocks, and cumulative energy delivered was not greater than 330 J. None of these patients had detectable injury. Two patients had CPK-MB release of 15.3% and 7.5%, respectively. One of these patients had a positive 99mTc pyrophosphate scan. These two patients received 12 and 17 rapid and consecutive AICD discharges, respectively, with cumulative delivered energy of 360 and 510 J, respectively. Twenty-one patients in this series developed nonspecific ST-T segment changes that normalized within 48-72 hours after AICD discharges. We conclude that 1) defibrillation efficacy testing limited to 85±29 J does not cause detectable myocardial injury; 2) spontaneous discharges of the AICD with a maximum cumulative energy of 330 J does not result in detectable myocardial injury when the rate of discharge for five rapid shocks is less than one shock per minute; 3) rapid consecutive (more than 12 at less than 1 minute apart) AICD discharges can result in a positive 9mTc pyrophosphate scan and CPK-MB release (however, electrocardiographic changes consistent with new myocardial infaretion are rare); 4) the appearance of new Q waves or persistent (after 48-72 hours) T wave changes, together with significant release of CPK isoenzymes, is probably because of myocardial infarction caused by vascular occlusion; and 5) transient (48-72 hours) ST-T segment changes are common after AICD discharges. (Circulation

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“…Myocardial injury was assessed using technetium99m stannous pyrophosphate (Tc-PYP), a radionuclide that binds to damage myocardium in direct proportion to the degree of injury in the postcountershock period. (This proportional binding does not occur when myocardial injury is secondary to coronary artery occlusion [5,6,22].) We also investigated the quantitative relationship between myocardial damage and the countershock dose by weight, expressed as joules (j) per kg body weight.…”

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confidence: 99%

Myocardial damage following transthoracic direct current countershock in newborn piglets

Gaba

Talner

1982

Pediatr Cardiol

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The effect of transthoracic direct current countershock on the myocardium of 21 newborn piglets was studied. Myocardial damage was quantified by measuring the myocardial uptake of technetium-99m pyrophosphate injected 24 hours after countershock. Substantial myocardial damage occurred in animals given greater than 150 joules/kg but not at lower energy doses. Damage occurred in both ventricular free walls, but more frequently in the right ventricle. The epicardial half of the myocardium was more severely affected than the endocardial half. The relationship between myocardial damage and total countershock energy dose was well modeled by an exponential function. Transthoracic direct current countershock appears unlikely to cause myocardial damage in newborn piglets unless greatly elevated energy doses are employed.

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Myocsrdial uptake of technetium-99m stannous pyrophosphate following direct current transthoracic countershock.

Cited by 78 publications

References 20 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

Automatic implantable cardioverter/defibrillator discharges and acute myocardial injury.

Myocardial damage following transthoracic direct current countershock in newborn piglets

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