Uptake Of Technetium-99m Pyrophosphate Research Articles

Non-cardiac uptake of technetium-99m pyrophosphate in transthyretin cardiac amyloidosis

BackgroundTechnetium-based bone scintigraphy is rapidly becoming the most common non-invasive imaging tool in the diagnosis of Transthyretin cardiac amyloidosis (ATTR). Skeletal muscle uptake has been described with technetium-99m-3,3-diphosphono-1,2-propanodicarboxylic acid (TcDPD), and may account for masking of bony uptake. We sought to investigate skeletal muscle uptake of technetium-99m-pyrophosphate (TcPYP) in patients with ATTR. Methods and ResultsThis was a retrospective analysis of 57 patients diagnosed with ATTR who underwent TcPYP scintigraphy. Cardiac uptake was assessed on whole-body planar imaging using a semiquantitative scale (grades 0 to 3) and on single-photon emission computed tomography (SPECT) with CT attenuation correction using total myocardial counts per voxel after a 3-hour incubation. Skeletal muscle (psoas and biceps), vertebral body, LV myocardium, and blood pool mean counts were calculated. In the cohort (age 78 ± 9 years, 77% male, and 30% hereditary ATTR), there was no visualized tracer uptake in skeletal muscle or soft tissue on qualitative SPECT assessment. Total and blood pool-corrected uptake in the muscle groups were significantly less than myocardium and bone (P < 0.001). Blood pool-corrected muscle uptake was not associated with semiquantitative grade 3 vs 2 uptake (psoas P = 0.66, biceps P = 0.13) or presence of hereditary ATTR (psoas P = 0.43, biceps P = 0.69). As bony uptake decreased, there was no corresponding increase in skeletal muscle uptake. ConclusionsIn patients with ATTR cardiac amyloidosis, skeletal muscle uptake of TcPYP is minimal when assessed by qualitative and quantitative metrics, and is not significantly different in patients with grade 2 vs 3 semiquantitative uptake. The properties of this tracer may be different than TcDPD with respect to non-cardiac uptake.

Regional Variation in Technetium Pyrophosphate Uptake in Transthyretin Cardiac Amyloidosis and Impact on Mortality

ObjectivesThis study sought to investigate the regional uptake of technetium 99m-pyrophosphate (TcPYP) in transthyretin cardiac amyloidosis (ATTR) and its association with mortality. BackgroundTcPYP nuclear scintigraphy is a diagnostic and prognostic tool in ATTR. Echocardiography has identified a pattern of regional variation in longitudinal strain (LS) with a gradient of improved strain from base to apex in ATTR. MethodsConsecutive patients with ATTR were evaluated who underwent TcPYP nuclear scintigraphy with planar and attenuation corrected single-photon emission computed tomography (SPECT). Heart-to-contralateral lung (H/CL) ratio was calculated on planar images, and left ventricular (LV) uptake was determined in each of the 17 segments using SPECT. A measure of apical-sparing of myocardial TcPYP uptake, termed the apical-sparing ratio (ASR), was calculated as basal + mid / apical counts. ResultsOverall, 54 patients with ATTR (age 78 ± 9 years, 76% male, 31% hereditary ATTR) were analyzed. There was increased TcPYP uptake in basal and mid relative to apical LV segments, and an apical-sparing LS pattern on echocardiography. The right ventricle similarly showed greater uptake in basal segments. There were 26 deaths over 1.8 years median follow-up. The ASR of TcPYP uptake was associated with age-adjusted all-cause mortality (p = 0.013) with worse prognosis seen at levels <2.75. Global LS was also prognostic (p = 0.01), whereas H/CL ratio and total LV uptake indexed to blood pool were not (p = 0.772 and p = 0.850, respectively). The prognostic utility of the ASR persisted in multivariable modeling (p = 0.003), whereas global LS did not. ConclusionsThere is decreased TcPYP uptake in apical as compared to mid and basal segments in the LV, mimicking apical-sparing LS seen on echocardiography. Regional distribution of LV TcPYP uptake is associated with mortality, whereas overall amount of uptake as measured by H/CL ratio and indexed LV SPECT uptake is not.

Technetium pyrophosphate uptake in transthyretin cardiac amyloidosis: Associations with echocardiographic disease severity and outcomes

BackgroundQuantitative uptake of Technetium 99 m-pyrophosphate (TcPYP) is sensitive and specific for diagnosing transthyretin cardiac amyloidosis (ATTR). We sought to examine the association between TcPYP uptake intensity and echocardiographic measures of disease severity and clinical outcomes. Methods and ResultsA retrospective analysis was performed of 75 patients who underwent TcPYP scintigraphy. Planar images were evaluated semiquantitatively and using heart-to-contralateral lung (H/CL) ratio. The associations between H/CL ratio and echocardiographic parameters and outcomes were evaluated using linear regression and Cox models, respectively. There were 48 patients diagnosed with ATTR with mean H/CL ratio 1.58 ± 0.22 (vs 1.08 ± 0.09 if semiquantitative score = 0). The H/CL ratio was not associated with any measured echocardiographic parameter. Both semiquantitative uptake grade and H/CL ratio were associated with all-cause mortality (P = 0.009 and 0.007, respectively) and all-cause mortality or heart failure hospitalization (P = 0.001 and 0.020, respectively); however, neither were associated with outcomes when limited to patients with confirmed ATTR (P = 0.18 and 0.465, respectively). ConclusionIn patients with suspected ATTR, quantitative and semiquantitative uptake intensity of TcPYP is associated with all-cause mortality as well as all-cause mortality or heart failure hospitalization. However, in those with confirmed ATTR, there is no association with echocardiographic disease severity or outcomes.

PROGNOSTIC VALUE OF TECHNETIUM PYROPHOSPHATE UPTAKE INTENSITY BY NUCLEAR SCINTIGRAPHY IN TRANSTHYRETIN AMYLOIDOSIS

In transthyretin cardiac amyloidosis (ATTR), nuclear scintigraphy using Technetium 99m-pyrophosphate (TcPYP) manifests as diffuse myocardial uptake and is sensitive and specific for this diagnosis. We examined the prognostic ability of TcPYP uptake intensity and its relationship with

The 1995 Lindberg Award

Joule heating has long been considered the principal component of tissue damage in electrical injury. Recent studies suggest electroporation, a nonthermally mediated mechanism of cell membrane damage, is also a factor. We investigated whether electroporation-mediated muscle necrosis can occur in vivo without significant Joule heating. Pulsed electric fields approximately 150 V/cm were produced in the hind limbs of anesthetized rats. In shocked limbs core muscle temperature rose less than 1.8 degrees C, yet significant damage occurred as determined by technetium-99m pyrophosphate uptake, elevated serum creatine phosphokinase, and prominent hypercontraction band degeneration of myofibers on histopathologic examination. This study is significant because it directly addresses whether nonthermal mechanisms of cell damage can cause tissue necrosis. These results indicate that electroporation effects can mediate skeletal muscle necrosis without visible thermal changes. Thus the phenomenon of "progressive recognition" may be characteristically largely explained by the occurrence of nonthermally mediated tissue damage.

Indium-111 myosin-specific antibodies and technetium-99m pyrophosphate in the detection of acute cardiac rejection of transplanted hearts: studies in a heterotopic rat heart model

111In-labelled myosin-specific antibodies were evaluated as an indicator of early changes in acute rejection in a rat heart heterotopic transplant model. Uptake of antibodies was measured in allograft and isograft hearts of animals undergoing different regimens of cyclosporine treatment and compared with the uptake of technetium-99m pyrophosphate. The data were correlated with histological estimation of the severity of myocyte necrosis and signs of early rejection (venous cuffing and endocardial inflammation, indicators of perivascular infiltrate and intermyocyte extension, respectively). Myocyte necrosis in transplanted hearts was reflected by increases in technetium-99m pyrophosphate accumulation (r = 0.88) but was poorly correlated with labelled antibody uptake (r = 0.58). There was no positive correlation between the degree of early cardiac rejection and uptake of either of the radiopharmaceuticals: accumulation of the labelled antibodies paradoxically declined with increased histological severity scores, whereas that of technetium-99m pyrophosphate remained unchanged. Cyclosporine treatment augmented the uptake of labelled antibodies in transplanted hearts. This may be due to alterations in plasma membrane permeability brought about by the drug, resulting in a rise in antibody binding to intracellular myosin.

The scoring system for early technetium-99m pyrophosphate scintigraphy as a method of evaluation of limiting the myocardial infarct size by thrombolysis.

The usefulness of a scoring system with early technetium-99m pyrophosphate scintigraphy as a method for evaluating the efficacy of myocardial preservation after thrombolysis was studied. The mean time from the onset of acute myocardial infarction to injection of the tracer was 5.6 +/- 1.5 h (range 2.8 to 11.9 h). All 36 patients underwent successful recanalization. Patients with strongly positive technetium-99m pyrophosphate uptake in anterior acute myocardial infarction had a significantly lower regional ejection fraction and a significantly larger thallium-201 defect score than those with 2+ positive results in chronic stage. Similarly, in inferior acute myocardial infarction, the thallium-201 defect score was significantly larger in patients with strongly positive uptake than in those with 2+ and negative uptake scores. In conclusion, strongly positive results in early technetium-99m pyrophosphate scintigraphy within 12h after the onset of acute myocardial infarction may indicate failure in limiting the infarct size by coronary thrombolysis.

Exacerbation of doxorubicin cardiotoxicity by digoxin administration in an experimental rabbit model

The relationship between digoxin administration and the development of doxorubicin cardiomyopathy was evaluated in a chronic experimental rabbit model. We graded the myocardial pathology by conventional light microscopic histologic techniques. Additionally, myocardial fibrosis was quantified by hydroxyproline determinations and myocardial cellular damage by technetium-99m pyrophosphate uptake. Twenty-four rabbits were studied: 6 control, 6 doxorubicin-treated, and 12 digoxin-doxorubicin-treated. Mortality in the digoxin-doxorubicin group was 50%. All other rabbits lived throughout the entire experiment. The severest grades of histologic lesions were seen only in the digoxin-doxorubicin group. Myocardial hydroxyproline content was greater (p less than 0.05) in the digoxin-doxorubicin group than in the doxorubicin or control groups. Myocardial technetium-99m pyrophosphate content was also significantly greater (p less than 0.05) in the digoxin-doxorubicin group than in controls. In conclusion, the pretreatment and continued administration of digoxin, together with doxorubicin, increased the severity of myocardial damage and reduced longevity in this experimental model of doxorubicin cardiotoxicity.

Replication of the Compartment Syndrome in a Canine Model: Experimental Evaluation of Treatment

The sequence of acute ischemia, reperfusion, and elevated tissue pressure, with subsequent neuromuscular damage, results in the clinical entity known as the compartment syndrome. We have developed a canine hindlimb model that successfully replicates these clinical features. Surgical devascularization of both hindlimbs at the popliteal level isolates perfusion to a single vascular pedicle. Total ischemia is produced in the left limb for 8 h, while the right limb serves as a surgical control. Ischemia is confirmed by measurement of transfascial oxygen tension (TF-PO2) as well as lactate and blood gases in the venous effluent. Pressure in the anterior compartment of the hindlimb is monitored by the slit catheter technique. After reperfusion, muscle damage is assessed by histology, creatine phosphokinase (CPK), and uptake of technetium-99m pyrophosphate (Tc-PyP), expressed as a ratio of the experimental (L) limb to the control (R) limb (L/R ratio). Muscle necrosis was greatest in untreated controls; the L/R ratio was 8.9 +/- 5.0. Significant diminution of muscle necrosis was achieved by fasciotomy prior to reperfusion (2.6 +/- 0.8), mannitol (1.8 +/- 0.6), albumin-conjugated superoxide dismutase (SOD) 2.8 +/- 0.8), native SOD (2.3 +/- 1.0), fasciotomy combined with SOD (1.9 +/- 0.7), and continuous heparin (1.6 +/- 0.4) (p less than .01 vs controls). When fasciotomy was delayed until 2 h after reperfusion, there was no significant decrease in the L/R ratio (5.4 +/- 1.5; p = .15). Early fasciotomy following prolonged severe limb ischemia remains the treatment of choice, although these results suggest an emerging role for nonsurgical therapies as well. A summary of work done with this model as well as a review of other techniques is presented, along with a discussion of the pathophysiology of the compartment syndrome.

Rate of reperfusion blood flow modulates reperfusion injury in skeletal muscle

The mechanisms of ischemia-reperfusion (I-R) injury in skeletal muscle remain controversial. We investigated the effect of the rate of reperfusion blood flow on I-R injury in an isolated in vivo canine gracilis muscle model in six anesthetized dogs. In all animals, both gracilis muscles were subjected to 6 hr of ischemia followed by 1 hr of reperfusion. During reperfusion, one gracilis artery was partially occluded to limit the rate of reperfusion blood flow to its preischemic rate (limited reperfusion, LR), while the contralateral artery was allowed to perfuse freely at a normal rate (normal reperfusion, NR). Muscle injury was quantified by histochemical staining (triphenyltetrazolium chloride, TTC) with computerized planimetry of the infarct size, and by spectrophotometric determination of technetium-99m pyrophosphate uptake. Endothelial permeability was quantified by measurement of gracilis muscle weight gain and 125I-albumin radioactivity after intravenous injection. Results are presented as the means ±SEM, and differences are considered to be statistically significant if P < 0.05 by Student's t test for paired data. LR resulted in significantly less blood flow (9.7 ± 1.7 cc/min/100 g) when compared to NR (55.7 ± 11.6 cc/min/100 g). I-R injury was significantly reduced by LR as evidenced by a decrease in TTC infarct size from 41 ± 7% to 11 ± 5%, and a decrease in technetium-99m pyrophosphate uptake from 512 ± 20 to 163 ± 44 × 10 3 counts/min/g. LR also significantly decreased the postreperfusion edema formation as evidenced by a reduction in the muscle weight gain from 27 ± 6 to 9 ± 1 g, and a reduction in the 125I-albumin radioactivity from 45 ± 14 to 32 ± 8 counts/min/g. These data suggest that the hyperemic rate of reperfusion blood flow is a significant factor in the pathophysiology of postreperfusion edema and that clinical control of reperfusion injury in skeletal muscle may be achieved by limiting the rate of reperfusion blood flow.

Experimental animal models of viral myocarditis

Animal models of congestive heart failure and dilated cardiomyopathy following encephalomyocarditis (EMC) virus infection have been developed. Differences were found between different strains of mice in the frequency of occurrence and severity of myocarditis, and even in the character of the pathological lesions. Genetic factors may play an important role in pathogenesis. Right ventricular aneurysm and arrhythmias were seen in these models. Viral myocarditis may play a pathogenetic role in right ventricular dysplasia. Auto-antibodies against heart developed and the distribution of cardiac myosin isoenzymes was altered during the course of myocarditis. Myocardial uptake of technetium-99m pyrophosphate and changes in NMR relaxation parameters have been studied in these models. Virus vaccine, passive immunization, recombinant interferon α A/D and ribavirin protected mice from developing myocarditis. Immunosuppressive agents such as prednisolone and cyclosporinwere studied, but had no beneficial effect on these models. An animal model of perimyocarditis induced by coxsackie virus B3 is also described. Because the myocardial lesions are severe and occur frequently, our animal models are considered suitable for studying pathogenetic mechanisms and for the evaluation of diagnostic methods and prevention and therapeutic interventions of viral myocarditis.

Comparison of early myocardial technetium-99m pyrophosphate uptake to early peaking of creatine kinase and creatine kinase-MB as indicators of early reperfusion in acute myocardial infarction

The value of technetium-99m pyrophosphate (Tc99m-PYP) scintigraphy as an indicator of reperlusion 2.8 to 8 hours after the onset of symptoms of acute myocardial infarction was compared with the value of early peak creatine kinase (CK) and CK-MB release within 16 hours after the onset of symptoms. In 29 patients who received thrombolytic therapy, recanalization was seen (group 1) and in 7 it was not (group 2). In 23 patients (79%) in group 1 scintigraphic findings were positive and in all 7 in group 2 they were negative. In 15 patients (52%) in group 1 and 1 patient (14%) in group 2, CK reached its peak level within 16 hours. In 20 patients (69%) in group 1 and 3 (43%) in group 2 the CK-MB level reached a peak within 16 hours. The sensitivity, specificity and predictive accuracy of positive results of early Tc-99m-PYP scintigraphy in predicting the reperfusion were 79%, 100% and 83%. These values are significantly higher than or similar to those of early peaking of CK and CK-MB release. In contrast to measurements of enzyme release, reperfusion data for Tc-99m-PYP scintigraphy are available immediately after thrombolytic therapy. Therefore, early Tc-99m-PYP scintigraphy (3 to 8 hours after onset of symptoms) is valuable as a noninvasive technique for early diagnosis of reperfusion.

Technetium-99m pyrophosphate imaging in acute renal failure associated with nontraumatic rhabdomyolysis.

Technetium-99m pyrophosphate (Tc-PYP) imaging was performed in five patients with acute renal failure associated with nontraumatic rhabdomyolysis. Four patients had phencyclidine intoxication and one had viral pneumonia. During the acute phase, marked uptake of pyrophosphate was seen in all patients in several muscle groups, but always in the thigh adductors. The results show that phencyclidine intoxication can result in diffuse muscle uptake of Tc-PYP without overt evidence of muscle injury. Tc-PYP imaging may provide a clue to the cause of acute renal failure in patients with suspected rhabdomyolysis in whom elevations of serum creatine phosphokinase concentrations are equivocal.

Measurement of myocardial infarction fraction using single photon emission computed tomography

Although infarct size correlates generally with prognosis after acute myocardial infarction, an absolute measure of infarct size may have differing prognostic significance depending on absolute left ventricular mass. To test the hypothesis that single photon emission computed tomography can accurately measure myocardial infarct size as a percent of total left ventricular mass ("infarction fraction"), thallium-201 and technetium-99m pyrophosphate tomograms were acquired in 21 dogs 24 to 48 hours after fixed occlusion of the left anterior descending or circumflex coronary artery. Pathologic infarct weight was measured as the myocardial mass that showed no staining with triphenyltetrazolium chloride. Scintigraphic infarct mass by technetium-99m pyrophosphate was calculated from the total number of left ventricular volume elements (voxels) demonstrating technetium-99m pyrophosphate uptake X voxel dimension [( 0.476 cm]3) X specific gravity of myocardium (1.05 g/cm3). Scintigraphic left ventricular mass was calculated in a similar fashion using an overlay of the thallium-201 and technetium-99m pyrophosphate scans. The "infarction fraction" was calculated as: infarction fraction = infarct mass/left ventricular mass. There was good correlation between single photon emission computed tomography and pathologic measurements of infarct mass (technetium-99m pyrophosphate mass = 1.01 X pathologic infarct mass + 0.96; r = 0.98), left ventricular mass (single photon emission computed tomographic left ventricular mass = 0.60 X pathologic left ventricular mass + 37.4; r = 0.86) and "infarction fraction" (single photon emission computed tomographic infarction fraction = 1.09 X pathologic infarction fraction - 1.7; r = 0.94).(ABSTRACT TRUNCATED AT 250 WORDS)

Postcountershock myocardial damage after pretreatment with adrenergic and calcium channel antagonists in halothane-anesthetized dogs.

Transthoracic electric countershock can cause necrotic myocardial lesions in humans as well as experimental animals. The authors investigated the effect on postcountershock myocardial damage of pretreatment with prazosin (0.1 mg/kg), an alpha-1 antagonist; L-metoprolol (0.5 mg/kg), a beta-1 antagonist, and verapamil (0.5 mg/kg), a calcium channel-blocking agent. Twenty dogs were anesthetized with halothane and given two transthoracic countershocks of 295 delivered joules each after drug or vehicle treatment. Myocardial injury was quantitated 24 h following countershock by measuring the uptake of technetium-99m pyrophosphate in the myocardium. Elevated technetium-99m pyrophosphate uptake occurred in visible lesions in most dogs regardless of drug treatment. For each of four parameters of myocardial damage there was no statistically significant difference between control animals and those treated with prazosin, metoprolol, or verapamil. These data suggest that adrenergic or calcium channel-mediated mechanisms are not involved in the pathogenesis of postcountershock myocardial damage.

Effect of coronary artery recanalizatiori on right ventricular function in patients with acute myocardial infarction

The effects of coronary artery recanalization by intracoronary administration of streptokinase on left ventricular function during acute myocardial infarction have received increasing attention in recent years. Although myocardial dysfunction is often more pronounced in the right ventricle than in the left ventricle in patients with acute inferior wall myocardial infarction, the effect of coronary artery recanalization on right ventricular dysfunction has not been previously addressed. Accordingly, in this investigation, 54 patients who participated in a prospective, controlled, randomized trial of recanalization during acute myocardial infarction were studied. Among 30 patients with inferior wall infarction, 19 had right ventricular dysfunction on admission; 11 of these 19 had positive uptake of technetium-99m pyrophosphate in the right ventricle, indicative of right ventricular infarction. Patients with successful recanalization (n = 6) exhibited improved right ventricular ejection fraction from admission to day 10 (26 +/- 7 to 39 +/- 14%, p less than 0.03). However, control patients (n = 6) and patients who did not undergo recanalization (n = 7) also exhibited improvement (20 +/- 7 to 29 +/- 11% [p less than 0.02] and 30 +/- 8 to 40 +/- 6% [p less than 0.03], respectively). Improvement in several other variables of right ventricular dysfunction evolved at an equal rate with the ejection fraction changes. Patients with or without right ventricular infarction improved similarly. These data indicate that the right ventricular dysfunction commonly associated with inferior wall infarction is often transient, and improvement is the rule, irrespective of early recanalization of the "infarct vessel."

Fatty acylcarnitine accumulation and membrane injury in ischemic canine myocardium

Although previous work has shown that long chain fatty acylcarnitine derivatives accumulate in ischemic canine myocardium, their role in the production of irreversible injury and associated sarcolemmal membrane injury is undefined. The present study examines the temporal and topographic relationship of the accumulation of long chain acylcarnitine with the uptake of technetium pyrophosphate and tissue calcium content during ligation of the left anterior descending coronary artery (LAD) in canine myocardium. After 60 minutes of fixed LAD ligation, there was no significant increase in long chain acylcarnitine content in the ischemic subendocardium compared with the corresponding nonischemic value. However, the ischemic subendocardium was irreversibly injured at this time, as assessed by a 4-fold increase in tissue calcium content and a 20-fold increase in technetium-99m pyrophosphate uptake after reperfusion. The ischemic subepicardium showed a 41% increase in long chain acylcarnitine content compared with the corresponding nonischemic subepicardium. However, the ischemic subepicardium contained only 50% of the calcium content and 10% of the technetium-99m pyrophosphate uptake found in the ischemic subendocardium. It is concluded that increases in fatty acylcarnitine can be dissociated from the development of irreversible ischemic injury during fixed LAD occlusion in ischemic canine myocardium.

Myocardial damage following transthoracic direct current countershock in newborn piglets.

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.

Detection of acute right ventricular infarction by right precordial electrocardiography

The value of 0.1 mV or greater of S-T segment elevation in at least one right precordial lead (V 4R to V 6R) in defining right ventricular myocardial infarction was assessed prospectively in 43 subjects (33 consecutive patients with enzymatically confirmed infarction of varying type and location, 4 patients with unstable angina and 6 healthy volunteers). Patients with acute myocardial infarction were studied with radionuclide ventriculography and technetium-99m stannous pyrophosphate myocardial scintigraphy 18.2 ± 14.3 (mean ± standard deviation) and 85.1 ± 18.0 hours after the onset of symptoms, respectively. Eleven patients (Group A: 9 patients with transmural inferior infarction, 1 with transmural inferolateral infarction and 1 with transmural anteroseptal infarction) demonstrated right precordial S-T segment elevation and 22 patients (Group B: 6 patients with transmural inferior infarction, 2 with transmural posterior infarction, 3 with transmural inferolateral infarction, 3 with transmural anteroseptal infarction, 3 with transmural extensive anterior infarction, 4 with subendocardial anterior infarction and 1 with unclassified infarction) did not. Right ventricular ejection fraction was significantly lower in Group A (0.47 ± 0.11) than in Group B (0.60 ± 0.12) (p < 0.01). Right ventricular total wall motion score was 63.8 ± 15.6 percent of normal in Group A versus 94.3 ± 8.5 percent in Group B (p < 0.001). Technetium-99m pyrophosphate uptake (2+ or greater) over the right ventricle occurred in nine patients (81.8 percent) in Group A and in one patient (4.5 percent) in Group B (p < 0.001). No patient with unstable angina and no healthy volunteer had S-T segment elevation in a right precordial lead. S-T segment elevation of 0.1 mV or greater in one or more of leads V 4R to V 6R is both highly sensitive (90 percent) and specific (91 percent) in identifying acute right ventricular infarction.

Technetium-99m pyrophosphate uptake in spontaneously occurring perimyocardial lesions in an inbred strain of DBA/2 mice.

The spontaneous occurrence of perimyocardial calcification localized in the right ventricle has been reported in an inbred strain of DBA/2 mice. In this paper we examined the correlation between the myocardial uptake ratio of technetium-99m pyrophosphate (99mTc-PYP) and pathological findings in these mice ranging in age from one to 12 months and became lower with age, while calcification and fibrosis in the perimyocardium of the right ventricle became more prominent in aged mice. This may be due to an insidious onset of degeneration with calcification and fibrosis in spontaneously occurring perimyocardial lesions in these mice. Persistent abnormal uptake of 99mTc-PYP observed in the present study suggests the usefulness of such scintigrams in the diagnosis of chronic perimyocardial disease.