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Concentrations of phosphoribosyl pyrophosphate (PP-ribose-P) in mouse liver were studied as a function of time of day and following injection of a number of metabolites and drugs. A twofold diurnal variation in liver PP-ribose-P concentration was observed. Liver PP-ribose-P concentrations were elevated following injection of glucagon, insulin, epinephrine, and ethylaminothiasiazole.
Two patients with carcinoma of the lung were studied with 99mTc-stannous pyrophosphate. Resolution of scintigraphic activity was observed postoperatively in one patient, while the second patient showed an asymmetric pattern of radionuclide uptake and radiographic changes as well as clinical findings of hypertrophic pulmonary osteoarthropathy.
99mTc-pyrophosphate was seen to be localized in the soft tissue in a patient with biopsy-proved polymyositis. Possible mechanisms of localization of 99mTc-phosphate complexes in bone and soft tissues are reviewed.
A "false-positive" 99mTc-stannous pyrophosphate (99mTc-PYP) myocardial image was seen in a patient with epidermoid carcinoma of the lung. The location of the increased activity corresponded to an area of direct invasion of the heart by carcinoma with associated multiple microscopic foci of myocardial necrosis. Metastatic carcinoma with myocardial necrosis should therefore be considered as a possible cause of a positive 99mTc-PYP myocardial image.
Of 70 consecutive cancer patients referred from radiotherapy for bone scans, 32% showed cardiac uptake of 99mTc-(Sn)-pyrophosphate; only 9% of a control group showed this uptake. Of those with prior left hemithorax irradiation, 60% showed cardiac uptake; only 12% of those with irradiation elsewhere showed this phenomenon (p less than .01). The patients who had no increased uptake tended to have shorter irradiation-to-scan time intervals (less than 10 months) than those who did show increased uptake (mean of 22 months).
Patients imaged with 99mTc pyrophosphate for myocardial infarction between October 1975 and March 1976 were reviewed. There were 103 patients and 114 images obtained. The clinical criteria of either or electrocardiographic changes were used to validate a myocardial infarct. We experienced 92.4% true negatives, 68.7% true positives, 7.5% false positives and 31.3% false negatives. It technically compromised scans were exclude (those with blood-pool activity, overlying costal cartilage), the false-negative rate was 15.4%. These data show that the presence of a negative phosphate scan does not rule out the possibility of a recent small, less than 2.5-cm subendocardial myocardial infarction.
In 3 patients, each of whom had previously had part of one kidney included within the field during radiation therapy, whole-body bone imaging using 99mTc-pyrophosphate showed increased activity in the irradiated renal segment. Possible mechanisms of such renal uptake are discussed.
Extensive mucosal small-bowel infarction was produced in 8 dogs by occluding the cranial mesenteric artery. After one hour of reperfusion, 15 mCi (555 MBq) of 99mTc-pyrophosphate was intra-arterially injected into 4 dogs and venously into the other 4. Positive images were obtained in all dogs except 1 which had received an intravenous injection. Diagnostic images were obtained consistently as early as 15 minutes after injection, and the infarcted bowel could still be visualized two hours later. The average tracer content in infarcted small bowel was 0.015% I.D./g. This was about eight times the uptake found in normal dogs. The results show that experimental small-bowel infarction can be detected as early as five hours after the onset of ischemia.
PURPOSE: To investigate the occurrence of calcification around the triangular fibrocartilage complex in calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. MATERIALS AND METHODS: The radiographs of 316 wrists in 181 patients with a definite or probable diagnosis of CPPD disease were reviewed to determine the occurrence of calcification in the inferior radioulnar joint cartilage, triangular fibrocartilage, lunotriquetral ligament, lunotriquetral cartilage, and triquetral cartilage. RESULTS: The distribution of calcification in the 316 wrists was as follows: inferior radioulnar joint cartilage, 87 wrists (28%), triangular fibrocartilage, 233 (74%); lunotriquetral ligament, 244 (77%); lunotriquetral cartilage, 167 (53%); and triquetral cartilage, 66 (21%). Forty-nine wrists had calcification in the lunotriquetral ligament or cartilage but not in the triangular fibrocartilage; 30 wrists had calcification in the triangular fibrocartilage but not in the lunotriquetral ligament or cartilage. This difference in prevalence was statistically significant (P = .0429). CONCLUSION: Radiologic diagnosis of CPPD crystal deposition disease in the wrist necessitates careful evaluation of the lunotriquetral ligament as well as the triangular fibrocartilage.
Inorganic pyrophosphate (PP(i)) regulates certain intracellular functions and extracellular crystal deposition. PP(i) is produced, degraded, and transported by specialized mechanisms. Moreover, dysregulated cellular PP(i) production, degradation, and transport all have been associated with disease, and PP(i) appears to directly mediate specific disease manifestations. In addition, natural and synthetic analogs of PP(i) are in use or currently under evaluation as prophylactic agents or therapies for disease. This review summarizes recent developments in the understanding of how PP(i) is made and disposed of by cells and assesses the body of evidence for potentially significant physiological functions of intracellular PP(i) in higher organisms. Major topics addressed are recent lines of molecular evidence that directly link decreased and increased extracellular PP(i) levels with diseases in which connective tissue matrix calcification is disordered. To illustrate in depth the effects of disordered PP(i) metabolism, this review weighs the roles in matrix calcification of the transmembrane protein ANK, which regulates intracellular to extracellular movement of PP(i), and the PP(i)-generating phosphodiesterase nucleotide pyrophosphatase family isoenzyme plasma cell membrane glycoprotein-1 (PC-1).
Technetium-99m stannous pyrophosphate (Tc-PYP) cardiac scintiphotos were performed on 101 of 221 patients admitted to the Coronary Care Unit to rule out acute myocardial infarction (AMI). Criteria were defined for the diagnosis of AMI, variant angina and unstable angina. 42 patients were diagnosed as having had an AMI. 22 patients had transmural and 20 patients had nontransmural AMI. 40 of the 42 patients with AMI (95%) had positive scintophotos; 2 (5%) had negative scintiphotos. 59 patients did not have an AMI; (97%) had negative scintiphotos. Four of these 59 patients had variant angina; all had negative scintiphotos. Seven of these 59 patients had unstable angina; 2 had positive scintiphotos. Tc-PYP scintiphotos have high sensitivity and specificity and are accurate in correctly classifying patients as having or not having AMI.
Enamel slabs and thin sections with artificially formed caries lesions were placed in the removable dentures of 15 subjects who brushed them three times daily for 2 weeks with a 1.3% pyrophosphate/1,100 ppm F/1.5% Gantrez dentifrice, a 1,100-ppm F dentifrice without pyrophosphate or Gantrez, or a placebo dentifrice in a double-blind, crossover study. Analysis of the thin sections by quantitative microradiography showed that the pyrophosphate/F dentifrice remineralized the lesions 15.9% (p less than 0.05) and the fluoride dentifrice 11.2%, whereas the placebo produced 4.4% demineralization. Fluoride uptake by the enamel slabs was similar for both fluoride dentifrices and significantly greater from the placebo dentifrice (p less than 0.05). The findings suggest that the anticaries mechanisms of fluoride include not only the prevention of demineralization, but also the promotion of remineralization.
Between October 1988 and March 1990, 173 urinary stone patients (average age 38.3 years) were evaluated metabolically, especially with regard to urinary magnesium, pyrophosphate (Ppi) citrate and glycosaminoglycans (GAG). 25 healthy subjects served as controls. Inhibitory deficiency was found to be the most frequent causal factor in our series, with an incidence of 48.7% in first-time stone formers and 51.08% in recurrent urolithiasis (p less than 0.1). Deficient citrate levels were present in 46.56%, hypomagnesiuria in 24.4%, hypopyrophosphaturia in 10.7% and deficient GAG in 2.7% of the patients. Deficient urinary Ppi was seen in only 2.7% of the stone formers as the only metabolic defect, while deficient GAG was never the only causal factor. All 4 inhibitors showed no correlation with age, sex, activity of stone disease, stone weight and burden. There were no statistically significant differences with controls. We think that routine metabolic evaluation must be performed both in recurrent patients and first-time stone formers and must include urinary citrate and Mg determinations in every case. Urinary Ppi should be determined in selected cases and GAG determinations are irrational.
Eighty-eight patients admitted to a coronary care unit with chest pain of varying etiology but without ECG evidence of an acute transmural myocardial infarction had myocardial scintigrams using technetium-99m stannour pyrophosphate (99m-Tc-PYP). Seventeen of these patients had ECG and enzymatic evidence suggestive of acute subendocardial myocardial infarction. In each of these the scintigrams were postivie demonstrating increased 99m-Tc-PYP uptake either in a faintly but diffusely positive pattern or in a well-localized strongly positive one. The remaining 71 patients did not evolve ECG or enzymatic evidence of acute myocardial infarction. In each of these patients the myocardial scintigram was negative. Thus 99m-Tc-PYP myocardial scintigrams are capable of identifying the presence of acute subendocardial myocardial infarction in patients. The absolute frequency with shich subendocardial myocardial infarction can be recognized utilizing this technique will have to be established in a larger number of patients in the future.
To obtain insight into the mechanism(s) responsible for the direct visualization of acute myocardial infarcts by myocardial scintigraphy with technetium-99m stannous pyrophosphate (99mTc-PYP), scintigraphic and morphologic studies were performed in 22 dogs subjected to occlusion of the proximal left anterior descending coronary artery (LAD). Grossly visible myocardial infarcts occurred in ten of 11 dogs with LAD occlusion for one day, five with LAD occlusion for two days, two with LAD occlusion for seven days and two with LAD occlusion for 13 days. Rare, microscopic foci of necrosis were observed in one dog with LAD occlusion for one day, and no lesions were present in two dogs subjected to temporary LAD occlusion for eight minutes and reflow for 24 hours. In the latter three dogs, 99mTc-PYP myocardial scintigrams were negative. In the 19 dogs with gross infarcts, 99mTc-PYP myocardial scintigrams were strongly positive at one and two days after LAD occlusion, much less positive at seven days and faintly positive at 13 days after occlusion. Positive myocardial scintigrams in most showed "doughnut" patterns, with marked peripheral concentration of radioactivity around central zones of much lower activity. On histologic examination, the one and two-day-old infarcts exhibited subendocardially located central zones and surrounding peripheral zones, both of which showed distinctive histopathological and histochemical features, including the selective occurrence in the peripheral zones of calcified muscle cells with ultrastructurally demonstrable apatite-like crystals in mitochondria. Selective occurrence of high tissue levels of 99mTc-PYP radioactivity also was demonstrated in the peripheral zones of four infarcts. Hearts with older infarcts (seven and 13 days) showed progressive replacement of necrotic myocardium by granulation tissue and progressive reduction in calcium deposits in the areas of damage. The data obtained in this study establish a temporal and topographical relationship between calcium accumulation in acute myocardial infarcts and 99mTc-PYP uptake responsible for scintigraphic detection of the lesions with this radionuclide in dogs subjected to proximal LAD occlusion.
We 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 hours after infarction and 75 to 90 min following the intravenous injection of 15 mCi of Technetium 99m pyrophosphate (Tc-PYP). Images were computer enhanced and area was calibrated with a radioactive grid source of known dimensions. Image radioactivity was normalized for decay and dose corrected for body weight. Animals were sacrificed two hours following the injection Tc-PYP. Postmortem images were also computer enhanced and calibrated. Gross infarct area and weight were estimated and transmural biopsies were evaluated for Tc-PYP activity and analyzed for creatine phosphokinase (CPK) content. Contiguous biopsies were pathologically analyzed and graded. There was a negative correlation between tissue Tc-PYP activity and CPK content (r=0.89). Pathologic severity worsened with increased Tc-PYP activity and diminished CPK content. There was a good correlation between gross infarct area and image infarct area, both in vivo (r
The dual radionuclide myocardial distributions of imaging agents potassium-43 (43K) and technetium-99m stannous pyrophosphate (99mTc-PYP) were studied in a 24-hour closed chest canine infarct preparation. In multiple myocardial biopsies in 20 dogs, tissue levels of both radionuclides were compared to either an index of tissue viability (myocardial creatine phosphokinase [CPK] depletion), or to estimates of regional myocardial blood flow as measured by the microsphere technique. Myocardial 43K uptake in the ischemic and infarcted zone correlated well with both CPK depletion (r = 0.73) and microsphere estimates of relative blood flow. The correlation with microspheres was excellent in the transmural sample (r = 0.93) as well as endocardial (r = 0.97) and epicardial (r = 0.86) portions. On the other hand, 99mTc-PYP myocardial uptake did not correlate with the extent of CPK depletion. Maximal uptake was frequently noted in border zones with only moderate CPK depletion, while lesser degrees of 99mTc-PYP uptake were noted in the central infarct zone where CPK activity was lowest. The relationship of 99mTc-PYP uptake to microsphere regional flow estimates demonstrated that 99mTc-PYP uptake was maximal at flows of 0.3 to 0.4 of normal. At lower flows, 99mTc-PYP uptake fell toward normal levels. A similar relationship was noted between the distributions of 99mTc-PYP and 43K. In relatively high flow border segments (larger than or equal to 0.80 of normal), abnormal 99mTc-PYP uptake of five to six times normal persisted. The transmural distribution of 99mTc-PYP demonstrated that in low flow regions 99mTc-PYP uptake was primarily epicardial, while in the higher flow ischemic periphery of the infarct endocardial uptake predominated. Thus, while there is a direct correlation between cationic 43K myocardial uptake and regional myocardial viability and blood flow, no such direct relationship exists for 99mTc-PYP. This is in part based on the necessity for delivery of the radioactive tracer to the infarct zone.
To further explore the usefulness of technetium 99m pyrophosphate (99mTc-PYP) myocardial imaging and test its validity in the diagnosis of acute myocardial infarction, 99mTc-PYP myocardial scintigrams were performed in 50 patients. Out of 28 patients with acute myocardial infarction, myocardial scintigrams demonstrated localized activity in the 15 patients with transmural, and diffuse activity in the 13 patients with subendocardial myocardial infarction. Twenty-two patients with significant coronary artery disease documented by coronary angiography but without acute myocardial infarction were also studied. Nine of ten patients with clinical evidence of left ventricular aneurysm from previous myocardial infarction and definite left ventricular dyskinesis had positive scintigrams with activity localized to the site of the wall motion abnormality. Two of five patients without definite aneurysm but with left ventricular akinesis also had localized uptake in the involved area of the left ventricle. Seven patients with normal left ventricular wall motion had negative scintigrams. These findings suggest caution in interpreting positive 99mTc-PYP scintigrams as being indicative of acute myocardial infarction when evidence of a left ventricular aneurysm is also present.