Indium-111 Platelet Scintigraphy Research Articles

Evaluation of Thrombogenicity by Indium-111 Platelet Scintigraphy in Endografting for Abdominal Aortic Aneurysms

Obstruction of the endograft limb by thrombosis has often been reported and may cause fatal complications such as leg necrosis or myonephropathic metabolic syndrome. The purpose of this study was to evaluate endograft antithrombogenicity by indium-111 platelet scintigraphy. Seventeen patients with abdominal aortic aneurysms were treated by endografting. Thirteen patients were treated with conventional open surgery using an artificial graft. The endograft was constructed from a self-expanding Z-shaped stent and woven polyester fabric. Autologous platelets labeled with indium-111 were injected at 2 weeks postoperatively. At 24 hours and 72 hours postinjection, the ratio of scintillation count of the endograft or graft to that of the native artery was calculated to assess platelet deposition. The normalization ratio was calculated as follows: (scintillation count per pixel of endograft or graft/circumference)/(scintillation count per pixel of the native femoral artery). Platelet factor 4 and beta-thromboglobulin were measured to evaluate the systemic platelets activity at 2 weeks postoperatively. There was no significant difference in platelet counts or labeling efficiency between the groups. The ratio was significantly higher in the endografting group than in the open surgery group at 72 hours postinjection (2.5-0.7 vs 3.9-1.1, P<.001). There was no significant difference in platelet factor 4 and beta-thromboglobulin between the groups. Although there was no difference in systemic platelet activity, endografting was associated with lower antithrombogenicity. It remains unclear whether lower antithrombogenicity causes thromboembolism as a complication of the procedure. The authors recommend the administration of antiplatelet drugs to prevent endograft obstruction in patients with very narrow iliac arteries.

Indium-111 platelet scintigraphy in vascular disease.

Indium-111 labelled platelet scintigraphy permits simple, accurate evaluation of platelet kinetics and sites of deposition. The most meaningful results are obtained from serial scans, although these are clinically useful in only a few of the many applications that have been suggested, principally in studies of acute thrombosis, prosthetic graft thrombogenicity and antiplatelet medication. Key pitfalls are associated with selection of regions and patient variation.

Hybrid Small-Caliber Vascular Prosthesis for Coronary Artery Bypass Grafting: A Preliminary Study of Plasmin-Treated Fibrin-Coated Vascular Prosthesis

The potential use of plasmin-treated fibrin-coated vascular prosthesis (PF-V) for coronary artery bypass grafting (CABG) in animal models was investigated. PF-V grafts, 3 mm in internal diameter, were studied on 5 sheep in off-pump CABG model and on 18 rabbits in abdominal aortic bypass grafting (AABG) model. Patency, blood flow, angiography, Indium-111 platelet scintigraphy, and histology of the graft were evaluated. In the sheep CABG model, the PF-V grafts were patent for a range of 12 to 22 days without postoperative antiplatelet therapy. Graft flows ranged 58 to 90 ml/min until the day before graft occlusion by thrombus. In rabbit AABG model, the fibrin coating of the PF-V grafts was completely absorbed and replaced with neofibrin net between 7 and 14 days after implantation. Platelet depositions on the graft between 7 and 14 days after implantation were significantly higher than those at other periods (p < 0.05). The small-caliber PF-V graft in sheep CABG model had a good blood flow with high antithrombogenicity in acute phase, but occluded over 2 to 3 weeks without antiplatelet agents after implantation. The current problem of the PF-V graft was a thrombus formation at the time of the degradation of fibrin coating. Further improvements are needed.

Clinical assessment of vascular thrombosis using indium-111 platelet scintigraphy.

The authors reviewed the clinical value of platelet scintigraphy by using autologous platelets labeled with indium-111-oxine to detect thrombotic activity at vascular thrombosis sites. Thirty-nine patients with deep vein thrombosis, 28 with arteriosclerosis obliterans, and 10 with pulmonary embolism were the subjects of this study. Platelet accumulation on scintigrams had a tendency to correlate with aggravation of acute thrombotic symptoms in deep vein thrombosis and arteriosclerosis obliterans. In addition, appropriate thrombolytic and anticoagulant therapy resulted in reduced platelet accumulation in conjunction with improvement of acute symptoms. On the other hand, this type of scintigraphy was not so sensitive for assessment of pulmonary embolism. Platelet scintigraphy could facilitate the assessment of thrombotic activity and might be useful for determining the optimal indication of thrombolytic and anticoagulant therapy for acute vascular thrombosis.

Platelet aggregability and in vivo platelet deposition in patients with ischemic cerebrovascular disease - evaluation by indium-111-platelet scintigraphy -

In ischemic cerebrovascular disease, it is not clear whether platelet function in vitro actually reflects the situation in vivo. Using indium-111 platelet scintigraphy as a method for detecting platelet activation in vivo, we tried to elucidate this problem. Twenty eight patients with chronic stage of ischemic cerebrovascular disease (CVD) and 17 control subjects were examined. Platelet scintigrams were positive in 9 of 28 patients in CVD, while all were negative in control. A comparison of the results obtained from qualitative platelet imaging and platelet aggregability was performed to evaluate whether threshold aggregation concentration (TAC) grade differed across the three groups(control, CVD patients without platelet deposition and CVD patients with platelet deposition). CVD patients with platelet deposition showed a higher TAC than those patients who did not show platelet deposition (P < 0.05) or control subjects without platelet deposition (P < 0.05). These results suggest that some patients in chronic stages of CVD may have active platelet deposition on carotid atheromatous lesions, and presence of platelet deposition in vivo could contribute to reduce platelet reactivity in peripheral blood.

Diagnosis of left ventricular thrombi by magnetic resonance imaging and comparison with angiocardiography, computed tomography and echocardiography

Left ventricular (LV) thrombi are common in patients with acute and healed anterior myocardial infarction. Although the reported incidence of clinically diagnosed embolism varies widely, 1–3 diagnosis of thrombus seems to carry an increased risk for this potentially life-threatening complication. It is not entirely clear whether long-term anticoagulation can reduce the embolism rate in patients with chronic aneurysms with an acceptable risk of bleeding. However, it is widely assumed that this is so; thus, the diagnosis of LV thrombus has far-reaching consequences. It is difficult to diagnose LV thrombus using currently available imaging techniques. LV angiography carries the risk of precipitating systemic emboli and has a low sensitivity in most reported studies. 4 Echocardiography has been reported to be fraught with false-positive results. 5,6 Indium-111 platelet scintigraphy reflects thrombus activity but has suboptimal sensitivity, especially for small thrombi. 7 More recently, computed tomography (CT) 8 and magnetic resonance imaging (MRI) 9,10 have shown encouraging results in the detection of LV thrombi. However, the diagnostic accuracy of MRI has not been evaluated with independent confirmation by surgery or autopsy. This study describes the sensitivity and specificity of MRI in the diagnosis of LV thrombi in patients with LV aneurysms undergoing surgical aneurysmectomy, and compares the results with those of angiography, 2-dimensional echocardiography and CT performed in the same patients.

Early image acquisition after administration of indium-111 platelets in clinically suspected deep venous thrombosis

Indium-111 platelet scintigraphy accurately detects acute deep venous thrombosis in asymptomatic high-risk patients and may be used as a surveillance test. However, its value in symptomatic patients and its accuracy early after platelet injection are not satisfactorily established. The latter is important for timely institution of therapy. Accordingly, 65 patients (67 limbs) with suspected deep venous thrombosis (symptom duration 8 ± 10 days, mean ± standard deviation) were prospectively studied with platelet scintigraphy and contrast venography. Platelets were labeled with 405 ± 101 mCi indium-111 oxine. The labeling efficiency was 80 ± 10%. All images were acquired within 120 minutes after intravenous administration of the platelet suspension. Both platelet scintigraphy and venography were interpreted independently by 2 blinded observers (for each technique). Five separate analyses were performed. Each scintigraphic reader was compared to each venographic reader. A fifth analysis—consisting of readings with blinded agreement of both readings of the platelet scans and both readings of the venograms—was performed. Interobserver agreement was 92% for venography and 79% for scintigraphy. Excluding anticoagulated patients, the sensitivity of platelet scintigraphy was between 38 and 46% and the specificity was between 92 and 100%. Thus, early imaging of labeled platelets for the diagnosis of symptomatic deep venous thrombosis carries a high specificity but a much lower sensitivity. It is speculated that the tow sensitivity is related to the inactivity of the thrombus. This may suggest that early imaging will only be useful in patients whose symptoms are of recent onset.

Effect of low dose acetylsalicylic acid on the frequency and hematologic activity of left ventricular thrombus in anterior wall acute myocardial infarction

In this prospective, randomized, placebo-controlled trial the effect of 100 mg acetylsalicylic acid (ASA) once daily on the incidence, hematologic activity and embolic potential of left ventricular (LV) thrombosis was studied in 100 consecutive patients with a first anterior wall acute myocardial infarction (AMI). Patients were randomized to ASA or placebo <12 hours after onset of symptoms. Heparin, 5,000 IU subcutaneously twice daily, was given to all patients during immobilization. Echocardiography was performed <24 hours, 48 to 72 hours and 1, 2, and 12 weeks after AMI. LV thrombosis was detected by echocardiography in 30 (33%) of the 92 evaluable patients (15 patients given ASA and 15 given placebo). Indium-111 platelet scintigraphy was done in 17 of the 22 patients with an LV thrombus at the second week echocardiogram. Among 7 ASA-treated patients, 4 had positive images; among 10 placebo patients, 5 had positive images. LV thrombus resolution was noted in 3 of 9 patients with a positive scan and in 5 of 8 patients with a negative platelet scan. In 7 of 10 ASA-treated patients and 5 of 12 placebo-treated patients thrombus resolution was observed (difference not significant). Systemic embolism occurred in 2 patients, both given ASA, during the first week after AMI. Thus, low dose ASA has no effect on the incidence, hematologic activity and embolic potential of LV thrombosis in anterior wall AMI.

Indium-111 platelet scintigraphy in carotid disease

Indium-111 platelet scintigraphy in carotid disease

Indium-111 platelet scintigraphy in carotid disease.

Forty-five patients (35 men, 10 women) undergoing carotid surgery had Indium-111 platelet scintigraphy as part of their preoperative work-up. Imaging was performed within three hours after injection of the Indium-111. A second series of views was obtained 24 hours later and repeated at 24 hour intervals for two days. Of 54 scintigrams, 22 were positive and 32 negative. Positive results were defined as a twofold or more increase in local activity on a visualized carotid after 24 hours. The sensitivity of the method was 41%, intraoperatively, and the specificity, 100%. The low sensitivity places this method behind sonography and duplex-scanning for screening patients for surgery. We believe that indications for platelet scintigraphy are limited to: 1. Repeated transient ischemic attacks in the same territory with minimal lesions on arteriography and non-homogeneous plaque on duplex scan; 2. Symptomatic patients being treated medically as a possible argument for surgery; 3. Determining therapeutic policy for patients having experienced a transient ischemic attack with a coexisting intracardiac thrombus.

Assessment of warfarin therapy under full dose using indium-111 platelet scintigraphy in patients with intracardiac thrombi.

Twenty patients in whom intracardiac thrombi were detected by indium-111 platelet scintigraphy (the first platelet scintigraphy) were prospectively studied to examine the effect of warfarin therapy under full dose on the intracardiac thrombogenicity. Eleven patients (group I) who received 2-6 mg/day of warfarin and 9 patients (group II) who did not receive warfarin had the second platelet scintigraphies 14-71 days after the first platelet scintigraphies. In group I, 10 platelet scintigraphies became negative and one remained positive for intracardiac thrombi after administration of warfarin, while in group II 8 platelet scintigraphies remained positive and only one changed to negative. The incidence of negative image at the second platelet scintigraphy was significantly lower in group II than that in group I. In group I, the degree of accumulation of platelets onto the surface of the thrombus (%IE), showed significant reduction (0.69 +/- 0.48 to 0.11 +/- 0.21) after warfarin therapy, while in group II %IE at the second scintigraphy (1.07 +/- 1.03) were not significantly different from those at the first scintigraphy (1.13 +/- 0.79). These results indicated that warfarin therapy under full dose inhibited the deposition of platelets on the intracardiac thrombi and thrombogenicity in the patients with intracardiac thrombi which were detected by indium-111 platelet scintigraphy.

Indium-111 platelet scintigraphy and two-dimensional echocardiography for detection of left ventricular thrombus: Influence of clot size and age

Two-dimensional echocardiography and indium-111 platelet scintigraphy were performed on 50 dogs to determine the influence of clot age and size on the detection of experimentally induced left ventricular mural thrombus. Thrombus was induced by apical infarction and injection of a sclerosing agent and thrombin. The animals were classified into four groups according to the time of indium-111 platelet injection after thrombus induction: Group I (17 dogs, 1/2 hour after induction; 3 dogs, before induction), Group II (12 dogs, 24 hours after induction) and Group III (12 dogs, 1 week after induction). In Group IV (six control dogs) apical infarction was produced, but thrombin was not injected; indium-111 platelets were injected 1/2 to 1 hour after infarction. The dogs were studied by indium-111 platelet scintigraphy and by two-dimensional echocardiography 1/2 to 5 hours (Group I) and 1 to 5 and up to 72 hours (Groups II to IV) after platelet administration and before death was induced. Two-dimensional echocardiography showed the best overall sensitivity for detection of acute thrombus (97%; 29 of 30). The sensitivity of indium-111 platelet scintigraphy was 86% (18 of 21) for clots greater than or equal to 0.08 ml in size, and 67% (20 of 30) for detection of all clots. Thrombus did not form in 14 dogs of Groups I to III and in 6 of 6 control dogs. The specificity of scintigraphy was 100% (20 of 20) compared with 80% (16 of 20) for echocardiography. Echocardiography was more sensitive than scintigraphy for detecting very small clots in this experimental model.(ABSTRACT TRUNCATED AT 250 WORDS)

Identification of intracardiac thrombi in stroke patients with indium-111 platelet scintigraphy.

Platelet scintigraphy (PSC) with indium-111 labelled platelets has been confirmed as an adequate method for the detection of intracardiac thrombi in patients with heart disease. We performed PSC of the heart and the neck vessels in 27 stroke patients with suspected cardiac embolism and as control on 10 patients with atherosclerotic lesions of the carotid arteries without evidence of heart disease. The carotid PSC was positive in 6 of 10 patients with carotid disease, and twice in the 27 with suspected cardiac embolism. In these 27 the PSC of the heart indicated pathological conditions 13 times. Pathological platelet accumulations could be visualized in 3 cases in the atrial space, in 9 cases in the region of the left ventricle, and once at the aortic valve. Scintigraphy was negative in all 10 patients with atherosclerosis of the neck vessels. The two-dimensional echocardiography revealed pathological findings in 8 of the 13 patients with positive heart PSC (3 with intraventricular thrombi, 3 with valvular disease, 2 with decreased ventricular contractility) and was normal in the 10 control patients. Open-heart surgery was performed in 2 patients with pathological PSC and revealed an intracardiac thrombus. Three of 4 patients with positive atrial PSC showed mitral or aortic valve disease. These results suggest that PSC can provide a valuable method for detecting cardiac thrombi in stroke patients.

Thrombosis and embolism from cardiac chambers and infected valves

In a number of cardiac conditions (acute myocardial infarction, chronic left ventricular aneurysm, dilated cardiomyopathy, infective endocarditis and atrial fibrillation in the absence of valvular disease), the risk of embolism gives cause for concern. Although anticoagulation with warfarin (Coumadin)-derivatives has been shown to be effective in some of these situations, there is no evidence regarding the role of antiplatelet agents. The common factor in the thromboembolic potential of acute myocardial infarction, chronic left ventricular aneurysm and dilated cardiomyopathy is mural thrombus. This can be detected by two-dimensional echocardiography and indium-111 platelet scintigraphy. Although of value in elucidating the natural history of mural thrombus, in most cases, management is not substantially aided by these investigations. In patients with extensive myocardial infarction, particularly anterior infarction, moderate intensity anticoagulation started soon after hospital admission reduces the rate of embolism. After 8 to 12 weeks, embolic risk is low so that anticoagulants can usually be discontinued. Patients with chronic left ventricular aneurysm have a low incidence of embolism; anticoagulation is, therefore, inappropriate. Dilated cardiomyopathy is associated with a high risk of embolism; moderate intensity anticoagulation may be advisable in many such cases. Little information is available regarding the incidence of thromboembolism or the role of antithrombotic therapy in the patient with a diffusely dilated left ventricle due to ischemic heart disease. In native valve infective endocarditis, the risk of hemorrhage is high, and the efficacy of conventional anticoagulants unclear; thus, anticoagulation should not be instituted for the cardiac condition as such. However, in prosthetic valve endocarditis, the risk of embolism seems to be very high, and anticoagulant therapy should be continued, but with great care because there is a substantial risk of cerebral hemorrhage. Atrial fibrillation in patients with valvular heart disease is dealt with in a previous review. Patients with nonvalvular atrial fibrillation are at varying risk of embolism, depending on the etiology of the arrhythmia; trials of antithrombotic therapy are needed for the various subsets of patients. In most elderly patients, the etiology is not known, and their stroke risk is high. The risk of embolism in younger patients with idiopathic atrial fibrillation is so low as to make any antithrombotic therapy unnecessary.(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of aspirin and ticlopidine on platelet deposition in carotid atherosclerosis: assessment by indium-111 platelet scintigraphy.

The antiplatelet effects of aspirin and ticlopidine were studied by a dual-tracer method, using indium-111 labeled platelets and technetium-99m human serum albumin, in a group of 12 patients with suspected ischemic cerebrovascular disease. The magnitude of platelet accumulation at the carotid bifurcation was expressed as the ratio of radioactivity of indium-111 platelets deposited on the vascular wall to those circulating in the blood-pool (PAI, platelet accumulation index), 48 hr after injection of labeled platelets. PAI values were measured before (baseline studies) and after the antithrombotic therapies (aspirin studies: 325 mg bid for 22.3 +/- 1.3 days, ticlopidine studies: 100 mg tid for 21.8 +/- 2.1 days). At the baseline, the mean PAI value at 24 carotid bifurcations in the patient group was 15.7 +/- 15.3% (mean +/- S.D.) compared to -4.3 +/- 9.1 at 24 carotid bifurcations in 12 normal subjects (p less than 0.01). We defined the upper limit for a normal PAI (%) value to be +13.9, namely the mean PAI plus 2 SD for the carotid bifurcation in normal subjects and used this value for semiquantitative analysis. At the baseline, significant elevation of PAI (more than 13.9%; positive scintigram) was observed at 12 of 24 vessels, while 12 other regions were negative (less than 13.9%). In the lesions with positive scintigraphic results at the baseline, the mean PAI (%) value from the baseline, aspirin and ticlopidine studies was 29.5 +/- 7.0, 11.2 +/- 8.5 (p less than 0.01 versus baseline) and 21.4 +/- 21.3 (not significant from baseline), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Possibilities and pitfalls of indium-111 platelet scintigraphy in the monitoring of renal transplant recipients.

During the last four years, we have performed two studies on the clinical application of 111In-platelet scintigraphy after renal transplantation. In the first study, we collected 75 patients who were treated with prednisolone and azathioprine. The platelet deposition in the graft was expressed as a platelet-uptake index (PUI). The results suggested that the platelet scan was a valuable tool for early detection of acute graft rejection, which was indicated by an increase in PUI. Quite different results were obtained in 50 patients immunosuppressed with cyclosporin A (CSA) and prednisolone. Acute interstitial rejection escaped detection by this diagnostic procedure. Significant elevations of PUI were observed in acute vascular rejection and microvascular CSA nephrotoxicity, resembling the haemolytic uraemic syndrome (HUS) only. Therefore, platelet deposition in the graft can be regarded as a non-specific phenomenon, occurring in two entities which require completely different therapeutic approaches. In spite of the monitoring by means of the platelet scan, percutaneous biopsy is still necessary for differential diagnosis of graft dysfunction.

Detection of platelet deposition at the site of peripheral balloon angioplasty using indium-111 platelet scintigraphy

Restenosis after balloon angioplasty may be mediated through platelet deposition at the site of arterial dilatation. The purpose of this study was to determine whether platelet deposition at the site of dilatation could be detected using indium-111 platelet scintigraphy. Fifteen patients, aged 60 ± 9 years, with iliac or femoral (n = 12), renal artery (n = 2) or distal aortic (n = 1) stenoses were studied. All patients received intravenous heparin at the time of dilatation. Labeled platelets containing 471 ± 65 μCi indium-111 were injected 0.25 to 4 hours after dilatation and 1 to 24 hours after imaging. In 11 of 12 patients with iliac and femoral dilatations, focal uptake was demonstrated at the angioplasty site. In 4 patients (2 patients with renal, 1 patient with iliofemoral, and 1 with distal aortic stenoses), uptake at the dilatation sites was not detected. This preliminary study indicates that despite intravenous heparin, platelets accumulate at sites of balloon dilatation. Platelet scintigraphy may be useful in predicting sites of future narrowing after angioplasty and may be used to test the efficacy of antiplatelet therapy in retarding restenosis.

Lack of elevation of platelet factor IV in plasma from patients with myocardial infarction

Platelet factor IV and beta-thromboglobulin are protein constituents of platelet granules. Elevated levels of these proteins in plasma have been used as sensitive indicators of platelet degranulation. Clearance of platelet factor IV is much faster than that of beta-thromboglobulin after release of the proteins in vivo. Although increases of platelet factor IV have been observed in patients with infarction, the implication that they reflect pathogenetic phenomena such as coronary thrombosis has not been assessed explicitly. Accordingly, plasma samples obtained serially from 52 patients with acute myocardial infarction under rigorous conditions verified to minimize platelet degranulation in vitro were evaluated prospectively. Correlative studies were performed to detect left ventricular mural thrombus, and coronary thrombosis was assessed independently in selected patients with indium-111 platelet scintigraphy. Platelet factor IV was normal at the time of admission in patients with infarction, averaging 6.3 +/- 3.3 ng/ml, similar to values in 44 other patients with chest pain without subsequent infarction (5.7 +/- 2.7 ng/ml) and in 25 normal subjects (4.3 +/- 1.6 ng/ml). Platelet factor IV generally did not increase during hospitalization in patients with infarction despite recurrent chest pain, development of left ventricular thrombus or documented recurrent infarction. However, platelet factor IV increased consistently after invasive procedures, accounting for 104 of the total of 110 increases due to platelet activation in vivo as reflected by persistence of elevated levels of beta-thromboglobulin. Thus, platelet factor IV values generally remain normal despite acute myocardial infarction. Rare increases that occur reflect platelet degranulation in vitro due to sampling artifact or perturbations of platelets in vivo due to invasive procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Detection of Active Left Ventricular Thrombosis during Acute Myocardial Infarction Using Indium-111 Platelet Scintigraphy

Platelet scintigraphy with radioactive indium-111 may be used both to identify and to reflect the activity of thrombin in vivo in man. Forty-one patients with acute myocardial infarction were studied for active left ventricular thrombosis by platelet scintigraphy and followed until in-hospital death, discharge, or same-admission cardiac surgery for evidence of systemic embolization. A total of 4.7 +/- 2.4 X 10(9) platelets (mean +/- 1 SD) labelled with 381 mu Ci +/- 51 mu Ci of indium-111 was injected intravenously at 91 +/- 88 hours following the onset of chest pain. Patients were imaged in multiple views on the day of and three to four days after injection of the platelet suspension. Group 1 (n = 29) had transmural myocardial infarctions, of which 21 were anterior (peak total level of creatine phosphokinase [CPK], 2,272 +/- 2,026 IU; mean +/- 1 SD) and eight were inferior (CPK level, 1,673 +/- 589 IU). Group 2 (n = 12) had subendocardial myocardial infarctions (CPK level 799 +/- 751 IU). Those with subendocardial and transmural inferior myocardial infarctions had neither left ventricular thrombosis nor emboli. Ten (48 percent) of 21 with anterior transmural myocardial infarctions had left ventricular thrombosis by platelet scintigraphy. Three with and one without such thrombosis by scintigraphy had acute neurologic episodes. In the group with anterior myocardial infarctions, seven of ten patients with and four of 11 without left ventricular thrombosis received heparin subcutaneously (chi 2 = 1.22 [Yates correction]; p greater than 0.30). We conclude that platelet scintigraphy may be used to monitor antiplatelet and anticoagulant therapy in patients with anterior transmural myocardial infarctions who are at risk for left ventricular thrombosis and systemic embolization.

Indium-111 platelet scintigraphy, a technique whose time has come

Indium-111 platelet scintigraphy, a technique whose time has come