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(Radiographics. 2000;20:1187-1193.)
© RSNA, 2000

PLENARY SESSION

1999 Plenary Session: Friday Imaging Symposium 1

Role of Small-Peptide Radiopharmaceuticals in the Evaluation of Deep Venous Thrombosis

Jay E. Blum, MD and Hirsch Handmaker, MD

1 From Cigna Healthcare of Arizona, Phoenix (J.E.B.); and Healthcare Technology Group, 2398 E Camelback Rd, Suite 695, Phoenix, AZ 85016 (H.H). From the Plenary Session, Friday Imaging Symposium: Algorithmic Controversies, at the 1999 RSNA scientific assembly. Received March 2, 2000; revision requested March 8 and received March 27; accepted March 27. Address correspondence to H.H. (e-mail: htg@azlink.com).

Index Terms: Radionuclide imaging, comparative studies, 935.12967 • Radionuclides, 935.12967 • Veins, extremities, 935.751 • Veins, thrombosis, 935.751

Learning Objective

Discuss the advantages and limitations of various modalities in the diagnosis of deep venous thrombosis.

Introduction

The morbidity, mortality, and socioeconomic consequences associated with venous thromboembolism are best viewed in terms of its well-studied sequelae including acute venous thrombosis, pulmonary embolism, and postphlebitic syndrome. The seriousness of these disease entities has been well documented and is generally well appreciated (1). Although risk stratification for venous thromboembolism has resulted in a heightened awareness of the need for prophylaxis in various milieus, the diagnosis of deep venous thrombosis has been less than optimal in patients with no discernible lower-extremity symptoms. The distribution of deep venous thrombosis includes the deep veins of the calf, the popliteal veins, the superficial and common femoral veins, and the iliac and pelvic veins. In addition, recent studies have supported the view that the greater saphenous vein, a superficial lower-extremity vein, is of clinical importance in deep venous thrombosis and venous thromboembolism due to its joining with the common femoral vein (2). Until recently, the lack of sensitivity of noninvasive diagnostic techniques did not allow consistent delineation of calf and pelvic vein disease. New techniques that make use of small-peptide radiopharmaceuticals and exploit the biologic properties of acute clot have shown significant promise in improving noninvasive delineation of deep venous thrombosis.

In this article, we discuss and illustrate the pathogenesis and diagnosis of deep venous thrombosis as well as the advantages and limitations of the new imaging modality known as small-peptide radiopharmaceutical thromboscintigraphy.

Pathogenesis of Deep Venous Thrombosis

The pathogenesis of deep venous thrombosis is classically determined with the Virchow triad, which includes evaluation of vessel damage, stasis, and hypercoagulability. More recently, the role of activated platelets in the formation of acute clot has been appreciated and exploited for diagnostic purposes with technetium-99m apcitide thromboscintigraphy. This new technique is performed with AcuTect (Diatide, Londonderry, NH), a synthetic peptide that binds to activated platelets. Deep venous thrombosis is generally thought to originate in the calf in 90% of cases (3). In approximately 15% of these cases, deep venous thrombosis will remain as isolated calf disease; in all other cases, it will rapidly propagate proximally (4). Symptomatic deep venous thrombosis involves the popliteal or more proximal veins in 80% of cases, and proximal thrombosis is the source of deep venous thrombosis and pulmonary emboli in the majority of cases (5,6). It has been reported that isolated calf disease is of questionable clinical importance (7). Although some studies suggest that proximal extension is uncommon in symptomatic patients and rarely occurs more than 1 week after presentation (8,9), other investigators point to data that show a 20% proximal propagation rate in addition to a small but definite prevalence of pulmonary emboli (10). In these patients, calf disease is a known cause of postphlebitic syndrome (10).

Diagnosis of Deep Venous Thrombosis

Acute deep venous thrombosis cannot be reliably diagnosed solely on the basis of clinical findings because over 50% of affected patients will be asymptomatic (11). Furthermore, only 20%–50% of patients with signs and symptoms that are considered consistent with deep venous thrombosis will have venographically proved disease (12). The implications of these facts are immediately clear: The frequent asymptomatic manifestation of acute deep venous thrombosis necessitates further testing to validate clinical suspicion, and venous thromboembolism is often missed with disastrous consequences. This clinical dilemma in the diagnosis of deep venous thrombosis is underscored by the fact that over 90% of pulmonary emboli arise from deep venous thrombosis but 73% of pulmonary emboli diagnosed at autopsy are not detected clinically (13). Again, this points to the absence of leg symptoms in over 50% of patients who subsequently prove to have deep venous thrombosis (14,15). Even the venerable Homan sign has a sensitivity of only 8% when it manifests as the sole clinical finding (16).

Objective tests for deep venous thrombosis include conventional venography, impedance plethysmography, venous ultrasonography (US), color flow Doppler imaging, magnetic resonance (MR) imaging, D-dimer assay, and Tc-99m apcitide scintigraphy. Although conventional venography is considered the standard of reference for diagnosis, its limitations are well known, and the technical difficulties involved result in an inadequate study in 20%–25% of patients (17).

Compression US of the lower extremities makes use of the phenomenon of the noncompressibility of a thrombosed vein with a US transducer. Real-time B-mode US is the standard of reference, and color flow Doppler imaging has not yet been validated as a means of improving accuracy (18,19). Pooled analysis of venous compression US in symptomatic patients suggests a sensitivity as high as 96% and a specificity of 98% (20). In asymptomatic patients, however, the sensitivity falls to 38%, with a negative predictive value of only 26% in high-risk asymptomatic patients (21). In addition, the sensitivity and specificity of compression US in calf and pelvic vein disease is poor (22). Data such as these indicate that compression US is useful in symptomatic patients but is of questionable utility in asymptomatic patients and in those with calf and pelvic disease.

There have been various attempts to improve diagnostic accuracy in deep venous thrombosis with the use of additional modalities such as clinical assessment with pretest probability. For moderate-risk patients with negative US findings and no serious underlying cardiopulmonary disease, follow-up with serial studies appears safe (23). Biochemical tests such as the D-dimer assay appear valid only when the expensive, difficult-to-perform enzyme-linked immunosorbent assay is used. Furthermore, these tests have high sensitivity but low specificity (24,25). Procedures such as MR venography have high sensitivity but are expensive and of limited availability (26).

Small-Peptide Radiopharmaceutical Scintigraphy

All of the aforementioned limitations have prompted investigators to take a new direction in the diagnosis of deep venous thrombosis. Whereas conventional imaging procedures rely on the morphologic properties of active tissue thrombus, a new imaging technique has been developed that takes advantage of the biologic properties of diseased tissue. Other examples of this nuclear medicine methodology include the use of small-peptide radiopharmaceutical tests that capitalize on the presence of somatostatin receptors expressed by neuroendocrine tumors and lung cancer. In both instances, somatostatin analogs (small peptides) are complexed with indium-111 or Tc-99m to localize malignancy in tissues. Small-peptide radiopharmaceutical single-photon-emission computed tomographic scintigraphy allows high-resolution delineation of and differentiation between malignant and benign causes in pulmonary nodules (27).

One biologic property of acute clot is the presence of activated platelets. The GPIIb/IIIa receptor resides exclusively on activated platelets, which are found only in acute clot, and is expressed on the surface of the platelets. This receptor binds both fibrinogen, which promotes platelet aggregation, and Tc-99m apcitide, which allows direct scintigraphic visualization of the activated platelet complex. Apcitide is a small peptide with a high affinity for this receptor (28). The resulting product, known as Tc-99m apcitide, allows high-resolution scintigraphic depiction of acute thrombi. This new and novel diagnostic modality has been generically termed thromboscintigraphy. Unlike current conventional methods of evaluating deep venous thrombosis, it exploits the biologic rather than the morphologic properties of acute clot, thereby allowing safe, rapid, and easily performed evaluation of the disease. Results can be obtained within 2 hours, and Tc-99m apcitide is not affected by anticoagulants (28,29). Figures 1 and 2 demonstrate platelet activation and aggregation in the setting of injured endothelium.



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  		Figure 1.   Platelet aggregation. Diagram illustrates how clot formation is initiated by the aggregation of platelets at the site of injured endothelium, which provides the substrate for platelet activation. Endothelial injury can occur by multiple mechanisms including trauma, surgery, and the adherence of small thrombi resulting from stasis. Activation results in the expression of GPIIb/IIIa receptors, which binds fibrinogen and leads to platelet aggregation.

 


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  		Figure 2.   Binding to GPIIb/IIIa receptors. Diagram illustrates how both fibrinogen and Tc-99m apcitide bind to the GPIIb/IIIa receptors on activated platelets, which are seen only in acute clot. This phenomenon also allows differentiation between acute and chronic clot with Tc-99m apcitide thromboscintigraphy.

 
There are immediate corollaries to the use of Tc-99m apcitide. The problem of recurrent deep venous thrombosis is illustrated by the fact that US findings in proximal deep venous thrombosis may remain abnormal for as long as 1 year. Non-filling of a venous segment at venography is not necessarily diagnostic. Nonacute clot is a consequence of deep venous thrombosis but has different therapeutic and clinical significance and must be distinguished from acute deep venous thrombosis for optimal treatment planning. Nonacute clot can lead to chronic pain and swelling due to venous insufficiency. This pathologic condition, known as postphlebitic syndrome, has a relatively high morbidity and develops in 50%–60% of patients with deep venous thrombosis (30,31). Venography and US allow only poor discrimination between deep venous thrombosis and acute clot, which can lead to unnecessary anticoagulation therapy (32,33).

Figure 3 illustrates the natural history of deep venous thrombosis. Platelet activation and thrombus formation are believed to originate at valve cusps. The thrombus may propagate and embolize or organize as chronic (nonacute) clot. Activated platelets are present only in acute clot, thus allowing differentiation between acute and chronic disease with Tc-99m apcitide thromboscintigraphy. In addition, Tc-99m apcitide imaging is reliable in noninvasively depicting the calf and pelvic veins, which is problematic with morphologic techniques such as US.



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  		Figure 3.   Natural history of deep venous thrombosis. Diagram illustrates how deep venous thrombosis begins with platelet aggregation at valve cusps and progresses to acute thrombus followed by embolic disease or thrombus organization and nonacute clot. Note that activated platelets (black dots) are present in acute but not in nonacute thrombus.

 
Technique

In Tc-99m apcitide thromboscintigraphy, no special bowel or other preparations are necessary, but bladder evacuation just prior to imaging is suggested for optimal evaluation of the pelvic veins. Urinary excretion occurs within 24 hours after scintigraphy, with 75% occurring within the first 8 hours. Approximately 100 µg of bibapcitide is labeled with approximately 20 mCi (740 MBq) of Tc-99m, and 20 mCi (740 MBq) of the compound Tc-99m apcitide is administered intravenously. Patients undergo planar gamma camera imaging of the lower extremities at 10, 60, and 120 minutes after injection.

Anterior and posterior static images are obtained from the level of the pelvis to the feet (8-10 min/view, 128 x 128 matrix). Images are obtained on the basis of counts, with 750,000 for pelvic images and 500,000 for the remaining images of the lower extremities. Studies are considered positive for acute deep venous thrombosis when a linear focus of increased tracer uptake is detected along the course of a deep vein.

Figures 4–6 illustrate specific findings at Tc-99m apcitide scintigraphy. Easily obtained, high-resolution studies have proved useful not only in acute proximal venous disease but also in calf disease. Note that the findings were not affected by the presence of anticoagulants. In Figure 5, Tc-99m apcitide scintigraphy demonstrated calf vein disease that was not detected with US.



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  		Figure 4.   Acute deep venous thrombosis in a 66-year-old man with a history of deep venous thrombosis and pulmonary embolism. The patient was undergoing heparin and warfarin therapy. Conventional venograms (not shown) demonstrated no filling of the deep calf veins and a thrombosed popliteal vein. Tc-99m apcitide thromboscintigram obtained 90 minutes after radiopharmaceutical injection 5 days after the onset of symptoms demonstrates acute deep venous thrombosis in the right calf and knee. Note that the accurate delineation of disease was not affected by the presence of heparin or warfarin.

 


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  		Figure 5a.   Acute deep venous thrombosis in a 23-year-old man who had sustained a gunshot wound to the left thigh 8 days earlier. The patient was undergoing heparin and warfarin therapy but had no history of deep venous thrombosis or pulmonary embolism. US images (not shown) demonstrated thrombosed left femoral and popliteal veins but no calf disease. Tc-99m thromboscintigram obtained 60 minutes after radiopharmaceutical injection 3 days after the onset of signs and symptoms demonstrates acute deep venous thrombosis in the left calf, knee, and thigh.

 


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  		Figure 5b.   Acute deep venous thrombosis in a 23-year-old man who had sustained a gunshot wound to the left thigh 8 days earlier. The patient was undergoing heparin and warfarin therapy but had no history of deep venous thrombosis or pulmonary embolism. US images (not shown) demonstrated thrombosed left femoral and popliteal veins but no calf disease. Tc-99m thromboscintigram obtained 60 minutes after radiopharmaceutical injection 3 days after the onset of signs and symptoms demonstrates acute deep venous thrombosis in the left calf, knee, and thigh.

 


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  		Figure 6.   Acute deep venous thrombosis in a 38-year-old man who was undergoing heparin therapy but had no history of deep venous thrombosis. Tc-99m thromboscintigram obtained 120 minutes after radiopharmaceutical injection 2 days after the onset of symptoms demonstrates acute deep venous thrombosis in the right calf and knee. Note the stark contrast between the affected and nonaffected extremity.

 
In a study by Taillefer et al (29) of 39 patients with acute signs or symptoms suggestive of acute deep venous thrombosis, findings at conventional venography (standard of reference) were compared with Tc-99m apcitide thromboscintigraphic findings. Twenty-two patients were considered to have deep venous thrombosis based on conventional venographic findings, which included infrapopliteal disease in six cases. Three sets of images were obtained with Tc-99m apcitide scintigraphy at 10, 60, and 120 minutes after radiopharmaceutical injection and interpreted by three separate readers, all of whom were blinded to clinical history and venographic findings. Comprehensive analysis of all three sets of images demonstrated development of a linear focus of increased uptake over time along the course of a deep vein. The sensitivity of Tc-99m apcitide scintigraphy for detection of acute deep venous thrombosis was 86.4% (19 of 22 cases), and the specificity was 88.2% (15 of 17). The results of this study were predicated on the accuracy of conventional venography in differentiating acute from nonacute deep venous thrombosis. It is likely that Tc-99m apcitide scintigraphy is more accurate than conventional venography in this regard.

Tc-99m apcitide thromboscintigraphy may also play a role in the evaluation of deep venous thrombosis when conventional morphologic imaging such as US or venography is problematic (eg, in obese patients, trauma victims, patients with orthopedic casts, suspected recurrent acute deep venous thrombosis, acute calf and pelvic disease, or evaluation of postphlebitic syndrome). Tc-99m apcitide thromboscintigraphy should also be useful in high-risk patients with negative US findings.

Data on the efficacy of Tc-99m apcitide continue to be collected. Two phase III trials involving patients with suspected deep venous thrombosis revealed specificities of 84%–88% and sensitivities of 86%–91% (34,35). These studies led to approval of the use of AcuTect (Diatide) by the U.S. Food and Drug Administration, and this radiopharmaceutical is now widely available commercially. A variety of phase IV studies are currently underway. The focus of these studies includes the evaluation of asymptomatic patients, which is clearly limited at US. Substantiation of the superiority of Tc-99m apcitide scintigraphy in this setting will be of great clinical importance, and in fact has already been achieved in one study involving asymptomatic orthopedic patients (36).

Nondiagnostic ventilation-perfusion scanning is often performed in patients with moderate or high clinical suspicion for pulmonary emboli. Documentation of lower-extremity acute clot in such cases would obviate further invasive procedures such as pulmonary angiography. US is frequently not helpful because lower-extremity involvement is often asymptomatic. Inclusion of Tc-99m apcitide scintigraphy instead of US in the algorithm for evaluation of pulmonary emboli could conceivably result in a substantial decrease in morbidity and cost. Because of the limitations of US in asymptomatic patients, new algorithms have been suggested for the evaluation of pulmonary emboli and acute deep venous thrombosis (Figs 7, 8). The capacity of Tc-99m apcitide scintigraphy to help detect acute clot in asymptomatic patients would reduce the need for more invasive diagnostic procedures.



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  		Figure 7.   Diagram illustrates a suggested algorithm for the noninvasive evaluation of acute deep venous thrombosis with Tc-99m apcitide scintigraphy.

 


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  		Figure 8.   Diagram illustrates a suggested algorithm for the noninvasive evaluation of pulmonary embolism with nondiagnostic ventilation-perfusion scanning.

 
Conclusions

Small-peptide radiopharmaceuticals are beginning to have an impact on diagnostic nuclear medicine. Tc-99m apcitide thromboscintigraphy is an example of this new methodology, which exploits the biologic rather than the morphologic characteristics of acute clot. Further substantiation of the superiority of Tc-99m apcitide thromboscintigraphy to US in asymptomatic patients should make this safe and readily available procedure extremely valuable.

Acknowledgments: The authors express their appreciation to Judy Endres, Carol Lewis, Bill Schmidt, Don Torre, Tracie Schnyder, Kevin Mohler, Helen Abernathy, and Yvonne Baran for their assistance in the performance of clinical patient studies, and to Kate McElroy and Sally Chambers for their assistance in the completion of patient records and in the preparation of this manuscript.

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