Venous Thromboembolism in the Intensive Care Unit Patient

Ken Leeper, MD

Section Chief, Pulmonary & Critical Care Medicine, Crawford Long Hospital, Atlanta, GA

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Prevalence of Venous Thromboembolism in Intensive Care Unit Patients: Intensive care unit (ICU) patients represent a heterogeneous population, and most information about the incidence of venous thromboembolism (VTE), and its prevention is from studies in trauma or surgical patients. Studies in which patients were prospectively screened for deep vein thrombosis (DVT), and the diagnosis confirmed by objective testing, suggest that in the absence of thromboprophylaxis the incidence of DVT ranges from approximately 7% to 33%, depending on the patient population and setting (1-8). In trauma patients approximately 60% will develop DVT within the first two weeks after admission (9).

In medical ICU patients, despite varying degrees of prophylaxis for DVT, the incidence of DVT remains unacceptable high. Nearly 13 years ago, a classic study by Hirsch et.al. highlighted the prevalence of DVT in a medical ICU population and the issue of inadequate prophylaxis in these patients In 100 patients admitted to the MICU for greater than 48 hours in whom 61% received DVT prophylaxis, lower extremity ultrasound (US) was performed and found that 33% had DVT, and those who had DVT were more likely to have had prior DVT and had a slightly higher hospital mortality rate (10). Ibrahim et.al. evaluated the incidence of DVT in a cohort of 110 patients requiring mechanical ventilation for > 7 days. Prophylaxis was administered to all the patients, but despite universal prophylaxis the incidence of DVT was 23.6%. This investigation also noted that 19% were upper extremity DVTs (11). Finally, in a prospective cohort study by Cook et.al. 261 medical-surgical ICU patients underwent bilateral US within 48 hours of admission and twice weekly or when DVT was suspected. These patients also received universal protocol-driven DVT prophylaxis. The investigators found that DVT was present in 2.7% of the patients on admission and subsequently occurred in 9.6% of patients during their ICU stay. Independent risk factors for DVT were family or personal history of DVT, end-stage renal disease (ESRD), platelet transfusions, and vasopressor use. This study also highlighted that the consequences of developing DVT during the ICU admission are longer length of stay in the ICU and hospital and longer duration on mechanical ventilation (12).

Risks Factors of VTE in the ICU Patient: A variety of factors may predispose ICU patients to VTE, and the majority have multiple risk factors.. In one prospective study conducted in a medical-surgical ICU, the mean number of VTE risk factors was 4.3 (13). Risk factors may be present on admission to the ICU, or may be acquired during the patient’s stay in the unit as a result of invasive procedures or treatments. Pre-existing risk factors include recent surgery, immobilization, estrogen treatment, and medical conditions such as cancer, trauma, or stroke. Interventions that may lead to an acquired risk of VTE in the ICU include sedation, mechanical ventilation and insertion of central venous catheters. In one randomized prospective trial, 25% of patients in a medical-surgical ICU who underwent central venous catheterization via a femoral vein, developed DVT, whereas no cases of DVT occurred in patients catheterized via a subclavian or internal jugular vein (14).

Diagnosis of VTE in the ICU Patient: The clinical diagnosis of a VTE event in the ICU is largely nonspecific (15). Clinical clues such as an unexplained increase in dead space ventilation or minute ventilation in a patient on mechanical ventilation or the development of unexplained fever may lead to the investigation of VTE. There is no role for d-dimer determination to exclude the possibility of VTE in this patient population. ICU patients have a number of comorbid diseases that would make the d-dimer test useless (16). The noninvasive diagnosis of DVT in the ICU patient is primarily performed by duplex ultrasonography. Screening for DVT with the new portable US devices has been advocated, but existing data suggest that screening for DVT may not be cost effective (17). CT venography in patients with normal renal function correlates well with duplex Doppler ultrasonography of the lower extremities. Evaluation of the upper extremities for DVT can be accomplished by ultrasound. In the evaluation for acute PE, if the patient is hemodynamically stable and with normal renal function, spiral CT scanning of the chest should be performed. There are only case series describing the role of spiral CT scanning for PE in ICU patients. The diagnostic accuracy of spiral CT-pulmonary angiography and CT venography are extrapolated from the recent PIOPED II investigation (18). The CT scan of the chest can also provide alternative diagnoses to explain the clinical suspicion of pulmonary embolism. Recently, there have been investigations that have shown that once PE is confirmed by CT scan, the finding of right ventricular diameter/left ventricular diameter (RV/LV) ratio >0.9 can be used in risk stratification of PE severity (19). In the patient who is unable to be moved from the ICU and may be hemodynamically unstable, either the transthoracic or transesophageal echocardiography can be used to demonstrate acute RV dysfunction and in some instances the presence of an acute pulmonary embolic event.

Thromboprophylaxis in ICU Patients: Although data specific to critical care patients are limited, the available evidence suggests that VTE thromboprophylaxis is often under-prescribed, or used sub-optimally in ICU patients (20). ACCP guidelines include general recommendations for the prevention of VTE in ICU patients, but make no specific recommendations for medical ICU patient. It is recommended that all patients should be assessed for their risk of VTE on admission to the ICU, and that most patients will require some form of thromboprophylaxis. Medical ICU patients are generally considered to be at moderate risk of VTE, and either LMWH or low-dose UFH is recommended for such patients (Grade 1A recommendation). If the risk of bleeding is considered to be high, mechanical prophylaxis with graduated compression stockings, intermittent pneumatic compression, or both, can be used until the risk decreases. The available data suggest that the efficacies of UFH and LMWH in the prevention of VTE in ICU patients are comparable. Moreover, the incidence of major bleeding appears to be similar with the two agents. It should be noted that thromboprophylaxis is not always effective, and that a proportion of high-risk patients may develop DVT despite prophylaxis. In a recent study, 23.6% of mechanically ventilated patients in a medical ICU developed DVT despite prophylaxis (11). Such findings suggest that some conditions common in the ICU setting, such as cardiac impairment or vasopressor use, might reduce the efficacy of thromboprophylaxis. (21,22).

Non-Pharmacological Thromboprophylaxis: The use of mechanical devices such has intermittent pneumatic compression (IPC) or sequential compression devices (SCD) are used primarily when there is a high risk of bleeding. Robust evidence supporting its efficacy as the only prophylaxis measure preventing DVT is lacking. If the risk of bleeding is considered to be high, mechanical prophylaxis with graduated compression stockings, intermittent pneumatic compression, or both, can be used until the risk decreases or resolves.

Treatment of Acute VTE in ICU Patients: Evidence-based consensus guidelines and individual studies have recommended that patients with confirmed VTE should receive either subcutaneous LMWH or intravenous UFH, together with vitamin K antagonists (20). If a patient presents to the ICU or develops a massive acute pulmonary embolism during their ICU stay, thrombolytic therapy should be considered if there are no contraindications. Surgical options are usually considered when there is a contraindication to more aggressive medical approach Heparin induced thrombocytopenia (HIT) is another source of venous thrombosis in ICU patients. HIT is characterized by a reduction in the platelet count by 50%, usually after five days of unfractionated heparin exposure, but rarely after LMWH exposure. The frequency in the cardiac surgical population can be has high as 1- 3% (23). Nearly 50% with documented HIT will develop either venous or arterial thrombosis. The treatment of HIT is the discontinuation of heparin and the treatment with direct thrombin inhibitors. Inferior vena cava filters are sometimes used in the treatment of VTE in cases where contraindications to anticoagulants exist. However, current guidelines recommend against the routine use of such devices in the majority of VTE patients (20), and it seems appropriate to adopt this recommendation in ICU patients.

Summary: Venous thromboembolism is a common problem in the intensive care unit. The occurrence of DVT, or acute pulmonary embolism in the ICU patient is associated with additional morbidity and increased cost. The clinical diagnosis of VTE in critically-ill patients is so nonspecific that the prevalence is underestimated. We need to ascertain whether DVT screening is justified and cost effective in this patient population. Diagnostic and treatment strategies need to be further studied on large groups of ICU patients with the appropriate stratification. Thromboprophylaxis in the ICU population must be universal, although it may not be as effective when compared to the non-ICU populations. Truly, prophylaxis against VTE in the ICU is the last frontier in our quest to appropriately protect our acutely ill hospitalized patients from VTE events (24).

References

1. Moser KM, LeMoine JR, Nachtwey FJ, et al. Deep venous thrombosis and pulmonary embolism. Frequency in a respiratory intensive care unit. JAMA 1981;246:1422-1424.
2. Cade JF. High risk of the critically ill for venous thromboembolism. Crit Care Med 1982;10:448-450.
3. Marik PE, Andrews L, Maini B. The incidence of deep venous thrombosis in ICU patients. Chest 1997;111:661-664.
4. Harris LM, Curl GR, Booth FV, et al. Screening for asymptomatic deep vein thrombosis in surgical intensive care patients. J Vasc Surg 1997;26:764-769.
5. Kapoor M, Kupfer YY, Tessler S. Subcutaneous heparin prophylaxis significantly reduces the incidence of venous thromboembolic events in the critically ill. Crit Care Med 1997;27 (12 Suppl):A69 [abstract 165].
6. Goldberg SK, Lippmann ML, Walkenstein MD, et al. The prevalence of DVT among patients in respiratory failure: the role of DVT prophylaxis. Am J Respir Crit Care Med 1996;153:A94 [abstract].
7. Fraisse F, Holzapfel L, Coulaud J-M, et al. Nadroparin in the prevention of deep vein thrombosis in acute decompensated COPD. Am J Respir Crit Care Med 2000;161:1109-1114.
8. Major KM, Wilson M, Nishi GK, et al. The incidence of thromboembolism in the surgical intensive care unit. Am Surg 2003;69:857-861.
9. Geerts WH, Code KI, Jay RM, Chen E, Szalai JP. A prospective study of venous thromboembolism after major trauma. N Engl J Med. 1994;331:1601–1606.
10. Hirsch DR, Ingenito EP, Goldhaber SZ. Prevalence of deep venous thrombosis among patients in medical intensive care. JAMA 1995;274:336-337.
11. Ibrahim EH, Iregui M, Prentice D, et al. Deep vein thrombosis during prolonged mechanical ventilation despite prophylaxis. Crit Care Med 2002;30:771-774.
12. Cook D, Attia J, Weaver B, et al. Venous thromboembolic disease: an observational study in medical-surgical intensive care unit patients. J Crit Care 2000;15:127-132.
13. Cook D, Meade M, Guyatt G, et al. Clinically important deep vein thrombosis in the intensive care unit: a survey of intensivists. Crit Care 2004;8:R145-R152.
14. Trottier SJ, Veremakis C, O’Brien J, et al. Femoral deep vein thrombosis associated with central venous catheterization: results from a prospective, randomized trial. Crit Care Med 1995;23:52-59.
15. Crowther MA, Cook DJ, Griffith L, et al.. Deep vein thrombosis: clinically silent in the ICU. J Crit Care. 2005;20:334–340.
16. Quinn DA, Fogel RB, Smith CD, Laposata M, Thompson BT, Johnson SM, Waltman AC, Hales CA. D dimers in the diagnosis of pulmonary embolism. Am J Resp Crit Care Med. 1999;159:1445–1449.
17. Harris LM, Curl GR, Booth FV, et al. Screening for asymptomatic deep vein thrombosis in surgical intensive care patients. J Vasc Surg 1997;26:764-769.
18. Stein PD, Fowler SE, Goodman LR, Gottschalk A. et.al. Multidetector computed tomography for acute pulmonary embolism. N Engl J Med. 2006;354: 2317-27
19. Sanchez 0., Trinquart L., Colombet I., Durieux P., HuismanMV, Chatellier G., Meyer G. Prognostic value of right ventricular dysfunction in patients with henmodynamically stable pulmonary embolism: systematic review. Eur Heart J 2008:12;1569-77.
20. Kearon C., Kahn SR., Agnelli G. Goldhaber S, Raskob GE., Comerota AJ. Antithrombotic treatment of venous thromboembolic disease: American college of Chest Physicians Evidence based Clinical Practic Guidelines (8th Esdition). Chest 2008;133:454S-545S.
21. Priglinger U, Delle Karth G, Geppert A, et al. Prophylactic anticoagulation with enoxaparin: is the subcutaneous route appropriate in the critically ill? Crit Care Med 2003;31:1405-1409.
22. Dörffler-Melly J, de Jonge E, de Pont A-C, et al. Bioavailability of subcutaneous low-molecular-weight heparin to patients on vasopressors. Lancet 2002;359:849-850.
23. Warkentin TE., Greinacher A. heparin-induced thrombocytopenia and cardiac surgery. Ann Thorac Surg 2003;76:638-648.
24. Goldhaber SZ. Venous thromboembolism in the intensive care unit. The last frontier of prophylaxis Chest 1998;113:5-7.

 

Contaminants in the Recalled Unfractionated Heparin Preparations: Pharmacologic and Clinical Implications

J. Fareed, Ph.D., J.M. Walenga, PhD, W. Jeske, PhD, D. Hoppensteadt, PhD, M. Prechel, PhD, O. Iqbal, MD, C. Adiguzel, MD, M. Clark, BS, E. Latinas, MD, J. Cunanan, MD, R. Linhardt, PhD, E. Ramacciotti, MD, PhD, R.L. Bick, MD PhD, H.L. Messmore, MD, J. Harenberg, MD

Loyola University Chicago, Maywood, IL; Rensealear Polytechnic, Albany, NY; Southwestern Texas University, Dallas, TX ; University Clinic Mannheim, Germany

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July 7, 2008; 1:04 p.m. (EST): The number of deaths of patients receiving heparin reported to the FDA, during the period from January 2007 through May 31, 2008, stands at 246.  Of these reported deaths, 149 are attributable to one or more allergic/hypotensive symptoms.  Of greater concern is the fact that since March 2008, a time span where stringent control measures and FDA alert were enforced, a total of 30 additional deaths were reported with 17 of these being linked to one or more allegeric/hypotensive symptoms.  Ironically, after the February 28, 2008 recall and subsequent monitoring by the US FDA, it was reported that heparin-associated deaths had returned to baseline (Kishimoto et al, NEJM, 2008;23:358).  Contaminated heparin containing oversulphated chondroitin sulphate was linked to the observed clinical adverse events.  If this is the case, the 17 additional deaths since March 2008 exhibiting one or more allergic/hypotensive causes requires further explanation.  This updated report also points to the fact that there may be additional factors responsible for the serious adverse events and deaths with the use of heparins.  Therefore, besides the reported role of oversulphated chondroitin sulphate, other factors may also be contributory to the deaths reported since March 2008.  It is likely that besides the reported activation of the contact system by oversulphated chondroitin sulphate, additional pathogenic mechanisms are contributing to the serious adverse events and deaths associated with the use of heparin, which may likely include immunogenic responses.  Heparin represents a very complex drug whose mechanism of action represents a collective response for both the therapeutic and adverse responses.  While contact system activation may contribute to the reported pathogenesis, it is unlikely to be the sole cause of reported deaths in patients treated with heparin.  Additional studies in animal models and retrospective analysis of biologic fluids and available autopsy data maybe helpful in the understanding of these adverse events and deaths (Hoppensteadt et al., Clin Appl Thromb Hemost, 2008;14:261).

As an initial step, the chemical and biological profiles of the contaminant in four recalled unfractionated heparins (UFH) (3 finished products and 1 powder) were investigated. To obtain the contaminant, each material was treated by exhaustive depolymerization with nitrous acid and heparinase 1 to remove heparin followed by ethanolic precipitation and anion exchange chromatography. The amount of non-digested material ranged 10-30%, most of which was characterized to be hypersulfated chondroitin sulfate (HSCS) by proton and 13C NMR spectroscopy. The molecular weight profile exhibited a wider dispersity index in comparison to contaminant-free UFH with oligosaccharides ranging from 5-30 kDa (average 16.8 kDa). In addition, a well-characterized porcine cartilage HSCS preparation with average molecular weight of 17.2 kDa was used as a reference material. While varying degrees of dermatan sulfate (high molecular weight) and minor impurities were detected, the HSCS appeared to be the major contaminant in these preparations. To investigate the biological profile of the isolated contaminant, it was subjected to chondroitinase A, B, and C and high potency heparinase 1 (2.5 U/ml) depolymerization. The material was resistant to the action of these enzymes. The contaminant was further profiled in routinely used anticoagulant and anti-protease assays. In the USP assay it exhibited a potency of 26.8 U/mg. It also produced a concentration dependent anticoagulant effect in the whole blood celite activated clotting time (ACT) and saline ACT tests, but was weaker than heparin. In the PT assay (extrinsic coagulation system) the contaminant only exhibited very weak activity and did not affect the INR up to a 50 µg/ml concentration. However, in global anticoagulant assays such as the aPTT (intrinsic coagulation system) and Heptest, in comparison to UFH, the contaminant produced varying degrees of concentration dependent anticoagulant activity (10-40 U/mg). In the amidolytic anti-thrombin assay it produced a concentration dependent inhibition of thrombin in citrated plasma (~ 25 U/mg). The contaminant did not exhibit any inhibition of FXa in the same systems. In antithrombin (AT) depleted plasma, while the anticoagulant and amidolytic activities of UFH were considerably reduced, the contaminant exhibited measurable concentration dependent effects indicating a non-AT dependence. In HCII depleted plasma the contaminant lost sizeable anticoagulant and anti-thrombin effects. The dermatan cofactor activity of pre- and post-heparinase digested contaminant was not different, whereas UFH showed a considerable decrease. The contaminant was readily neutralizable by protamine sulfate, polybrene, and PF4 in a similar fashion as UFH. The contaminant-mediated contact factor activation, as measured by the generation of kallikrein and bradykinin, was concentration dependent in plasma and whole blood. UFH also showed this activity in both systems. Significant differences in contact activation by UFH and the contaminant were noted between citrated and hirudinized whole blood. The contaminant also produced HIT mediated antibody activation of platelets; however, it had a faster onset of action and longer lasting time course of platelet aggregation than UFH. In the 14C-Serotonin Release Assay (SRA) the contaminant produced a strong release of serotonin which sustained at high concentrations and did not follow the parabolic response usually observed with UFH. Studies of the contaminant mixed with UFH in proportions of 3, 6, 12, 25, and 50% (amount of contaminant) in plasma and whole blood revealed a non-additive assay dependent synergistic effect of the contaminant on the anticoagulant and anti-thrombin activities. At a 25% level, the contaminant produced a marked increase of the anticoagulant activity of the mixture mimicking the pharmacopoeial potency of ~ 150 U/mg; however, this increase was dependent on different contaminant preparations (different batches). Similar augmentation of the effects of UFH were noted in the thrombin and FXa generation tests as measured by amidolytic methods and measurements of such thrombin generation markers as FPA, TAT, and F1.2. Preliminary studies show that the contaminant may also exhibit direct anti-protease effects by complexing with FVIIa and the prothrombinase complex. To study the in vivo effect of the contaminant, the effect of contaminated UFH and a potency equivalent contaminant-free preparation were studied in animal models of bleeding and thrombosis. In comparison to the contaminant-free UFH at an identical dosage of 200-800 U/kg, the contaminated UFH produced a marked increase in bleeding. Similarly, the antithrombotic effect in terms of ED50 was markedly stronger with the contaminated preparation. Blood pressure measurements provided variable effects in which both the contaminated and contaminant-free preparations exhibited a hypotensive response in some rats. The contaminated heparin exhibited stronger and longer lasting anticoagulant effects in primates, and produced a stronger release of TFPI. Similar studies carried out on two hemi-synthetic HSCS preparations mixed with non-contaminated UFH provided comparable results. Since the contaminated batches of UFH also contain variable amounts of dermatan sulfate, additional studies are in progress at this time on the pharmacologic profile of the contaminated UFH, isolated contaminant, hemi-synthetic HSCS, hyper-sulfated dermatan sulfate, and their precursors. Furthermore, additional investigations on the contaminant isolated from commercially available/branded and generic LMWHs are in progress at this time with particular reference to the molecular profile of the contaminant, its subcutaneous PK/PD profile, and immunogenic potential. Until the availability of such data and additional information on the cause of adverse reactions and deaths in patients treated with recalled heparins is available, the true cause of these events remains unknown. 

Global Registry on PMT for Acute PE – Development of a Case Report Form

William T. Kuo, MD, FCCP

Vascular and Interventional Radiology, Stanford University Medical Center, Stanford, CA 94305

INTRODUCTION: The Stanford Division of Vascular and Interventional Radiology has drafted a case report form (CRF) for the Global Registry on Percutaneous Mechanical Thrombectomy (PMT) for Acute Pulmonary Embolism.  This draft serves as an initial template for gathering data relevant to the endovascular treatment of massive PE.

We realize there is no widely accepted protocol for catheter-directed treatment of pulmonary embolism, and the PE management algorithm itself varies among institutions.  Furthermore, existing treatment regimens are continuously evolving with the development of new catheters, devices, and treatment protocols.  Consequently, this Case Report Form has been designed to capture data not only on existing catheter-based methods but also on emerging techniques. 

In the final step of completing this document, and prior to its official launch, we open the CRF via the web to commentary and feedback from all interested participants of the North American Thrombosis Forum (NATF).  We are seeking input from all potential collaborators and investigators.  Acceptable ideas and recommendations by consensus will be incorporated into the CRF and contributors acknowledged. 

As part of a worldwide multidisciplinary effort, our goal is to create an effective web-based registry that will study the effects of PMT for acute PE.  Please contact us with questions, comments, and feedback.  We greatly appreciate your input in the creation of this international registry. 

 

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NATF Traveling Fellowship Program: APPLICATION DEADLINE IS JULY 15, 2008

With the goal of exploring the cross-disciplinary diagnosis, treatment, education, and research related to thrombosis, the NATF Traveling Fellowship Program is an annual scientific exchange opportunity for physicians (either Junior Faculty or physicians-in-training), scientists, nurses, or pharmacists.  NATF will provide an award equivalent to $5,000 for lodging and travel for one Fellow selected to visit a North American thrombosis research and education center of his or her choice for up to 10-30 days.

The NATF Traveling Fellow will:

• Work on a joint project with hosting center
• Contribute to the development of a cross-disciplinary approach for the research, diagnosis, treatment, and education thrombosis
• View research facilities and thrombosis diagnosis, treatment, and prevention methods
• Participate in scientific symposia with members of the NATF Board and Scientific Advisory Committee
• Free participation in the 2008 North American Thrombosis Forum Thrombosis Summit (Boston, MA, September 27, 2008) attended by cross-disciplinary medical and scientific leaders
• Present learnings gained through NATF Traveling Fellowship at the Fall 2009 North American Thrombosis Forum Thrombosis Summit
• Serve as an NATF Ambassador

To learn more about the NATF Traveling Fellowship or to apply, please click here.

Benefits of the NATF Traveling Fellowship

• Foster an exchange of scientific information, stimulate research and expanded education, and develop friendships among leaders in thrombosis research, treatment, and patient education
• Serve as a bridge that may be used to forge the future of thrombosis treatment and prevention that includes a cross-disciplinary approach
• Provide a stimulus for leadership by recognizing young medical personnel or scientists with the potential for nationally lowering the rate of life-threatening thrombotic episodes through education, research, and prevention

NATF Committment to Future Leaders

The NATF Traveling Fellowship Program was conceptualized to allow scientists and health professionals (MD, DO, PhD, RN, or PharmD) the opportunity to expand their fund of knowledge, as well as build positive and enduring relationships with others concerned with thrombotic disorders. NATF recognizes the vital impact training programs have on the future of thrombosis research, diagnosis, treatment, and prevention.

Application Requirements

• The Fellow will be selected by the NATF Advisory Committee, Chaired by Dr. Arthur A. Sasahara, MD, Professor of Medicine, Emeritus, Harvard Medical School, and NATF Director.
• The fellowship will be granted based on a demonstrated commitment to excellence in education, research, or clinical practice.
• 3 Letters of reference are required.
• Applicants must be practicing in North America:  Application Deadline is July 15, 2008

The North American Thrombosis Forum is a 501(c)(3) nonprofit organization that focuses on unmet needs and issues related to thrombosis and cardiovascular diseases such as deep vein thrombosis, pulmonary embolism, myocardial infarction, peripheral arterial occlusive disease, and stroke. The five areas of major focus are: 1) basic translational research, 2) clinical research, especially diagnosis and therapy, 3) prevention and education, 4) public policy, and 5) advocacy. NATF's legacy will be to improve patient care, outcomes, and public health by supporting thrombosis-related programs, such as novel research projects, innovative educational programs, public policy initiatives, regulatory issues and advocacy, and to broaden training opportunities for scientists and health professionals (physicians, nurses, pharmacists).

Our offices are located at 1620 Tremont Street, Suite 3022; Roxbury Crossing, MA 02120.  For general information, please call (617) 525-8326 or email: info@NATFonline.org.

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