Aortic thromboembolism occurs commonly in cats and has been addressed extensively in the literature.1–6 Typical clinical signs in feline patients consist of acute-onset hind limb paresis, pain, absent femoral pulses, and nail bed cyanosis.2,3 Although idiopathic cases have been reported,7 most cats have underlying cardiac disease, with congestive heart failure reported in 40% to 66% of cats.2,3,7 Prognosis is typically poor, with a reported rate of survival to discharge of 0% to 50% and 6-month recurrence rate of 45% to 75%.2,8 Low rectal temperature, bradycardia, and multiple limb involvement have all been associated with decreased survival rate.3 Euthanasia is common, occurring in 24% to 35% of cases.3
Clinical information regarding aortic thrombosis in dogs is less thoroughly documented in the current literature. In canine patients, aortic thrombosis has been associated with multiple conditions, including hyperadrenocorticism, protein-losing glomerulonephropathy, infective endocarditis, and neoplasia.9–12 Both acute and chronic onset of disease has been reported,9 and clinical signs include exercise intolerance, hind limb paresis, absent femoral pulses, cold extremities, and signs of pain.9,11,13 Survival rate in dogs with aortic thrombosis has been reported to exceed that of cats with ATE; however, the prognosis and rate of recurrence have not been fully addressed.9,13
In feline patients, the outcome of therapeutic interventions, including thrombolytic treatment with streptokinase or t-PA or long-term anticoagulant treatment with acetylsalicylic acid, clopidogrel, warfarin, and heparin, has been reported.1,5,6,8,14 The literature concerning therapeutic intervention in dogs is sparse and conflicting.9 Two case reports14,15 of dogs reported streptokinase or t-PA administration to result in partial or complete thrombus resolution. However, another case report9 indicated that t-PA treatment was ineffective. To our knowledge, there are no reports of long-term management of the disease.
The purpose of the study reported here was to describe the clinical signs and diagnostic findings for dogs with aortic thrombosis and assess associations with survival data. We also aimed to describe short-term (thrombolytic drug treatment and rheolytic thrombectomy) and long-term (anticoagulant and antiplatelet treatment) therapeutic interventions. Clinical decision making for the management of dogs with aortic thrombosis is critically dependent on a greater understanding of initial clinical signs, prognostic associations, and future prospective assessment of treatment options.
Materials and Methods
Case selection—The University of California-Davis Veterinary Medical Teaching Hospital medical record system was searched for records of dogs initially examined between September 2000 and October 2010 with aortic thrombosis identified on abdominal ultrasonography or postmortem examination.
Procedures—Records were retrospectively reviewed and data collected regarding signalment (age, breed, and sex), historical signs, physical examination findings, laboratory testing, definitive diagnosis, and presence of concurrent disease. Acute disease was defined as clinical signs that developed in < 24 hours, whereas chronic disease was defined as clinical signs that developed over a period of > 24 hours. All laboratory testing was performed at the University of California-Davis clinical pathology laboratory. Digitally captured, still ultrasonographic images and written ultrasonographic reports were reviewed by a board-certified radiologist (EGJ) for the presence or absence of an aortic thrombus on a dedicated workstation.
An aortic thrombus was defined as a discrete intraarterial space-occupying lesion that altered blood flow. Two echocardiographic machinesa,b equipped with an S5–1 and S8–3 MHz blended transducer were used for all echocardiographic examinations. The location and anatomic extent of the thrombus were determined from this information. Additionally, the echogenicity of the thrombus, compared with adjacent muscle, was recorded, as was the presence or absence of patency through or around the thrombus identified via color flow Doppler echocardiography. Echocardiographic images were retrospectively reviewed (GALB), with echocardiographic diagnosis, presence, and severity of valvular insufficiency and evidence of clot or spontaneous contrast recorded. When performed, results from other diagnostic tests (radiography, CT, MRI, or necropsy) were obtained from the medical record. Therapeutic interventions, selected at the discretion of the treating clinician, were recorded. Gross and histologic necropsy findings were extracted from the record when performed. If the last medical record entry indicated that the dog was alive, an attempt was made to contact the owner, referring veterinarian, or both via email or telephone. For the 9 cases lost to follow-up, survival time was censored on the last date in the record at which the dog was known to be alive.
Statistical analysis—Categorical data (ie, breed, sex, and examination findings) are summarized as percentages and frequencies. Continuous data (ie, age, body weight, and laboratory results) were tested for normality of distribution via the Kolmogorov-Smirnov test. Normally distributed variables are reported as mean ± SD, and nonnormally distributed variables are reported as median and range. To avoid excessive manipulation of the data set, outliers, when present, were not removed from calculations of mean and SD. The Kruskal-Wallis rank sum test was used to evaluate differences in survival data. χ2 Analysis was used to analyze breed distributions. All statistical evaluations were performed with a statistical software program.c Values of P < 0.05 were considered significant.
Results
From a hospital caseload of 68,414 canine patients within the 10-year search period, 31 cases of aortic thrombosis were identified (prevalence, 0.0005%). Thirteen (42%) dogs were castrated males, 17 (55%) were spayed females, and 1 (3%) was a sexually intact female. No breed was found to be overrepresented, compared with hospital intake. Mean age was 9.9 ± 3.6 years, and mean body weight was 21.5 ± 11.2 kg (47.3 ± 24.6 lb). The onset of clinical signs was acute in 14 (45%) dogs and chronic in 15 (48%). Two dogs had unclear progression of signs.
Physical examination findings included absent femoral pulses (17 [55%]), subjectively cool extremities (11 [35%]), and cyanotic hind limb nail beds (2 [6%]). Mean rectal temperature was 38.4 ± 1.8°C (101.2 ± 1°F). The owner or veterinarian perceived signs of pain in 9 (29%) dogs. Paresis or paralysis was characterized in 28 dogs. The majority of dogs were initially examined because of paresis (23 [82%]). Single limb involvement was present in acute cases only: right hind limb in 3 dogs and left hind limb in 2 dogs. All chronic cases involved both hind limbs. Overall, bilateral hind limb involvement was present in 19 (68%) dogs, of which 6 had acute disease and 13 chronic. Three dogs developed tetraparesis (1 had acute disease, 1 had chronic disease, and 1 had disease with unclear progression). In 1 dog, 2 acute events involved the right hind limb and then left hind limb. Twelve of the 15 dogs with chronic signs had bilateral hind limb involvement.
Echocardiography was performed on 14 (45%) dogs. A cardiac murmur was auscultated in 9 (29%) dogs, and echocardiography was performed in 7 of these. Seven dogs did not have heart murmurs but underwent echocardiography as part of the diagnostic evaluation for thromboembolic disease. Two of the dogs undergoing echocardiography had mild left atrial enlargement; the remaining 12 dogs had no evidence of left atrial enlargement (left atrial-to-aortic root diameter ratio < 1.6). No dogs had spontaneous echocardiographic contrast in the left atrium or ventricle. Of the dogs with murmurs, 6 were determined to have myxomatous mitral valve degeneration, 1 of which also had a mass in the left ventricle. The remaining dog had vegetative endocarditis of the mitral valve. Of the dogs without heart murmurs, 1 had a mass associated with the left ventricular free wall, 1 had a thickened interventricular septum suggestive of infiltrative disease, 1 had a possible vegetative lesion associated with the mitral chordae tendinae, and 1 had a proximal aortic thrombus.
A CBC was evaluated in all dogs. A stress leukogram was present in 9 (29%) dogs. Neutrophilia (without stress leukogram) was present in 6 dogs (4 had acute disease and 2 had chronic disease), with a mean of 13,318 ± 2,310 neutrophils/μL (reference value, < 10,500 neutrophils/μL). Thrombocytopenia (< 100,000 platelets/μL) was present in 3 chronically affected dogs, with a median of 69,000 (reference range, 51,000 to 91,000 platelets/μL). Thrombocytosis (> 400,000 platelets/μL) was present in 4 dogs (3 had acute disease and 1 had chronic disease), with a median of 472,500 (range, 423,000 to 859,000 platelets/μL). The mean BUN concentration was 41.0 ± 38.2 mg/dL (reference range, 5 to 21 mg/dL), and the mean creatinine concentration was 2.2 ± 2.6 mg/dL (reference range, 0.3 to 1.2 mg/dL). Azotemia was present in 19 (68%) dogs (6 had acute disease and 13 had chronic disease). The mean albumin concentration was 2.8 ± 0.7 g/dL (reference range, 3.0 to 4.4 g/dL). The median creatinine kinase activity was 384 U/L, with a range of 78 to 52,756 U/L (reference range, 51 to 399 U/L). No other remarkable clinical biochemical abnormalities were noted. Eighteen of the 19 dogs in which urinalysis was performed had proteinuria at the time of initial examination. Determination of UPC was performed in 12 of these dogs, and all dogs had proteinuria with a UPC > 0.5 and a mean UPC of 5.7 ± 4.8.16 Ten of these dogs also had hypoalbuminemia, and 4 of these dogs also had a prior history of chronic renal disease.
Concentration of ATIII was low in 5 of the 12 dogs tested, with a mean concentration of 69.2 ± 7.1%, (reference range, 80% to 120%). All of the dogs with low ATIII concentrations had a UPC > 0.5. Seventeen dogs had PT and partial thromboplastin time determined. Five of 17 dogs had a prolonged PT, with a mean of 11.8 ± 2.6 seconds (reference range, 7 to 9.3 seconds). Ten of 17 dogs had a prolonged partial thromboplastin time, with a mean of 15.1 ± 2.6 seconds (reference range, 10.4 to 12.9 seconds). Fibrinogen concentration was elevated in 11 of the 17 dogs tested (median, 417 mg/dL; range, 315 to > 1,000 mg/dL; reference range, 109 to 311 mg/dL). D-dimer concentration was elevated in 9 of the 11 dogs evaluated. Thromboelastographyd was performed in 5 dogs. Four dogs (1 had acute disease and 3 had chronic disease) had results of thromboelastography consistent with hypercoagulable state as indicated by decreased K-kinetics, increased α angle, maximum amplitude, and G (clot strength). The remaining dog (with chronic disease) had normal thromboelastography results.
Abdominal ultrasonography was performed in 25 dogs, and an aortic thrombus was identified in all dogs. The aorta and external iliac arteries were involved in 10 dogs. The distal portion of the aorta and external iliac, internal iliac, and femoral arteries were affected in 7 dogs. The thrombus was located exclusively in the distal portion of the aorta near the iliac arterial bifurcation in 4 dogs. The distal portion of the aorta and external iliac and internal iliac arteries were involved in 1 dog. A thrombus in the aorta, external iliac arteries, and left renal artery was found in 1 dog. One dog had involvement of the distal portion of the aorta, internal and external iliac arteries, femoral arteries, and both renal arteries. A sole thrombus in the left external iliac artery was identified in 1 dog. An ultrasonographic evaluation of the left brachial artery was performed in 1 dog and identified a thrombus in this artery as well.
Of the 25 ultrasonographic examinations performed, 21 included color flow Doppler examination of the affected arteries to evaluate for patency through or around the thrombus. Of these, 13 had some documented flow through or around the thrombus and 8 did not. The echogenicity of the thrombus, compared with the adjacent muscle, was also recorded in 21 cases. Six of the thrombi identified were hyperechoic to the adjacent muscle, 11 were isoechoic to adjacent muscle, and 4 were hypoechoic in comparison with adjacent muscle.
Eight (26%) dogs had renal disease. Four of these dogs had prior chronic renal disease: 3 had protein-losing nephropathy, and 1 had glomerulonephritis. Two (6%) dogs had immune-mediated thrombocytopenia (one dog in remission received 0.5 mg of prednisone/kg [0.23 mg/lb], q 24 h, and the other dog received 1 mg/kg [0.45 mg/lb], q 12 h). Two (6%) dogs had endocarditis. Other concurrent diseases included hyperadrenocorticism (n = 1), hypoadrenocorticism (1), and diabetes mellitus (1). Six (19%) dogs had received systemic corticosteroids < 1 month prior to initial examination.
A necropsy was performed in 10 dogs. Eight of these dogs had received antemortem abdominal ultrasonography, and the diagnosis of an aortic thrombus was correct in all of these dogs. Six (19%) dogs had neoplastic disease identified on necropsy, with final diagnoses of lymphoma (n = 2), osteosarcoma (1), adrenocortical carcinoma (1), cardiac sarcoma (1), and adrenal mass (1), which was not classified histologically. One dog had a left ventricular thrombus that was suspected to be of neoplastic origin (hemangiosarcoma). One dog was found to have a chronic thrombus associated with the left atrium. No underlying disease process was determined in 2 dogs, although 1 had a history of chronic renal disease (Figure 1).
Necropsy specimen from a 13-year-old castrated male Whippet with chronic hind limb paresis, chronic kidney disease, and aortic thrombosis. The thrombus fills the caudal portion of the abdominal aorta extending from the renal arteries to the aortic trifurcation. The thrombus also extends into the internal iliac arteries, into part of the left external iliac artery, and down the entire right external iliac artery and into a portion of the right femoral artery. The left renal artery was also found to contain a portion of the thrombus.
Citation: Journal of the American Veterinary Medical Association 241, 7; 10.2460/javma.241.7.910
Necropsy specimen from a 13-year-old castrated male Whippet with chronic hind limb paresis, chronic kidney disease, and aortic thrombosis. The thrombus fills the caudal portion of the abdominal aorta extending from the renal arteries to the aortic trifurcation. The thrombus also extends into the internal iliac arteries, into part of the left external iliac artery, and down the entire right external iliac artery and into a portion of the right femoral artery. The left renal artery was also found to contain a portion of the thrombus.
Citation: Journal of the American Veterinary Medical Association 241, 7; 10.2460/javma.241.7.910
Necropsy specimen from a 13-year-old castrated male Whippet with chronic hind limb paresis, chronic kidney disease, and aortic thrombosis. The thrombus fills the caudal portion of the abdominal aorta extending from the renal arteries to the aortic trifurcation. The thrombus also extends into the internal iliac arteries, into part of the left external iliac artery, and down the entire right external iliac artery and into a portion of the right femoral artery. The left renal artery was also found to contain a portion of the thrombus.
Citation: Journal of the American Veterinary Medical Association 241, 7; 10.2460/javma.241.7.910
Median survival time of dogs with chronic disease (30 days; range, 0 to 959 days) was significantly (P = 0.04) longer than that of dogs with acute disease (1.5 days; range, 0 to 120 days). Eighteen dogs were euthanized (10 had acute disease and 8 had chronic disease), 14 of which were euthanized without treatment (7 had acute disease and 7 had chronic disease). Nine dogs (3 had acute disease and 6 had chronic disease) were lost to follow-up. Survival data for those dogs in which owners had an intention to treat demonstrated that median survival time of dogs with chronic disease (293 days; range, 7 to 959 days) was significantly (P = 0.0045) longer than that of dogs with acute disease (9 days; range, 1 to 120 days). Evaluation of physical examination and diagnostic findings revealed no significant differences between dogs euthanized at initial examination and those that were not.
Median survival time for the 14 untreated dogs (7 had acute disease and 7 had chronic disease) was 1 day (range, 0 to 5 days). Eight of these dogs had neoplastic or suspected neoplastic disease. No untreated dogs were documented as having any improvement in clinical signs or diagnostic findings during their follow-up period. Data regarding treatment were summarized (Table 1).
Outcomes of 17 of dogs receiving treatment for aortic thrombosis between 2000 and 2010.
| Type of treatment | Dosage range | No. of dogs | Median duration of treatment (d) | Resolved | Improved | No change | Chronic progression | Acute recurrence | Euthanized | Adverse effects |
|---|---|---|---|---|---|---|---|---|---|---|
| Acetylsalicylic acid | 0.5–0.7 mg/kg, q 24 h | 9 | 25 | 1 | 2 | 0 | 2 | 3 | 1 | NR |
| Acetylsalicylic acid and clopidogrel | 0.5–0.6 mg/kg, PO, q 24 h, and 1–2 mg/kg, PO, q 24 h | 3 | 16 | 1* | 1* | 0 | 1 | 1 | 0 | NR |
| Enoxaparin | 1 mg/kg, SC, q 12–24 h | 2 | 13 | 0 | 0 | 1 | 0 | 0 | 1 | NR |
| Enoxaparin and acetylsalicylic acid | 1 mg/kg, SC, q 12–24 h, and 0.5–0.6 mg/kg, q 24 h | 2 | 9 | 0 | 1 | 1* | 0 | 0 | 1*† | NR |
| Heparin | 90 U/kg, SC, q 8 h | 1 | 4 | 0 | 0 | 1 | 0 | 0 | 0 | NR |
| Rheolytic treatment | NA | 2 | NA | 0 | 0 | 1 | NA | NA | 1 | Necrotizing pancreatitis, acute renal failure |
| Surgical removal | NA | 1 | NA | 0 | 1* | 0 | 0 | NA | 1*† | Acute renal failure |
| t-PA and heparin | 0.2 mg/kg/h and 90 U/kg, SC, q 8 h | 1 | 2 + 10 | 0 | 1 | 0 | 0 | 0 | 0 | NR |
| Warfarin | NA | 2 | 103 | 0 | 2 | 0 | 0 | 0 | 0 | NR |
Indicates the same patient within a horizontal column.
Indicates the same patient within a vertical column.
NA = Information not available or not applicable. NR = None reported.
Resolution of clot was considered to have been achieved when a previously identified thrombus was found to be absent on abdominal ultrasonography. Improvement of clinical signs was considered to have occurred when improved exercise tolerance or improvement in degree of paresis was recorded. Chronic progression was considered to be present when gradual worsening of exercise intolerance, paresis, or both were documented. Acute recurrence was considered to have occurred when acute exacerbation of clinical signs was documented. Some patients received multiple treatments and are therefore represented in multiple rows.
Discussion
In the present study, aortic thrombosis was found to be a rare condition in dogs and accounted for only 0.0005% of hospital admissions during the 10-year study period. The initial clinical signs for dogs with aortic thrombosis differ from those seen in feline patients with ATE. Median survival time for dogs with chronic clinical signs was significantly longer than for dogs with acute signs. Despite treatment, outcomes were typically poor, although protracted survival time was achieved in some dogs in this series.
In cats, ATE is a disease characterized by acute clinical manifestation2 and recurrence is common.12 By contrast, approximately half of dogs of the present study and a previous report9 had chronic disease and recurrence rate was low. Similarly, hypothermia, severe underlying cardiac disease, cardiac murmur, severe left atrium enlargement, and congestive heart failure are common findings in cats with ATE2,8,17 but were found to be uncommon in dogs of the present study. These differences suggest that the pathophysiology underlying acute versus chronic aortic thrombosis in canine patients may be different. Therefore, the possibility of disease due to thrombosis in situ, rather than thromboembolism should be considered in dogs, although further investigation is needed to clarify whether this etiology is present in any or all cases.
In this study, survival time of dogs with chronic clinical signs was significantly (P = 0.04) longer than that of dogs with acute clinical signs and was also longer than reported survival time for cats.2,8 These survival differences are not explained by differences in the rate of euthanasia (18 dogs were euthanized [10 had acute disease and 8 had chronic disease]). There were no clear historical, clinical, or diagnostic differences between dogs that were euthanized and those that were treated. Reasons for euthanasia were rarely recorded but may have been influenced by suspected poor prognosis.
In the present study, mild azotemia (68%), hypoalbuminemia (53%), and proteinuria with a UPC > 0.5 (95%) were common findings. Only 4 dogs had prior chronic renal disease, and it is unclear whether the remaining dogs developed renal disease secondary to the aortic thrombus or whether renal disease was a predisposing factor. The finding that only 2 dogs had a renal artery thrombus and that all of the dogs with azotemia and proteinuria had low ATIII concentrations is suggestive of the latter. In human patients, chronic renal disease and low ATIII concentrations have been associated with a hypercoagulable state.18,19
Although the pathogenesis of aortic thrombosis in dogs is unknown, the presence of a hypercoagulable state is a reasonable assumption. Thromboelastography, in conjunction with standard coagulation profiles, has been used as an additional means for assessment of coagulation and presence of hypercoagulable state through measuring the speed and strength of clot formation.20,21 In this study, the results of thromboelastography analysis were consistent with a hypercoagulable state in 4 of the 5 dogs in which the test was performed. Although the number of cases was small, our findings suggested that thromboelastography may be a valuable supplemental diagnostic test for the evaluation of these patients at risk for thrombosis as well as potentially for response to treatment.20 Interestingly, in the present study, cardiac lesions were found in 4 of the 7 dogs without murmurs in which echocardiography was performed. This finding supports including echocardiography, regardless of the presence of a murmur, as part of routine diagnostic testing for dogs with aortic thrombosis.
Abdominal ultrasonographic findings suggest that the distal portion of the aorta and external iliac arteries are the most common site of aortic thrombi in dogs, accounting for 10 of 25 (40%) of dogs in this study. This site was second only to a more extensive thrombus involving the distal portion of the aorta, internal and external iliac arteries, and the femoral arteries seen in 7 of 25 (28%) dogs. Thirteen of 21 (62%) dogs had some flow through or around the thrombus. It was impossible from still images to evaluate the degree of blood flow; therefore, this finding is of unknown clinical importance at this time. Eight of 21 (38%) dogs of the present study had no documented flow through or around the thrombus. It is unknown from this study how this finding correlates with prognosis. There was a striking difference in the echogenicities of the thrombi detected with ultrasonography. The echogenicities varied from isoechoic to adjacent muscle to hyperechoic and hypoechoic to adjacent muscle. This may be related to the age of the thrombi and is likely related to the histologic composition of thrombi. The clinical relevance of this finding is unknown at this time and is an area that requires further research.
In human patients, aortic thrombosis occurring in the absence of underlying disease such as atherosclerosis or aortic aneurysm is rarely reported in the literature.22 No consensus exists in terms of optimal treatment strategy for human patients with aortic thrombosis. However, a recent report by Tsilimparis et al22 reviewed outcome for thrombectomy, thrombolytic treatment, and systemic anticoagulation alone as treatment options for aortic thrombosis. The authors concluded that anticoagulation treatment should represent the first line of treatment for patients with aortic thrombosis.22 Conservative medical treatment in human patients typically consists of IV administration of heparin followed by anticoagulation with orally administered warfarin derivatives (target INR, 2.5 to 3.5) and has been documented as resulting in complete resolution of the thrombus without recurrence.23,24 Optimal duration of heparin treatment and target INR have not been fully addressed in the literature. Calculation of INR is an important consideration for monitoring warfarin treatment because the reported PT varies between laboratories on the basis of the strength of the tissue thromboplastin reagent used for the test. Conversion of the patient's PT value to an INR allows for comparison of results between laboratories:
where ISI is the international sensitivity index, a measure of the tissue thromboplastin activity of the test. In the present study, both dogs receiving anticoagulant (warfarin) treatment with a target INR of 2 to 3 had an improvement in clinical signs, without recurrence of the aortic thrombus while they were receiving the medication. Both of these patients had acute recurrence after warfarin treatment was discontinued. Surgical treatment followed by anticoagulation and acetylsalicylic acid treatment has also been reported to result in thrombus resolution without recurrence in human patients; however, surgical intervention is typically reserved for patients with contraindications to long-term anticoagulation or with a mobile thrombus, due to high risk of embolism.23
The limitations of this study are inherent to a retrospective study and include lack of standardized examination, diagnostic, and treatment protocols. Additionally, there was inconsistency of patient follow-up, with 9 patients (3 with acute disease and 6 with chronic disease) eventually lost to follow-up. However, given that most dogs lost to follow-up had chronic disease, this was unlikely to have affected our acute versus chronic survival data and, if anything, resulted in underestimation of survival rate in the dogs with chronic disease. It is also possible that lack of information on survival rate of canine patients with aortic thrombosis may have influenced owner decision to euthanize, resulting in premature euthanasia in some patients. Further prospective study is required to determine the effect of treatment on thrombus resolution and survival rate in canine patients with aortic thrombosis.
In dogs with aortic thrombosis, underlying predisposing causes should be thoroughly evaluated at the time of initial examination. Particular emphasis should be placed on diagnosis of subclinical cardiac disease, renal disease, or presence of concurrent underlying neoplastic lesions. Currently, there is no consensus in the veterinary literature regarding the appropriate treatment of acute or chronic aortic thrombi in dogs. Protracted survival periods were documented in some canine patients with aortic thrombosis in the present study. This finding supports future prospective investigation of long-term treatment modalities for these patients.
ABBREVIATIONS
| ATIII | Antithrombin III |
| ATE | Aortic thromboembolism |
| INR | International normalized ratio |
| PT | Prothrombin time |
| t-PA | Tissue plasminogen activator |
| UPC | Urine protein-to-creatinine concentration ratio |
Hewlett Packard Sonos 5500 echocardiograph machine, Philips Medical Systems NA, Bothell, Wash.
Phillips IE33, Philips Healthcare, Andover, Mass.
JMP, version 8.0, SAS Institute Inc, Cary, NC.
Haemonetics TEG analyzer, Haemonetics Corp, Braintree, Mass.
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