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PubMed1981

Blood tests for the diagnosis of venous and arterial thrombosis.

There are many reports in the literature of blood test abnormalities occurring in patients with venous or arterial thrombosis. Most of these have not used acceptable criteria for establishing an association between thrombosis and blood tests and, therefore, their interpretation is questionable. Recently, sensitive and specific assays have been developed for the detection of products of intravascular thrombin formation, of plasmin digests of fibrin or fibrinogen and of platelet specific proteins that are released into the plasma when platelets react with stimuli. Blood abnormalities have been sought that can either predict or detect venous thrombosis. Many of the predictive tests evaluated are nonspecific acute phase reactant responses to inflammation; of these, only reduced fibrinolytic activity has been consistently reported to be associated with postoperative venous thrombosis. Hereditary antithrombin III deficiency has been consistently shown to predispose patients to venous thrombosis. Abnormalities of the plasminogen and fibrinogen molecule have also been described in patients with familial or recurrent venous thrombosis but these are rare and the association could be coincidental. Two blood tests, the fibrinopeptide A assay and the assay for fibrin/fibrinogen fragment E are highly sensitive to acute venous thromboembolism in symptomatic patients but both are nonspecific. Elevated levels of beta thromboglobulin and platelet factor 4 have been reported in patients with arterial thromboembolism but the sensitivity and specificity of these findings is presently unknown.

Antithrombin III↗
PubMed1978

[Recurrent familial thromboembolic disease due to congenital deficiency in anti-thrombin III. Preliminary study of 3 cases (author's transl)].

The three cases reported, two mesenteric venous infarctions and one asymptomatic carrier, prove the responsibility of the anti-thrombin III deficiency in the development of apparently primary entero-mesenteric venous infarctions. Thus such a deficiency should be sought routibs. Furthermore, these 3 cases confirm the usual characteristics of the 10 familial cases collected since the princeps description of Egeberg: recurrent thromboembolic disease in the young subject involving essentially the lower limbs, relative resistance to heparin, family history of thromboembolic disease confirming the hereditary nature of the disease with dominant transmission, laboratory confirmation of the quantitative deficiency in antithrombin III, the levels and activity of which are reduced by half, and decrease in laboratory sensitivity to heparin contrasting with normal clotting studies. The family history reveals associated conditions within the syndrome: asthma and Biermer's anemia as well as similarities in leucocyte HLA groups.

Antithrombin III Deficiency↗
PubMed2005

Thrombophilia is significantly associated with severe preeclampsia: results of a large-scale, case-controlled study.

The role of thrombophilia in the pathogenesis of preeclampsia is controversial. The aim of this case-controlled study was to determine whether thrombophilia increases the risk of preeclampsia or interferes with its clinical course. A total of 808 white patients who developed preeclampsia (cases) and 808 women with previous uneventful pregnancies (controls) matched for age and parity were evaluated for inherited and acquired thrombophilia (factor V Leiden; factor II G20210A; methylenetetrahydrofolate reductase C677T; protein S, protein C, and antithrombin III deficiency; anticardiolipin antibodies; lupus anticoagulant; and hyperhomocysteinemia). Odds ratios (ORs) with 95% confidence intervals (CIs) for risk of being carriers of thrombophilia in cases compared with controls and for risk of maternal life-threatening complications and adverse perinatal outcomes in preeclamptic patients with or without thrombophilia were calculated. Women with severe preeclampsia (406 cases) had a higher risk (OR, 4.9; 95% CI, 3.5 to 6.9) of being carriers of either an inherited or acquired thrombophilic factor, except for protein S, protein C, and antithrombin deficiency. In women with mild preeclampsia (402 cases), only prothrombin and homozygous methylenetetrahydrofolate reductase gene mutations were significantly more prevalent than in the controls. Thrombophilic patients with severe preeclampsia are at increased risk of acute renal failure (OR, 1.8; 95% CI, 1.5 to 2.2), disseminated intravascular coagulation (OR, 2.7; 95% CI, 1.1 to 6.4), abruptio placentae (OR, 2.6; 95% CI, 1.2 to 6.0) and perinatal mortality (OR, 1.7; 95% CI, 1.5 to 2.2) compared with nonthrombophilic preeclamptic patients. Our study demonstrates a significant association between maternal thrombophilia and severe preeclampsia in white women. Thrombophilia also augments the risk of life-threatening maternal complications and adverse perinatal outcomes in preeclamptic patients.

Case-Control Studies↗
PubMed2002

Hematological risk factors for coronary heart disease.

Coronary heart disease (CHD) is a leading cause of morbidity and mortality in the developed and developing countries. Several underlying genetic and environmental factors have been implicated in its etiology. Some of the hematological risk factors implicated in the development of coronary heart disease include antithrombin III deficiency, protein C and protein S deficiency, factor V Leiden mutation, prothrombin gene (20210A) mutation hyperhomocystinaemia, elevated factor VIII levels, plasminogen activator inhibitor type 1 and dysfibrinogenaemia. In general, these factors result in thrombosis, thus having a negative effect on the heart and blood vessels. This paper presents an overview of some of the hematological risk factors involved in the development of CHD.

Antithrombins↗
PubMed2000

Factor V Leiden and antiphospholipid antibodies are significant risk factors for ischemic stroke in children.

BACKGROUND AND PURPOSE: The association between ischemic childhood stroke and thrombophilia has been debated. We studied the prevalence of thrombophilia risk factors in 65 unrelated children with ischemic stroke compared with 145 control subjects. METHODS: Patients and control subjects were tested for antithrombin protein C and protein S deficiencies, the presence of antiphospholipid antibodies (APLA), factor V Leiden (FVL), G20210A polymorphism of factor II gene (FII G20210A), and C677T polymorphism of 5,10-methylenetetrahydrofolate reductase gene (C677T MTHFR). RESULTS: Of 65 children, 7 had a stroke in the neonatal/perinatal period and therefore were analyzed separately. Thirty-one of the remaining 58 patients with pediatric stroke (53.4%) were found to have at least 1 thrombophilia marker compared with only 25.5% of control subjects. None of the patients or control subjects had protein S or antithrombin III deficiency. The prevalence of protein C deficiency was higher among pediatric stroke patients than among control subjects, but the difference was not statistically significant (OR=7, 95% CI 0.75 to 65.1). Heterozygous FII G20210A and homozygous MTHFR 677T were not associated with an increased risk for stroke (OR=1.29, 95% CI 0.2 to 8.2; and OR=1.06, 95% CI 0.4 to 2.7, respectively). In contrast, the presence of APLA was associated with a >6-fold risk of stroke (OR=6. 08, 95% CI 1.5 to 24.3), and the heterozygosity for FVL increased the risk of stroke by almost 5-fold (OR=4.82, 95% CI 1.4 to 16.5). Five patients with pediatric stroke had a combination of > or =2 thrombophilia markers, whereas none of the control subjects had a combination of the markers. Most of the patients with neonatal/perinatal stroke were found to have at least 1 thrombophilia marker. CONCLUSIONS: These data suggest that the prevalence of thrombophilia markers is increased in children with stroke compared with control subjects and, specifically, that FVL and APLA contribute significantly to stroke occurrence.

3' Untranslated Regions↗
PubMed2002

Thrombophilia is common in women with idiopathic pregnancy loss and is associated with late pregnancy wastage.

OBJECTIVE: To describe the characteristics of thrombophilia in women with idiopathic pregnancy loss. DESIGN: Prospective observational study. SETTING: Tertiary referral center in a teaching academic hospital. PATIENT(S): One hundred forty-five patients with repeated pregnancy loss and 145 matched controls. INTERVENTION(S): Prospective assessment of thrombophilia in patients and controls. MAIN OUTCOME MEASURE(S): Prevalence of activated protein C (APC) resistance, protein C, protein S, and antithrombin III deficiencies, antiphospholipid antibodies, factor V Leiden, factor II G20210A, and MTHFR C677T mutations. RESULT(S): At least one thrombophilic defect was found in 66% of study group patients compared with 28% in control group patients. Combined thrombophilic defects were documented in 21% of women with pregnancy loss compared with 5.5% of control patients. Late pregnancy wastage occurred more frequently in women with thrombophilia compared with women without thrombophilia (160/429 [37%] vs. 39/162 [24%], respectively). APC resistance was documented in 39% of women with pregnancy loss compared with 3% of the control patients. APC resistance without factor V Leiden mutation was documented in 18% of women with pregnancy loss compared with none of the controls. While factor V Leiden mutation was more common in women with pregnancy loss (25% vs. 7.6%), factor II G20210A and homozygosity for MTHFR C677T contributed to pregnancy loss only in the presence of other thrombophilia. CONCLUSION(S): Thrombophilia was found in the majority (66%) of women with idiopathic pregnancy loss. APC resistance with or without factor V Leiden mutation is the most common thrombophilic defect, and combined thrombophilia is a frequent finding in women with pregnancy loss. Thrombophilia is associated with increased frequency of late pregnancy wastage.

Abortion, Habitual↗
PubMed2004

Heparinless cardiopulmonary bypass with argatroban in dogs.

OBJECTIVES: Systemic heparinization is usually required for cardiopulmonary bypass (CPB). However, problems such as heparin-induced thrombocytopenia, protamine shock, and antithrombin III deficiency exist related to CPB with heparinization. The aim of this study was to evaluate argatroban (ARG) as a substitute for heparin during CPB. METHODS: In the pilot study, blood samples were sequentially obtained from dogs with continuous infusion of ARG at a dose of 10 (n = 6), 20 (n = 6), or 30 (n = 6) microg/kg per min for 2 h without CPB. In the main study, dogs underwent CPB for 2 h with 10 (n = 6) or 30 (n = 6) microg/kg per min of ARG or with heparin with blood samples obtained sequentially. Thrombogenicity in each group was evaluated by observation of the blood-contacting surfaces of the CPB circuits with scanning electron microscopy (SEM). Evidence of thromboembolism in the dogs was also investigated in histological specimens of the kidney and spleen in addition to microscopic observation at autopsy. RESULTS: In the pilot study, the activated coagulation time (ACT) reached a maximum level dose-dependently after continuous infusion of ARG for 30 min. ACT returned to the baseline value within 60 min after the termination of continuous infusion. In the main study, CPB with 30 microg/kg per min of ARG achieved thrombin-antithrombin III complex (TAT) level similar to that achieved by CPB with heparin. Platelet count with 30 microg/kg per min of ARG tended to be higher than that with heparin or 10 microg/kg per min of ARG. The SEM appearance of blood-contacting surfaces of the CPB circuits after infusion with 30 microg/kg per min of ARG appeared to be similar to that after infusion with heparin. Depositions on the blood-contacting surfaces of the CPB circuits were also frequently observed with 10 microg/kg per min of ARG. CONCLUSIONS: Coagulability related to CPB was controlled by the appropriate ARG dosage without the use of heparin in dogs. ARG may be a substitute for heparin in CPB.

Animals↗
PubMed1990

[Anti-coagulant therapy--antithrombin III].

Biological properties and the efficacy of AT III concentrate for the treatment of thromboembolic disorders were evaluated in the patients with AT III deficiency. Commercially available AT III concentrates showed heterogeneity on agarose gel isoelectric focusing, however, they inhibited thrombin in the same manner. At III concentrates were infused to 11 patients with congenital AT III deficiency (4 with thrombosis). Pharmacokinetic parameters of infused AT III were calculated as follows; half time 61.1 +/- 23.0 hr. (58.4 +/- 22.6 hr. in the cases with thrombosis), max increase rate 1.01 +/- 0.3%/U/kg and recovery rate 95.4 +/- 33.3%. Simulation curves adjusted to the multiple administration were correlated well with the actually determined values in the patients and steady state concentration of AT III was achieved by the administration of this concentrate in 12 or 24 hour intervals. Clinically, substitution with AT III concentrate was proved to be effective for the treatment of thromboembolism in these patients. 16 patients with disseminated intravascular coagulation were treated with heparin (6,000 U/day) followed by AT III concentrate (1,500 U/day) administration. Clinical symptoms and laboratory findings were improved in 11 patients. From these results substitution with AT III concentrate was suggested to be beneficial for the prevention or the treatment of thromboembolic disorders in the patients with AT III deficiency.

Antithrombin III↗
PubMed2005

Inherited antithrombin deficiency and end stage renal disease.

Antithrombin is a potent inhibitor of the coagulant effect of thrombin. In the latter half of 20th century, many families have been described in which an autosomaly dominant inherited antithrombin deficiency has caused severe venous thromboembolic disease in successive generations. The important complication is severe venoocclusive disease by deep venous thrombus. Some inherited antithrombin deficient patients developed renal failure because of fibrin deposition in the kidney glomeruli or renal vein thrombus, and therefore the need for replacement therapy for end stage renal disease (ESRD). Although an inherited antithrombin deficiency with renal failure is rare, prevention against renal failure in such patients, and their renal replacement therapy for ESRD are important. Proteinuria decreases plasma antithrombin level leading to more severe hyper-coagulation state. Therefore early in renal disease, it may be prudent for adaptation of anti-coagulation therapy even if recurrent thrombosis has not occurred. All replacement therapy (hemodialysis, transplantation or peritoneal dialysis) for ESRD are available for such thrombophilic disorders. Anticoagulation agents working without aggravation of antithrombin effects (Argatroban, Nafamostat mesilate etc.) are useful for hemodialysis. The renal allograft recipients with thrombophilia seem to be at risk of developing an acute rejection or other vascular event. Peritoneal dialysis is potentially a good adaptation for such thrombophilic disorders. However which therapy has the best mortality and morbidity outcomes is not clear. Physicians and Surgeons must pay attention to the coagulation state and thrombophilia in ESRD patients, give strong consideration for adequate anti-coagulation therapy and review the best renal replacement modality for each patient.

Animals↗
PubMed1998

Antithrombins Wibble and Wobble (T85M/K): archetypal conformational diseases with in vivo latent-transition, thrombosis, and heparin activation.

The inherent variability of conformational diseases is demonstrated by two families with different mutations of the same conserved aminoacid in antithrombin. Threonine 85 underlies the opening of the main beta-sheet of the molecule and its replacement, by the polar lysine, in antithrombin Wobble, resulted in a plasma deficiency of antithrombin with an uncharacteristically severe onset of thrombosis at 10 years of age, whereas the replacement of the same residue by a nonpolar methionine, antithrombin Wibble, gave near-normal levels of plasma antithrombin and more typical adult thromboembolic disease. Isolated antithrombin Wibble had a decreased thermal stability (Tm 56.2, normal 57.6 degreesC) but was fully stabilized by the heparin pentasaccharide (Tm 71.8, normal 71.0 degreesC), indicating that the prime abnormality is a laxity in the transition of the main sheet of the molecule from the 5- to 6-stranded form, as was confirmed by the ready conversion of antithrombin Wibble to the 6-stranded latent form on incubation. That this transition can occur in vivo was shown by the finding of nearly 10% of the proband's plasma antithrombin in the latent form and also, surprisingly, of small but definitive amounts of latent antithrombin in normal plasma. The latent transition will be predictably accelerated not only by gross mutations, as with antithrombin Wobble, to give severe episodic thrombosis, but also by milder mutations, as with antithrombin Wibble, to trigger thrombosis in the presence of other predisposing factors, including the conformational stress imposed by the raised body temperatures of fevers. Both antithrombin variants had an exceptional (25-fold) increase in heparin affinity and this, together with an increased inhibitory activity against factor Xa, provides evidence of the direct linkage of A-sheet opening to the conformational basis of heparin binding and activation.

Amino Acid Substitution↗
PubMed2006

Recombinant human antithrombin expressed in Chinese hamster ovary cells shows in vivo efficacy on rat DIC model similarly to plasma-derived antithrombin regardless of different N-glycosylation.

Plasma-derived human antithrombin (pAT) is used for the treatments of disseminated intravascular coagulation (DIC) and hereditary antithrombin deficiencies. We expressed recombinant human antithrombin (rAT) in Chinese hamster ovary (CHO) cells. The purified rAT is composed of 55% alpha-isoform and 45% beta-isoform. The structure of the N-linked oligosaccharides of rAT is the same biantennary complex type as previously found in pAT with less sialylated on the non-reducing ends. Most of the oligosaccharides of rAT are fucosylated at the reducing ends of N-acetylglucosamine, while those of pAT are not fucosylated. Despite of the difference in sialylation and fucosylation of the oligosaccharide units, rAT and pAT showed indistinguishable heparin cofactor and progressive activities, and they bound to thrombin in a one-to-one stoichiometric manner. In lipopolysaccharide (LPS)-induced and thromboplastin-induced DIC rat models, rAT reduced fibrinogen and platelet consumption to a similar extent with pAT. In LPS-induced DIC model, both ATs similarly restrained the increase of alanine aminotransferase and aspartate aminotransferase activities. Finally, pharmacokinetic analysis showed that both ATs had similar half-lives in the circulation of normal rats. Together, the present study demonstrated that rAT prepared in CHO cells has potential for a substitute of pAT in therapeutic use.

Alanine Transaminase↗
PubMed1990

A hypercoagulable state follows orthotopic liver transplantation.

Orthotopic liver transplantation may be associated during the postoperative period with hepatic artery thrombosis, a catastrophic occurrence generally necessitating emergency retransplantation. To assess the contribution of the coagulation mechanism to this complication, the levels of procoagulant and anticoagulant proteins were followed in 41 liver transplant patients during the first 10 postoperative days. The mean activities of all procoagulant factors reach normal values on day 1 except for factors V and VII, which achieve normal activity by day 3. Supernormal levels of factor VIII activity and antigen are noted (peak values on day 5 of 334% +/- 113% and 481% +/- 260%, respectively). The anticoagulant proteins show delayed recovery, with deficient antithrombin III levels seen in 81% of patients on day 3 and 57% on day 5. Similarly, proteins C and S are subnormal in 24% and 21%, respectively on day 3, and 20% and 10%, respectively, on day 5. During this period, elevated levels of thrombin/antithrombin complexes are encountered, reflecting in vivo activation of the coagulation mechanism. Activated thrombin is, therefore, being generated at a time when a decrease in the major regulatory anticoagulant proteins exists. These data suggest an imbalance between the hemostatic and thrombotic mechanisms and indicate a sustained prothrombotic state that may contribute to the risk for hepatic artery thrombosis. Using a regimen of low-dose heparin and fresh frozen plasma infusion, no thromboses have been seen in 65 consecutive liver transplants.

Blood Coagulation Disorders↗
PubMed1993

Thrombectomy with arteriovenous fistula for embolizing deep venous thrombosis: an alternative therapy for prevention of recurrent pulmonary embolism.

Thrombectomy with arteriovenous fistula was performed between 1977 and 1988 in 103 patients (41 females, 62 males, mean age 46.7 years, 114 involved extremities) with embolizing deep-vein thrombosis (DVT). The sole aim of the surgical procedure was prevention of recurrent embolization. On the basis of the proximal extent of the thrombosis the source of embolization was identified as the iliac veins or inferior vena cava in 63% of the patients; 48% presented with a post-phlebitic vein and/or an older thrombosis, and 46% had already had recurrent pulmonary emboli. Unsuccessful aggressive procedures had been carried out previously in 11%. The rate of intraoperative pulmonary embolism (PE) was 3% (one fatal case). The perioperative mortality was 6.8%, but only one death was related to the surgical treatment itself. During follow-up (8-140 months postoperatively, mean 55 +/- 34 months) late recurrent PE was confirmed in two patients (antithrombin III deficiency, contralateral DVT) and was reported as the suspected cause of death in a third (3.6%). Venous thrombectomy with arteriovenous fistula is a reliable and effective procedure for management of embolizing DVT and is indicated especially in young patients. The rates of early- and late-recurrent PE are low, introduction of artificial material into the vein can be avoided, and long-term preservation of valve function is occasionally possible.

Adolescent↗
PubMedDate not supplied

Acquired and congenital clotting syndromes.

Although Virchow postulated 100 years ago that hypercoagulability states exist, it has only been in recent years that methods of documenting hypercoagulability have been developed. These clotting tendencies can be acquired or congenital. The common causes of acquired clotting tendencies include conditions which result in tissue and cellular damage, shock, transfusion reactions, and tissue necrosis. Certain drugs and drug reactions, and certain disease states which include blood dyscrasias and cancer are also associated with clotting problems. In certain diseases such as homocystinuria, hyperlipidemia, and lupus erythematosus, abnormal clotting tendencies may also develop. Important advances in the recognition of hypercoagulability have come with the documentation that congenital clotting abnormalities exist. Moreover, these abnormalities are proving to be more common than are congenital bleeding syndromes. Patients who appear to have spontaneous clotting manifestations and are under 40 years of age should be screened for one of these abnormalities. These congenital clotting tendencies can be classified as defects in thrombosis inhibitors, dysfibrinogenemias, or defects in fibrinolysis. The first thrombotic inhibitor defect recognized was antithrombin III deficiency which was reported in 1965. Subsequently, Protein C, Protein S, and Heparin cofactor II deficiencies have been recognized as contributing to thrombotic tendencies. Dysfibrinogenemias are relatively rare and most are associated with bleeding problems; however, 11% of the abnormal fibrinogens are associated with a clotting tendency. The reason appears to be that these fibrins are resistant to fibrinolysis. The most common defects which are associated with thrombotic tendencies appear, at the present time, to be due to defects in fibrinolysis. These include hypoplasminogenemia, decreases in plasminogen activator, increases in plasminogen activator inhibitor, and Factor XII deficiency.

Blood Coagulation Disorders↗
PubMed1991

Hirudin, a new therapeutic tool?

Hirudin is the most potent natural inhibitor of thrombin known to date. It is gaining popularity as an anticoagulant now that recombinant and synthesized forms are available. It is a monospecific and co-factor-independent thrombin inhibitor with otherwise inert pharmacological properties. Being a surprisingly weak immunogen, its administration has exhibited no side effects, particularly on platelets. Bleeding complications are not to be expected at therapeutic doses. Effective anticoagulatory doses can be easily predicted and laboratory control is no problem. Application of hirudin or derivatives thereof may be indicated for: prophylaxis and treatment of postoperative venous thrombosis and diffuse microthrombosis; prevention of arterial thrombosis, especially in cardiac surgery; enhancement of fibrinolytic therapy and/or angioplasty to prevent reocclusion; extracorporeal circulation; and plastic surgery. Hirudin may be a particularly useful alternative anticoagulatory agent in patients sensitized to heparin or in patients with hereditary or acquired antithrombin III deficiency. However, whether hirudin is really an effective therapeutic tool and whether it can replace heparin in certain clinical indications can be judged only after extended clinical experience has been accumulated.

Animals↗
PubMed2005

Evaluation of thrombotic children with malignancy.

The purpose of this study was to evaluate inherited and acquired prothrombotic risk factors among children with malignancies who have thrombosis and emphasize the importance of inherited prothrombotic risk factors. Thirty-seven consecutive children with thrombosis and malignancy were included in this study. The patients were evaluated separately for time of development of thrombosis, insertion of a central venous line (CVL), history of L: -asparaginase usage, and recent infections. Prothrombotic risk factors such as factor V G1691A and prothrombin G20210A mutation, protein C, protein S, antithrombin III deficiencies, factor VIII and lipoprotein(a) elevation, and antiphospholipid antibodies were analyzed for all patients. Of 387 children with thrombosis, 37 (9.5%) had a malignancy. Thrombosis was detected in 9 patients at the time of diagnosis, during maintenance therapy in 25 patients, and after the discontinuation of treatment in 3 patients. One or two additional prothrombotic risk factors other than L: -asparaginase therapy and insertion of central venous lines were present in 20 of these patients (54%). It was found that eight patients had the factor V G1691A mutation in the heterozygote state. One of them had the factor V G1691A mutation associated with a history of infection and one patient had the factor V G1691A mutation associated with factor VIII elevation. One had the the prothrombin G20210A mutation in the heterozygote state, four had lipoprotein(a) elevation, two had factor VIII elevation, one had a decreased protein S level, one had a decreased protein C level, one had antiphospholipid positivity, and two had histories of infection. Malignancy is an important risk factor for the development of childhood thrombosis. However, the risk of thrombosis increases when accompanied by additional prothrombotic risk factors. For this reason, especially children with malignancy and at high risk for the development of thrombosis, such as those who have received L: -asparaginase or a replaced CVL during their therapy, might be screened for additional prothrombotic risk factors and appropriate measures might be taken to prevent the development of thrombosis.

Activated Protein C Resistance↗
PubMed2002

Comparing the interpretations of CT pulmonary angiograms by attending and resident radiologists: can residents identify life-threatening pulmonary emboli in hospitalized patients?

OBJECTIVE: CT pulmonary angiography is now often the first-line investigation for pulmonary emboli. When these studies are performed after hours in teaching hospitals, they are often initially interpreted by trainees. It is of great significance whether the interpretations of trainees and certified radiologists with regard to the presence of pulmonary emboli on CT pulmonary angiograms correspond, because of the morbidity and mortality of both the condition and its treatment. MATERIAL AND METHODS: Twenty-five consecutive CT pulmonary angiograms (CTPAs) of hospitalized patients were viewed at lung and soft tissue windows both on a workstation and on hard copies, at the observers' discretion. Each CTPA was divided into 28 arterial zones based on pulmonary anatomy (including the subsegmental arteries), giving a total of 700 arterial zones, and analyzed retrospectively and independently by two cross-sectional imaging specialists and four residents. Each arterial segment was rated with regard to pulmonary embolus as either high, intermediate, or low probability or not visualized. The kappa (Kappa) test, which tests for interobserver agreement, was used for statistical analysis. RESULTS: At the time of the scan all patients were hospitalized for underlying conditions. Of the 25 patients studied, 9 were referred from the ICU, 7 experienced severe acute shortness of breath and respiratory failure, 5 were post-partum women, 2 had had a recent stroke, 1 patient had antithrombin III deficiency, and 1 had a diagnosis of breast cancer. The incidence of pulmonary emboli was 44%. For the main pulmonary arteries interobserver agreement was good (Kappa=0.61) and for the segmental pulmonary arteries it was fair (Kappa=0.26). For the subsegmental arteries interobserver agreement was poor (Kappa=0.16). The zones where interobserver agreement was greatest (Kappa>0.4) were the left main, left lower lobe, and the right main pulmonary arteries. Interobserver agreement was poorest (Kappa<0.05) in the left interlobar, left lower lobe lateral basal segment, right lower lobe superior segment, and left lower lobe superior segment branches. None of the patients expired due to pulmonary emboli. CONCLUSION: Most life-threatening pulmonary emboli requiring urgent treatment are the more central emboli. This study demonstrates that trainees and certified radiologists can make similar conclusions regarding these central pulmonary emboli in hospitalized patients and that preliminary interpretations by trainees should not therefore adversely affect patient care.

Journal Article↗