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PubMed1984

Left ventricular thrombosis and cerebrovascular accident in acute myocardial infarction.

In a prospective study of 90 consecutive patients with acute myocardial infarction, 15 (28.3%) of 53 patients with an anterior wall infarction developed a left ventricular thrombosis diagnosed by cross sectional echocardiography. Patients received anticoagulants only after a left ventricular thrombosis had been diagnosed. Twenty eight patients had an inferior infarction, but none of these had a left ventricular thrombosis. Five (5.5%) of the 90 patients suffered a cerebrovascular accident, and all had an anterior wall infarction. In four of these five patients a left ventricular thrombosis was confirmed by echocardiography before the cerebrovascular accident. All patients with left ventricular thrombosis had apical akinesis. The incidence of a thrombosis did not differ in patients with a first anterior myocardial infarction and with reinfarctions. Among the 40 patients with a first anterior wall infarction, 12 with a thrombosis had a significantly higher incidence of enlarged heart on chest radiographs and significantly higher serum aspartate aminotransferase enzyme activity than those without. Thus patients with a large anterior wall infarction and with akinesis in the apical region are at high risk of developing a left ventricular thrombosis, which may be a source of peripheral emboli. Left ventricular thrombosis appears to be rare with infarctions in other locations.

Aspartate Aminotransferases↗
PubMed1986

Asynchronous left ventricular wall motion early after coronary thrombosis.

To study regional wall motion early in the development of acute myocardial infarction, left ventriculograms performed in 24 patients before thrombolysis and within 3.5(1.2) (mean (SD] hours of the onset of pain were digitised frame by frame. Isometric and contour plots of regional wall motion were constructed. In 19 patients (seven with anterior descending, eight with right, and four with circumflex disease) thrombosis was demonstrated on an underlying stenosis. In 10 patients the two remaining coronary arteries were normal, and in nine, one or both showed important disease. Mean values of global indices of left ventricular function, including end diastolic volume, ejection fraction, peak ejection and filling rates, and cavity shape changes were all within normal limits, though end systolic volume was significantly raised. Total systolic amplitude of wall motion was normal in the affected area in all but seven patients (four with anterior descending, two with right, and one with circumflex thrombosis). Dyskinesis of more than 2 mm was seen in only three patients, all with thrombosis of the anterior anterior descending coronary artery, and hyperkinesis was present in four. The commonest abnormality of wall motion was hypokinesis during ejection followed by prolonged inward motion during isovolumic relaxation, which was seen in four patients with anterior descending, seven with right, and three with circumflex artery thrombosis. This was preceded by outward motion during isovolumic contraction and delayed inward motion during ejection in eight with right or circumflex thrombosis. Five of six patients without thrombosis had simple hypokinesis or dyskinesis without asynchrony. Disease of other coronary arteries did not affect the pattern of wall motion seen after right or circumflex coronary artery occlusion but it reduced the incidence of delayed inward motion along the free wall after thrombosis of anterior descending artery. Thus early after acute coronary thrombosis asynchronous wall motion is commoner than simple hypokinesis or dyskinesis. Its persistence suggests that in the setting of coronary artery thrombosis in man, residual contractile activity may persist for up to six hours after the onset of symptoms.

Acute Disease↗
PubMed1996

Prophylaxis against deep venous thrombosis after total knee arthroplasty. Pneumatic plantar compression and aspirin compared with aspirin alone.

A prospective, randomized study was conducted to assess the efficacy of pulsatile pneumatic plantar compression for prophylaxis against deep venous thrombosis after total knee arthroplasty performed with use of regional anesthesia. One hundred and twenty-two patients (164 knees) who were scheduled to have a unilateral or a one-stage bilateral total knee arthroplasty were separately randomized to be managed with either aspirin alone or the pulsatile pneumatic plantar-compression device and aspirin. The prevalence of deep venous thrombosis was 27 per cent (twenty-two of eighty-one knees) in the group treated with pneumatic plantar compression compared with 59 per cent (forty-nine of eighty-three knees) in the patients managed with aspirin alone (the control group) (p < 0.001). A significant difference was also noted in the group that had had a unilateral arthroplasty (a prevalence of 27 per cent [eleven of forty-one knees] in the group treated with pneumatic plantar compression, compared with 67 per cent [twenty-six of thirty-nine knees] in that treated with aspirin alone; p < 0.006) and in the group that had had a one-stage bilateral procedure (a prevalence of 28 per cent [eleven of forty knees] in the group treated with pneumatic plantar compression, compared with 52 per cent [twenty-three of forty-four knees] in that treated with aspirin alone; p < 0.03). No proximal thrombi were noted in any patient who used the pulsatile pneumatic plantar-compression device, while the prevalence of proximal thrombosis in the popliteal or femoral veins was 14 per cent (twelve of eighty-three knees) in the group treated with aspirin alone (p < 0.0003). In the group treated with a unilateral procedure and aspirin alone the prevalence of proximal thrombosis was 13 per cent (five of thirty-nine knees; p < 0.02), while in the group treated with a bilateral procedure and aspirin alone it was 16 per cent (seven of forty-four knees; p < 0.01). Only in the patients who had had a unilateral procedure was use of the compression device associated with significantly less edema postoperatively than was use of aspirin alone. The change between the preoperative and postoperative circumferences of the thigh and leg was significantly less (9 +/- 4.1 millimeters [mean and standard deviation] less for the thigh [p < 0.01] and 6 +/- 3.9 millimeters less for the leg [p < 0.049]) with the compression device than with aspirin alone. In addition, there was significantly less mean drainage (98 +/- 61.1 milliliters) in the group treated with a unilateral procedure and pneumatic compression, compared with that treated with a unilateral procedure and aspirin alone (p < 0.041). An internal timer of the compression device was used to assess the compliance of the patient with use of the device, and a relationship between deep venous thrombosis and the total duration of treatment with the device was found. The patients in whom deep venous thrombosis did not develop used the device for a mean of 96 +/- 23.4 hours (range, sixty to 164 hours) postoperatively, or 19.2 +/- 5.1 hours a day, while those in whom thrombosis developed used it for a mean of 67 +/- 21.1 hours (range, twenty-six to 101 hours), or 13.4 +/- 4.3 hours a day (p < 0.001). No untoward effects were noted in any patient who used the device. This study confirms the safety and efficacy of pulsatile pneumatic plantar compression and aspirin compared with aspirin alone and supports the use of mechanical compression for prophylaxis against deep venous thrombosis and for reduction of edema in patients who have had a total knee arthroplasty. In addition, we found a direct relationship between compliance with the use of this device and its efficacy in reducing deep venous thrombosis.

Arthritis, Rheumatoid↗
PubMed1997

Venous thrombosis of pancreatic transplants: diagnosis by duplex sonography.

OBJECTIVE: Our objective was to determine whether elevated pancreatic transplant arterial resistive index (RI) and absence of venous flow correlate with pancreatic transplant venous thrombosis. MATERIALS AND METHODS: Thirteen episodes of surgically documented pancreatic venous thrombosis occurred in 175 pancreases that had been transplanted over a 3-year period. Duplex sonography was performed before surgical exploration in 11 cases. We retrospectively reviewed these 11 sonograms to determine whether blood was flowing in the veins and arteries of the graft. The RI was calculated from all pancreatic artery waveforms. We compared these arterial RIs and the presence or absence of venous flow with those of pancreatic grafts without venous thrombosis to determine sensitivity and specificity. RESULTS: In the venous thrombosis group, thrombosis occurred within 12 days of transplantation (mean, 3.5 days) in all 11 cases. Six cases of thrombosis (55%) occurred within 1 day. Arterial flow was detected within the graft in nine cases (82%) and in the stump of the donor artery between the graft and the recipient iliac artery in the two remaining cases. Antegrade diastolic flow was absent in all arterial tracings. Diastolic flow reversal was present in seven (78%) of nine grafts with detectable intrapancreatic arterial flow. Arterial RIs ranged from 1.00 to 2.00 (mean +/- SD, 1.27 +/- 0.29). Intrapancreatic venous flow was absent in all 11 cases. In the control group (43 examinations in 34 patients) RIs ranged from 0.46 to 1.29 (mean +/- SD, 0.72 +/- 0.18). Two of 43 arterial tracings had diastolic flow reversal (RI > 1.0). Venous flow was present in all examinations in the control group. A statistically significant difference existed between the RIs in the thrombosis group and the RIs in the control group (p = .0001). CONCLUSION: Reversal of diastolic flow in pancreatic transplant arteries is highly specific for detection of graft venous thrombosis during the first 12 days after transplantation. Our findings suggest that an RI greater than or equal to 1.00 and absence of venous flow, in combination, are highly sensitive and specific for the diagnosis of pancreatic graft venous thrombosis.

Adult↗
PubMed1996

The long-term clinical course of acute deep venous thrombosis.

BACKGROUND: In patients who have symptomatic deep venous thrombosis, the long-term risk for recurrent venous thromboembolism and the incidence and severity of post-thrombotic sequelae have not been well documented. OBJECTIVE: To determine the clinical course of patients during the 8 years after their first episode of symptomatic deep venous thrombosis. DESIGN: Prospective cohort study. SETTING: University outpatient thrombosis clinic. PATIENTS: 355 consecutive patients with a first episode of symptomatic deep venous thrombosis. MEASUREMENTS: Recurrent venous thromboembolism, the post-thrombotic syndrome, and death. Potential risk factors for these outcomes were also evaluated. RESULTS: The cumulative incidence of recurrent venous thromboembolism was 17.5% after 2 years of follow-up (95% CI, 13.6% to 22.2%), 24.6% after 5 years (CI, 19.6% to 29.7%), and 30.3% after 8 years (CI, 23.6% to 37.0%). The presence of cancer and of impaired coagulation inhibition increased the risk for recurrent venous thromboembolism (hazard ratios, 1.72 [CI, 1.31 to 2.25] and 1.44 [CI, 1.02 to 2.01], respectively). In contrast, surgery and recent trauma or fracture were associated with a decreased risk for recurrent venous thromboembolism (hazard ratios, 0.36 [CI, 0.21 to 0.62] and 0.51 [CI, 0.32 to 0.87], respectively). The cumulative incidence of the post-thrombotic syndrome was 22.8% after 2 years (CI, 18.0% to 27.5%), 28.0% after 5 years (CI, 22.7% to 33.3%), and 29.1% after 8 years (CI, 23.4% to 34.7%). The development of ipsilateral recurrent deep venous thrombosis was strongly associated with the risk for the post-thrombotic syndrome (hazard ratio, 6.4; CI, 3.1 to 13.3). Survival after 8 years was 70.2% (CI, 64.7% to 75.6%). The presence of cancer increased the risk for death (hazard ratio, 8.1; CI, 3.6 to 18.1). CONCLUSION: Patients with symptomatic deep venous thrombosis, especially those without transient risk factors for deep venous thrombosis, have a high risk for recurrent venous thromboembolism that persists for many years. The post-thrombotic syndrome occurs in almost one third of these patients and is strongly related to ipsilateral recurrent deep venous thrombosis. These findings challenge the widely adopted use of short-course anticoagulation therapy in patients with symptomatic deep venous thrombosis.

Adult↗
PubMed1996

Importance of findings on the initial evaluation for cancer in patients with symptomatic idiopathic deep venous thrombosis.

BACKGROUND: The relation between thrombosis and cancer is well documented, but the clinical evaluation appropriate for detecting underlying cancer in patients with deep venous thrombosis remains unknown. OBJECTIVES: To 1) determine the appropriate initial evaluation for cancer in patients with idiopathic deep venous thrombosis and 2) estimate the incidence of subsequently diagnosed cancer in patients who were not found to have cancer when deep venous thrombosis was diagnosed. DESIGN: Retrospective cohort study. SETTING: Urban, tertiary care teaching hospital. PATIENTS: 986 consecutive patients (637 women and 349 men; mean age +/- SD, 53 +/- 17 years) who had no risk factors for venous disease and had venous ultrasonography because idiopathic deep venous thrombosis was suspected. MEASUREMENTS: Initial clinical evaluation was assessed by using chart review. The incidence of cancer at a median of 34 months after diagnosis of deep venous thrombosis was obtained through hospital chart review (38%), computerized record extraction (54%), mailed questionnaires (6%), telephone interviews (1%), or a death registry (1%). RESULTS: Deep venous thrombosis was diagnosed in 142 patients (14%); 136 of the 142 were hospitalized. Cancer was diagnosed in 16 of these 136 patients (12%) during the index hospitalization. All 16 of these patients had one or more abnormalities on at least one of the four components of the clinical examination: history, physical examination, basic laboratory testing, or chest radiography. The probability of detecting cancer increased as the number of findings suggestive of cancer on the four components of the clinical evaluation increased. Cancer was diagnosed in none of the 56 patients with deep venous thrombosis who did not have findings on the clinical evaluation. The probability of cancer-free survival during follow-up (median, 34 months) was similar in patients with (3 of 122 [2.5%]) and without (23 of 844 [2.7%]) deep venous thrombosis and in the age- and sex-matched U.S. population. CONCLUSIONS: A clinical evaluation that includes a comprehensive medical history, physical examination, routine laboratory testing, and chest radiography seems to be appropriate for detecting cancer in these patients. Additional testing should be guided by any abnormalities detected by this clinical evaluation.

Adult↗
PubMedDate not supplied

Use of deep venous thrombosis prophylaxis by family physicians.

BACKGROUND: Accumulated data indicate that the administration of low-dose subcutaneous heparin reduces the incidence of deep venous thrombosis in high-risk surgical and medical patients. Because deep venous thrombosis predisposes to pulmonary embolism, it is generally accepted that reducing deep venous thrombosis will reduce pulmonary embolism, the most common preventable cause of death in hospitalized patients. There are few data, however, regarding physicians' use of heparin for deep venous thrombosis prophylaxis in medical patients. METHODS: We reviewed charts of medical patients aged 50 years and older who were admitted to family practice services in a community teaching hospital and excluded patients who were not candidates for heparin prophylaxis. RESULTS: Eighty (65 percent) of 123 patients received heparin for deep venous thrombosis prophylaxis. Patients admitted to a residency teaching service were more likely to receive heparin for deep venous thrombosis prophylaxis than were patients admitted to nonteaching services (odds ratio 3.37, 95 percent confidence interval 1.26-9.21, P = 0.012). An association between the patient's number of risk factors for deep venous thrombosis and likelihood of receiving deep venous thrombosis prophylaxis approached statistical significance (P = 0.078). CONCLUSIONS: In our institution, heparin for deep venous thrombosis prophylaxis is frequently but not uniformly prescribed for appropriately selected family practice inpatients. No similar data for nonsurgical patients were found for comparison.

Aged↗
PubMed1992

Comparison of warfarin and external pneumatic compression in prevention of venous thrombosis after total hip replacement.

OBJECTIVE: To compare the effectiveness and safety of warfarin and external pneumatic compression (EPC) in prevention of venous thrombosis after total hip replacement. DESIGN: Prospective, randomized trial in consecutive patients, with blinded assessment of the primary end point. SETTING: University medical center and large community hospital. PATIENTS: Patients over age 18 years scheduled for elective primary total hip replacement were eligible. Of 254 patients interviewed, 232 were randomized, 220 patients had surgery and received prophylaxis, and 201 had venography. INTERVENTIONS: Patients were randomly assigned to prophylaxis with a device providing bilateral sequential EPC to both the calf and thigh or to receive warfarin in a low-intensity regimen beginning 10 to 14 days preoperatively. Prophylaxis was continued until venography. MAIN OUTCOME MEASURES: Venous thrombosis was diagnosed by venography between postoperative days 6 and 8. Bleeding was assessed by surgical blood loss, transfusion requirements, changes in hematocrit, and clinically identified bleeding complications. RESULTS: The total incidence of venous thrombosis was virtually the same in the warfarin and EPC groups (31% vs 27%), but the distribution of thrombi was different. Proximal thrombosis occurred in 12% of patients in the EPC group compared with only 3% in the warfarin group (P = .012, 95% confidence interval for difference, 2% to 18%). In contrast, calf vein thrombosis was more frequent in the warfarin group (21%) than in the EPC group (12%) (P = .021, 95% confidence interval for difference, 0% to 18%). Most proximal thrombi in EPC-treated patients were located within 15 cm of the femoral head and were not continuous with thrombi in deep calf veins. The high incidence of proximal thrombosis in the EPC group resulted in termination of the study by the safety monitoring committee. Blood loss and bleeding complications were similar in the two groups. CONCLUSION: Warfarin therapy is significantly more effective than EPC in preventing serious proximal vein thrombosis after total hip replacement. The greater effectiveness of warfarin therapy in preventing proximal vein thrombi and of EPC in preventing thrombosis in the calf suggests that there are differences in the pathogenesis of thrombosis in these two locations.

Aged↗
PubMed1990

[Compression sonography as a procedure in the diagnosis of acute deep venous thrombosis of the leg].

It is well known that clinical symptoms of deep venous thrombosis of the leg are not reliable. We studied the diagnostic value of compression sonography in the diagnosis of venous thrombosis of the lower extremity. Ultrasound examination was performed in patients in the supine position. The venous segments were evaluated almost exclusively with transversal scanning. In the thigh lacking compressibility of the venous lumen was the only criterion for thrombosis. In the calf, unobstructed veins can usually not be seen in the patient supine. In thrombosis however the vessel is dilated by the clot and appears as sonolucent incompressible channel. 178 patients were examined comparatively by venography and ultrasound (226 one extremity phlebogramms). Phlebography demonstrated 113 thromboses which could be demonstrated by ultrasound with a sensitivity of 95% and a specificity of 100%. In 92% the extension of thrombosis was estimated accurately. Thigh vein thrombosis was detected with a sensitivity of 97% and a specificity of 99%. Occlusion or patency of the common femoral vein was seen correctly in each case. Ultrasonic diagnosis of the superficial femoral vein thrombosis had a sensitivity of 97%, that of the popliteal vein of 98% and a specificity of 100% in both. Venous occlusion confined to the calf was detected with a sensitivity of 89% and a specificity of 99%. We conclude that compression sonography is a highly accurate diagnostic procedure for the diagnosis of deep venous thrombosis of the thigh as well as the calf. It should be the first choice of imaging method in the diagnosis of venous thrombosis of the leg.

Acute Disease↗
PubMedDate not supplied

[Plasminogen depletion and incorporation in experimental venous thrombosis].

The objective of this piece of work is to study (using animals): venous thrombosis, the depletion and incorporation of plasminogen in thrombus of different stages of time, in order to devise better guide lines for the treatment of thrombosis than the conventional treatment. The studies relating to the plasminogen content of the thrombus show us that, on experimental venous thrombosis, as from the fifth day after which it occurred, the content of the plasminogen thrombus is reduced considerably. This data underlines the fact some venous thrombosis of over five days are resistant to conventional thrombolytic treatment. In relation to this we have to report that the mean lifespan according to our experiments of the plasminogen on beagle dogs is approximately sixteen hours. On the other hand the study of the addition of 125Lis-plasminogen, on experimental thrombosis of different stages of oldness show us that the above addition results in a 54% intake into the thrombus on three day, old thrombosis and 17% on five day old thrombosis. In conclusion we can suggest that the resistance to conventional thrombolytic treatment of old venous thrombosis (5-7 days old) is probably due to a reduction of efficiency of the thrombus plasminogen. At the same time the contribution of exogenous lis-plasminogen does not produce a sufficient enrichment of the thrombus in plasminogen. Therefore the therapeutic exogenous plasminogen addition is not advisable for relatively old thrombosis (less than or equal to 5 days old).

Animals↗
PubMed1995

[Prevention of deep venous thrombosis].

The positive and negative clinical symptoms and signs of deep venous thrombosis are both insensitive and non-specific. Venography is the reference investigation: Duplex ultrasonography is the usual diagnostic procedure for distal deep venous thrombosis but it is less reliable in proximal lesions. The sensitivity of plethysmography in proximal deep venous thrombosis is high but the diagnosis of isolated calf vein thrombosis and non-obstructive proximal thrombosis escape diagnosis in this technique. Most cases of deep venous thrombosis occur after major surgery, during pregnancy, in the post-partum period, after prolonged immobilisation and in obese patients or those with varicose veins. Congenital and acquired causes should also be investigated when spontaneous deep venous thrombosis occurs or when the condition complicates minor surgical trauma in a young patient. The incidence of deep venous thrombosis varies with the type of surgical procedure: 25% in general surgery, 50% after hip or knee arthroplasty, 43% after fracture of femur, 24% after neurosurgery. Graduated pressure stockings should be used for the prevention of deep venous thrombosis. Other measures include aspirin, dextran, oral and subcutaneous anticoagulants, non-fractionated and low molecular weight heparins. The relative efficacy of these different measures is discussed with respect to each type of surgical procedure.

Humans↗
PubMed1998

Different risks of thrombosis in four coagulation defects associated with inherited thrombophilia: a study of 150 families.

Deficiency of the naturally occurring anticoagulant proteins, such as antithrombin, protein C and protein S, and activated protein C resistance due to the factor V Leiden gene mutation is associated with inherited thrombophilia. So far, no direct comparison of the thrombotic risk associated with these genetic defects is available. In this study, we wish to compare the lifetime probability of developing thrombosis, the type of thrombotic symptoms, and the role of circumstantial triggering factors in 723 first- and second-degree relatives of 150 index patients with different thrombophilic defects. We found higher risks for thrombosis for subjects with antithrombin (risk ratio 8.1, 95% confidence interval [CI], 3.4 to 19.6), protein C (7.3, 95% CI, 2.9 to 18.4) or protein S deficiency (8.5, 95% CI, 3. 5 to 20.8), and factor V Leiden (2.2, 95% CI, 1.1 to 4.7) than for individuals with normal coagulation. The risk of thrombosis for subjects with factor V Leiden was lower than that for those with all three other coagulation defects (0.3, 95% CI, 0.1 to 1.6), even when arterial and superficial vein thromboses were excluded and the analysis was restricted to deep vein thrombosis (0.3, 95% CI, 0.2 to 0.5). No association between coagulation defects and arterial thrombosis was found. The most frequent venous thrombotic manifestation was deep vein thrombosis with or without pulmonary embolism (90% in antithrombin, 88% in protein C, 100% in protein S deficiency, and 57% in factor V Leiden), but a relatively mild manifestation such as superficial vein thrombosis was common in factor V Leiden (43%). There was a predisposing factor at the time of venous thromboembolism in approximately 50% of cases for each of the four defects. In conclusion, factor V Leiden is associated with a relatively small risk of thrombosis, lower than that for antithrombin, protein C, or protein S deficiency. In addition, individuals with factor V Leiden develop less severe thrombotic manifestations, such as superficial vein thrombosis.

Adolescent↗
PubMed2000

Anticoagulant proteins in childhood venous and arterial thrombosis: a review.

Thrombotic disease is less frequent in children than in adults, but may result in severe morbidity and mortality. The coagulation system is balanced to provide rapid activation to stop bleeding and appropriate inhibition to prevent unwanted clot extension. It is regulated by fibrinolysis and by three major anticoagulant pathways: the protein C, antithrombin, and tissue factor pathway inhibitor systems. Acquired or inherited abnormalities of coagulation proteins or hemostatic regulatory mechanisms, particularly when combined with dehydration or the presence of indwelling catheters, may pose a high risk for thrombosis. Thrombosis in a child warrants investigation of potential underlying prothrombotic conditions. These include acquired antiphospholipid antibodies or the lupus anticoagulant as well as abnormalities of the inherited anticoagulant factors including protein C, protein S, antithrombin, and Factor V Leiden. Other abnormalities may result in heightened levels of otherwise normal coagulation proteins such as hyperprothrombinemia due to the prothrombin 20210 mutation. A large survey of children with thrombosis indicated that Factor V Leiden, protein C deficiency, and increased lipoprotein(a) were found most commonly. The most severe predisposition occurs with homozygous protein S or protein C deficiency with resultant purpura fulminans in the newborn. The risk of thrombosis in children with heterozygous deficiencies of anticoagulant proteins is not well defined, although it is clear that combined heterozygotes or a combination of an inherited and an acquired defect heightens the risk for thrombosis. Treatment of thrombosis primarily involves a rapidly acting anticoagulant such as heparin or low-molecular-weight heparin to prevent extension, and long-term anticoagulation with warfarin may be instituted to prevent recurrence. Fibrinolytic therapy is infrequently used because of the risk of serious bleeding complications and is reserved for selected cases of arterial thrombosis to initiate rapid reperfusion of ischemic tissue or used in those patients with a large venous thrombosis and pulmonary emboli causing hemodynamic compromise.

Anticoagulants↗
PubMed2006

Increased venous versus arterial thrombosis in the Factor V Leiden mouse.

BACKGROUND: Deep vein thrombosis (DVT) occurs with high prevalence in association with the Factor V Leiden (R506Q) mutation, whereas most evidence suggests no correlation with clinical arterial thrombosis. OBJECTIVE: This study compared arterial to venous thrombosis in the mutationally analogous Factor V Leiden mouse. METHODS: Three separate vascular thrombosis models were evaluated in Fv(+/+) (wild-type), Fv(Q/+) (heterozygous) and Fv(Q/Q) (homozygous) Factor V Leiden mice. RESULTS: In a FeCl(3)-induced arterial thrombosis model, no statistical differences among the three genotypes were found in the time to thrombotic occlusion. In contrast, Fv(Q/+) and Fv(Q/Q) mice demonstrated larger femoral vein thrombi at 30 and 60 min compared to wild-types, with Fv(Q/Q) mice having statistically larger thrombi than both wild-type and Fv(Q/+) mice at 10 and 60 min and 24 h (p<0.05). In a model of thrombotic occlusion following arterial and venous anastomotic repair, both Fv(Q/+) and Fv(Q/Q) mice had higher rates of venous thrombosis than wild-types, but only Fv(Q/Q) homozygotes showed a statistically greater arterial occlusion rate than wild-types. CONCLUSION: The Factor V Leiden mouse demonstrated a greater propensity for venous vs. arterial thrombosis, paralleling clinical epidemiologic findings and supporting its use for research on deep vein thrombosis.

Amino Acid Substitution↗
PubMed2006

Arterial and venous thrombosis in rare congenital bleeding disorders: a critical review.

A thorough review of the literature and of personal files has allowed the gathering of 81 patients with rare congenital bleeding disorders and thrombotic phenomena. Sixteen of these patients had congenital afibrinogenemia, eight involved factor V deficiency, 20 factor VII defects, 33 factor XI deficiencies and only one, a factor XIII defect. Altogether 42 patients showed arterial thrombosis (myocardial infarction [MI] in 28 cases; ischemic stroke in 4; arterial occlusion in 8; 2 patients with disseminated intravascular coagulation (DIC)). Ages varied between 13 and 74. Twenty-two patients were males and 16 females. In four cases, sex was not reported. There were three fatalities: two after a MI and one because of heart failure. With regard to venous thrombosis: 9 patients had pulmonary embolism, 15 patients had deep vein thrombosis, 9 patients had both pulmonary embolism and deep vein thrombosis; 1 patient had superficial vein thrombosis, whereas, 5 cases had an unusual site venous thrombosis (two portal systems, two cerebral sinuses, one inferior vena cava) for a total of 39 cases. Age varied between 3 and 86. In this case, 20 patients were males and 17 were females. In two cases, sex was not reported. There were three fatalities: two because of pulmonary embolism and one because of inferior vena cava thrombosis. The fact that thrombosis has never been described in patients with factor II or factor X seems to underscore the central antithrombotic role that these two factors have in the coagulation system.

Adolescent↗
PubMed2005

Homozygosity for factor V Leiden leads to enhanced thrombosis and atherosclerosis in mice.

BACKGROUND: Activated protein C resistance due to factor V Leiden (FVL) is a common genetic risk factor for venous thrombosis in humans. Although the impact of FVL on the development of venous thrombosis is well established, its effect on arterial thrombosis and atherosclerosis is controversial. METHODS AND RESULTS: To determine the effect of the FVL mutation on arterial thrombosis in the mouse, wild-type (Fv+/+), heterozygous FVL (FvQ/+), and homozygous FVL (FvQ/Q) mice underwent photochemical carotid arterial injury to induce occlusive thrombosis. FvQ/Q mice formed occlusive thromboses 27+/-3 minutes (n=7) after the onset of injury, which was significantly shorter than that observed for Fv+/+ mice (56+/-7 minutes, n=9, P<0.01), whereas FvQ/+ mice (41+/-7 minutes, n=5) were intermediate (P=0.5, compared with Fv+/+). To determine the source of FVL relevant to the enhanced vascular thrombosis, bone marrow transplantation experiments were performed between Fv+/+ and FvQ/Q mice. FvQ/Q mice transplanted with Fv+/+ bone marrow formed occlusive thromboses at 35+/-5 minutes (n=7, P<0.05 compared with Fv+/+ mice), whereas Fv+/+ mice transplanted with FvQ/Q bone marrow occluded at 59+/-7 minutes (n=6, P<0.001 compared with FvQ/Q mice). To assess the effect of the FVL mutation on the development of atherosclerosis, FvQ/Q mice were crossed with the atherosclerosis-prone apolipoprotein E (ApoE)-deficient strain (ApoE-/-) to generate FvQ/Q,ApoE-/- mice. By 52 weeks of age, FvQ/Q,ApoE-/- mice (n=8) had developed more aortic atherosclerosis (40+/-6% lesion area) compared with Fv+/+,ApoE-/- mice (15+/-3% lesion area; n=12, P<0.02). CONCLUSIONS: In conclusion, homozygosity for the FVL mutation in mice leads to enhanced arterial thrombosis and atherosclerosis. The source of the FVL leading to accelerated thrombosis appears to be circulating, non-platelet-derived plasma FVL.

Animals↗
PubMed1995

Triggering of plaque disruption and arterial thrombosis in an atherosclerotic rabbit model.

BACKGROUND: It is now recognized that plaque disruption and thrombosis, a process often triggered by activities of the patient, is generally the cause of the onset of acute coronary syndromes. Understanding of disease onset could be greatly enhanced by the availability of a suitable animal model of plaque disruption and thrombosis. The aim of this study was to replicate and further characterize an atherosclerotic rabbit model of triggering of arterial thrombosis that was introduced by Constantinides and Chakravarti more than 30 years ago but not subsequently used. Aortic plaques were induced by a high-cholesterol diet, by mechanical balloon injury of the artery, or by a combination of the two. Triggering was attempted by injection of Russell's viper venom (RVV), which is a proteolytic procoagulant, and histamine. METHODS AND RESULTS: A total of 53 New Zealand White rabbits were exposed to one of four preparatory regimens: rabbits in group I (n = 9) were fed a regular diet for 8 months; rabbits in group II (n = 13) were fed a diet of 1% cholesterol for 2 months alternated with 2 months of a regular diet for a total of 8 months; rabbits in group III (n = 5) underwent balloon-induced arterial wall injury, then were given a regular diet for 8 months; and rabbits in group IV (n = 14) underwent balloon-induced arterial wall injury, then were given a diet of 1% cholesterol for 2 months followed by a regular diet for 2 months for a total of 4 months. After completion of the preparatory regimen, triggering of plaque disruption and thrombosis was attempted by injection of RVV (0.15 mg/kg IP) and histamine (0.02 mg/kg IV). In group I, normal control rabbits without atherosclerosis, only one small thrombus was noted in 1 of 9 rabbits. In group II, cholesterol-fed rabbits, thrombosis occurred in 3 of 13 rabbits. Thrombus occurred in all rabbits in group III (5 of 5) and in 10 of 14 rabbits in group IV. Although the frequency of thrombosis was not significantly different between groups I and II, possibly due to a small sample size, it was significantly different among all four groups (P < .001). Also, the frequency and amount of thrombus formation were significantly different among all four groups (P < .001; P < .0001) but not between groups I and II. Rabbits with atherosclerosis (those in groups II and IV) demonstrated plaque disruption and overlying platelet-rich thrombus formation similar to that observed in patients with acute coronary syndromes. The surface area covered by thrombus was 2 mm2 in group I, 15.3 +/- 19.2 mm2 in group II, 223 +/- 119 mm2 in group III, and 263 +/- 222 mm2 in group IV. Rabbits in groups III and IV had the greatest amount of thrombus, and this amount was significantly greater than in rabbits in groups I and II (P < .001 and P < .03, respectively). CONCLUSIONS: A suitable animal model is available for the study of plaque disruption and arterial thrombosis. Hypercholesterolemia and mechanical arterial wall injury seemed to produce plaques vulnerable to triggering of disruption and thrombosis, whereas normal arteries were relatively resistant to triggering. This model provides a method to evaluate agents that might decrease the occurrence of vulnerable plaques or the amount of thrombus formed after triggering. Most important, the model can be used to identify the features of vulnerable plaques and the pharmacological stressors that trigger plaque disruption and thrombus formation.

Animals↗
PubMed2006

Infantile spasms as an adverse outcome of neonatal cortical sinovenous thrombosis.

Cerebral sinovenous thrombosis is a rare but potentially serious condition often occurring in children with nonspecific presenting features. Much remains to be learned about the long-term outcome of infants with cerebral sinovenous thrombosis. We report a series of four patients taken from a prospective database of neonates with sinovenous thrombosis who subsequently developed infantile spasms, three with hypsarrythmia on electroencephalography and one with multiple independent spike foci. The first patient presented at 2 weeks of age with hypernatremia, dehydration, and seizures. He was found to have extensive thrombosis and hemorrhagic infarction of the right basal ganglia. The second patient presented at 5 weeks of life and was found to have sagittal sinus thrombosis with bilateral intracranial hemorrhage. The third patient presented with seizures on day 1 of life and was found to have venous thrombosis involving the torcular, extending into the sagittal sinus. The fourth patient presented at 3 weeks with lethargy and seizures. He was diagnosed with bacterial meningitis and also had extensive sinus thrombosis. All patients developed infantile spasms at ages 9, 7, 11, and 10 months, respectively. This is the first report in the English literature describing infantile spasms as a possible outcome of sinovenous thrombosis in early infancy.

Anticoagulants↗