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PubMed2001

Acute arterial thrombosis causes endothelial dysfunction: a new paradigm for thrombolytic therapy.

PURPOSE: The goals of this study were to delineate the time course of endothelial dysfunction after arterial thrombosis, to determine the cause of endothelial dysfunction in this setting, and to determine whether modulating standard thrombolytic therapy would ameliorate the thrombosis-mediated endothelial dysfunction. METHODS: Male adult rats underwent infrarenal aortic occlusion by means of clip ligature to induce arterial thrombosis. After 30 minutes, 1, 2, and 3 hours, ring segments from the infrarenal aorta were harvested and placed into physiologic buffer baths. With the use of a force transducer, both endothelial-dependent relaxation (EDR) and endothelial-independent relaxation (EIR) were measured. Endothelial function and presence were determined by means of factor VIII immunohistochemical staining. Endothelial morphology was evaluated with scanning electron microscopy (SEM). Nitric oxide (NO) levels were determined with a chemiluminescent assay of its nitrite/nitrate metabolites (NO(x)). Standard thrombolytic therapy with urokinase (UK) was infused into thrombosed aortic ring segments and compared with UK supplemented with both low-dose L -arginine (2 mmol) and high-dose L -arginine (20 mmol). RESULTS: Arterial thrombosis decreases EDR. The nadir of EDR occurs 1 hour after thrombosis (mean +/- SE, 13% +/- 6.4% vs 94% +/- 2.6% for controls, P <.005), with persistent lowering of EDR as long as 3 hours after thrombosis. EIR is preserved, and vasoconstriction with norepinephrine or potassium buffer is unaltered. Both endothelial function and presence (n = 6 per group) were documented by means of factor VIII immunohistochemistry. An intact monolayer of endothelium at all time intervals after thrombosis was revealed by means of SEM analysis. No differences between control and thrombosed specimens were revealed by means of the grading of SEM images. Local NO(x) levels were lower after 1 hour of thrombosis, with an increase higher than baseline values at 3 hours. The addition of low-dose L -arginine resulted in a minor increase in EDR. However, high-dose L -arginine resulted in a significant increase in EDR versus controls receiving UK alone (64% +/- 6.3% vs 38% +/- 4.4%, P <.05). Correspondingly, local NO(x) levels were 20-fold higher after the high-dose L -arginine supplementation when compared with UK thrombolysis alone (2.8 +/- 0.52 micromol/L vs 0.133 +/- 0.02 micromol/L, n = 6 samples/group, P <.005). CONCLUSION: Acute arterial thrombosis causes endothelial dysfunction, without causing endothelial cell loss. Endothelial function reaches a nadir after 1 hour of thrombosis. EIR and vasoconstriction remain unaffected, indicating normal smooth muscle cell function. NO(x) levels suggest that NO levels are decreased acutely after thrombosis. Supplementing standard thrombolytic therapy with the NO precursor, l-arginine, ameliorates the endothelial dysfunction seen after acute thrombosis by increasing local NO production.

Acute Disease↗
PubMed1991

Graft thrombosis in pediatric renal transplant recipients. A report of the North American Pediatric Renal Transplant Cooperative Study.

Data from the North American Pediatric Renal Transplant Cooperative Study were analyzed to determine the incidence and possible causes of graft thrombosis in pediatric renal transplant recipients. Between January 1987, and November 1989, 1045 renal transplants in recipients less than 18 years of age were registered in the study, including 484 living-related donor and 561 cadaver donor transplants. There were 213 graft failures (67 LRD, 146 CAD), and of these 27 were caused by thrombosis (8 LRD, 19 CAD). Thrombosis occurred in 2.6% of all transplants and accounted for 22.5% (27/120) of all graft failures that occurred in the first 60 days following transplantation. Among the LRD recipients, there were 24 graft failures in those less than 6 years of age, and 7 of these were due to thrombosis, compared to 1 thrombosis in 43 graft losses in recipients greater than 6 years (P less than 0.01). In recipients less than 6 years old, the thrombosis rate for those who received transplants without prior dialysis was 4/32 (12.5%) versus 3/109 (2.8%) with prior dialysis. Among the CAD recipients, age of the recipient did not influence graft thrombosis. Donor age, however, was strongly associated with the risk of thrombosis, as was cold storage time. Donor age and cold storage time were not independently distributed within the population, with longer cold storage times required for younger donors. Both factors, however, independently affected outcome. Other factors, including prior nephrectomy, prior transplant, center size, and use of cyclosporine were not associated with increased risk of thrombosis in LRD or CAD recipients. We conclude that graft thrombosis is an important cause of renal graft loss in children. In LRD transplants the risk of graft thrombosis is increased in recipients less than 6 years old, and preliminary data suggest that the lack of prior dialysis may be associated with thrombotic risk in these patients. CAD transplant recipients who receive grafts from young donors, particularly those with long cold storage time, are at increased risk for graft failure due to thrombosis.

Adolescent↗
PubMed2001

Hypercoagulable states in renal transplant candidates: impact of anticoagulation upon incidence of renal allograft thrombosis.

INTRODUCTION: Although multiple studies of demographic variables have been associated with allograft thrombosis, these results are not routinely reproducible. Are ESRD patients with hypercoagulable states (HCS) (antithrombin III deficiency, protein S or C deficiency, activated protein C resistance, and anticardiolipin antibodies) at predictably greater risk for allograft thrombosis? METHODS: Between 1996 and 1999, all renal transplant candidates were screened for hypercoagulability risk factors [HRF] (multiple arteriovenous access thromboses, prior deep vein thrombosis, prior allograft thrombosis, collagen vascular disease, multiple miscarriages, diabetes, autoimmune disease, and Fabry's disease). HRF(+) candidates were then tested for HCS status. We administered preemptive posttransplant i.v. Heparin in HCS(+) patients and observed the impact of this intervention upon the incidence of allograft thrombosis. We compared demographic data and incidence of allograft thrombosis in an historic control (346 patients transplanted between June 31, 1992, and March 5, 1996) not tested for HCS and a study cohort (502 patients transplanted between March 6, 1996, and June 31, 1999) prospectively screened for HRF. HRF(+) patients who were HCS(+) in the study cohort received i.v. heparin immediately after transplant and p.o. warfarin as outpatients. RESULTS: Demographic characteristics previously implicated in allograft thrombosis were equivalently distributed in both cohorts with the exceptions that more living-donor transplants (33.1% vs. 15.3%) were performed in study cohort, CIT>24 hr occurred in more control patients (37.3% vs. 22.1%) and more study patients (16.7% vs. 0%) received tacrolimus. Hypercoagulable states were found upon reevaluating five of seven controls (71.4%), who lost prior allografts to thrombosis. Hypercoagulable states were prospectively detected in 10 study patients with hypercoagulability risk factors. Most (9 of 10) study patients receiving anticoagulation have achieved long-term allograft function. Study group allograft thrombosis incidence was reduced (1.59% vs. 4.05%). Hypercoagulable states were demonstrated in most episodes of allograft thrombosis. Control patients who lost prior allografts to thrombosis were anticoagulated after retransplantation and 100% achieved long-term allograft function. CONCLUSIONS: Long-term allograft function has been achieved in 90% of study patients when prophylactically anticoagulating study patients with hypercoagulable states. A 2.6-fold reduction in the expected incidence of allograft thrombosis was observed in anticoagulated patients with hypercoagulable states.

Adult↗
PubMed1993

Efficacy and cost of low-molecular-weight heparin compared with standard heparin for the prevention of deep vein thrombosis after total hip arthroplasty.

PURPOSE: To compare the efficacy, safety, and cost-effectiveness of low-molecular-weight heparin with standard heparin for the prevention of deep vein thrombosis after total hip arthroplasty. DATA IDENTIFICATION: Studies were identified by MEDLINE search and review of bibliographies of retrieved articles. Hospital resources used in treating deep vein thrombosis and bleeding complications after total hip arthroplasty were estimated using retrospectively collected data from 447 patients who participated in a recently completed randomized controlled deep vein thrombosis prophylaxis trial at our center. STUDY SELECTION: Randomized controlled trials directly comparing a low-molecular-weight heparin preparation with standard heparin for the prevention of deep vein thrombosis after total hip arthroplasty were potentially eligible for the meta-analysis. DATA EXTRACTION: Data from eligible studies were extracted independently by two of the authors. Multiple regression analysis of data from the patient cohort was used to estimate the effect of deep vein thrombosis and bleeding on length of hospital stay. A hypothetical North American price for low-molecular-weight heparin was determined based on the ratio between low-molecular-weight heparin and standard heparin in France. Costs were based on weighted per-diem hospital expenditures and physician fees for procedures and reported in 1992 U.S. dollars. RESULTS OF DATA SYNTHESIS: Meta-analysis of six eligible trials determined that low-molecular-weight heparin was significantly more effective than standard heparin at preventing deep vein thrombosis after total hip arthroplasty (common odds ratio, 0.72; 95% CI, 0.53 to 0.95). However, this benefit was restricted to the prevention of proximal deep vein thrombosis (common odds ratio, 0.40; CI, 0.28 to 0.59). No significant differences were found in the rates of distal deep vein thrombosis or total, major, or minor bleeding between the two groups. Based on a 2.6 to 1 price ratio between low-molecular-weight heparin and standard heparin, use of low-molecular-weight heparin would save the health care system about $50,000 per 1000 patients treated. Sensitivity analysis shows that if the low-molecular-weight heparin/standard heparin price ratio exceeds 3.7 (the threshold value lies between 0.8 and 5.5 based on the extremes of the 95% CI of the common odds ratios for deep vein thrombosis and bleeding complications), use of low-molecular-weight heparin is more expensive. At a price ratio of 10, it would cost more than $250,000 to treat 1000 patients with low-molecular-weight heparin compared with standard heparin or about $5000 for each additional deep vein thrombosis prevented with low-molecular-weight heparin. CONCLUSIONS: Low-molecular-weight heparin is more effective and is at least as safe as standard heparin for the prevention of deep vein thrombosis after total hip arthroplasty. Based on the current French price ratio of low-molecular-weight heparin to standard heparin, the use of low-molecular-weight heparin in North America would result in overall savings in cost; however, the relative cost-effectiveness is critically dependent on the price ratio between the two drugs. Further research is needed to compare the cost-effectiveness of low-molecular-weight heparin with other prophylactic regimens and postoperative deep vein thrombosis management strategies.

Cost-Benefit Analysis↗
PubMed2000

Do patients with acute deep vein thrombosis have fever?

The purpose of this study was to determine whether those with lower extremity acute venous thrombosis have fever. During a recent 14.5-month period, 1847 patients undergoing lower extremity venous duplex scanning also had their oral temperature measured using a digital thermometer at the time of duplex examination. Patients were 57.8 +/- 17.3 years of age (range, 14 to 99). Temperature was 98.5 +/- 1.1 degrees F. Twenty-three patients had acute inferior vena cava thrombosis, 60 had acute iliac vein thrombosis, 138 had acute femoral venous thrombosis, and 131 had acute popliteal venous thrombosis. Calf vein thromboses were present in 102 patients, and 43 patients had superficial venous thrombosis. A total of 228 patients had acute lower extremity venous thrombosis in one or more of these venous segments. Temperature with acute lower extremity venous thrombosis was 98.7 +/- 1.05 degrees F versus 98.5 +/- 1.10 degrees F in those with no acute thrombosis. Although small, this temperature difference was statistically significant (P < 0.02). Acute deep venous thrombosis (DVT) was defined as acute popliteal or more proximal femoral, iliac, or vena cava thrombosis. The temperature for the 175 patients with acute DVT was 98.7 +/- 1.10 degrees F versus 98.5 +/- 1.10 degrees F for those without DVT (P < or = 0.035). There was no temperature that served to accurately differentiate those who did from those who did not have DVT. The frequency that patients with DVT had fever, defined as a temperature > or = 100 degrees F, was 9.1 per cent (16 of 175) with DVT versus 7.5 per cent (126 of 1678) without DVT (not significant). In the subgroup with a temperature > or = 101 degrees F, 4.6 per cent (8 of 175) with DVT had such a fever versus 3.4 per cent (57 of 1672) without DVT (not significant). Those undergoing venous duplex who were found to have acute lower extremity venous thrombosis, including acute DVT, had statistically higher temperatures, but such temperature differences were minimal. The incidence of fever, defined as a temperature > or = 100 degrees F or > or = 101 degrees F, was not different between those with and those without acute DVT. It appears that the presence of fever may not be a sensitive or specific indicator for the presence of underlying acute DVT.

Acute Disease↗
PubMed2002

Factor V Leiden, prothrombin gene mutation, and thrombosis risk in patients with antiphospholipid antibodies.

OBJECTIVE: To determine if the prevalence of 2 prothrombotic genetic factors, factor V Leiden and prothrombin gene mutation, is increased in patients with antiphospholipid (aPL) antibodies with a history of venous/arterial thrombosis compared to patients with aPL antibodies with no history of thrombosis. METHODS: One hundred fifty-seven patients with aPL antibodies were studied. The occurrence of venous and arterial thrombotic events since the time of antibody detection was determined retrospectively, using appropriate clinical and diagnostic criteria. Clinical risk factors for thrombosis were documented and included hypertension, hyperlipidemia, cigarette smoking, diabetes, positive family history, use of oral contraceptive, pregnancy, trauma, hospitalization, varicose veins, and malignancy. Genomic DNA was extracted from blood cells for determination of factor V Leiden mutation G1691 --> A and prothrombin mutation G20210 --> A by polymerase chain reaction and restriction fragment length polymorphism analysis. RESULTS: Of 157 patients, 69 had a history of thrombosis (venous 37, arterial 32); 147 (94%) patients had anticardiolipin (aCL) antibodies; 69 (45%) had lupus anticoagulant (LAC). The prevalence of factor V Leiden in patients with thrombosis was 13% compared to 4.6% in patients without thrombosis (OR 3.11, CI 0.92-10.6). In patients with aCL antibodies, 15% of patients with arterial thrombosis had factor V mutation compared to 3.5% of patients without thrombosis (OR 4.9, CI 1.2-19.3). The prothrombin gene mutation was identified in 5 patients, none of whom had thrombosis. Stepwise logistic regression analysis indicated that LAC (p = 0.005), male sex (p = 0.04), and hypertension (p = 0.03) were the strongest risk factors for developing thrombosis and that no additional risk was conferred by factor V Leiden (p = 0.13) and prothrombin gene mutation. CONCLUSION: Although the prevalence of factor V Leiden is modestly increased in patients with autoimmune aPL antibodies and thrombosis, these results suggest that its detection does not significantly increase the risk of a thrombotic event, once other clinical risk factors have been considered. Prothrombin gene mutation is not associated with thrombosis in patients with aPL antibodies.

Adult↗
PubMed2004

Laparoscopic procedures as a risk factor of deep venous thrombosis, superficial ascending thrombophlebitis and pulmonary embolism--case report and review of the literature.

UNLABELLED: Since its introduction laparoscopic surgery has been used for many indications, e.g., cholecystolithiasis, hernia, appendicitis, fundoplication, benign large bowel disease and gynaecological disorders. It has been considered as safe and efficient procedure for most patients with only few contraindications, mostly heart-lung disease. When the initial enthusiasm has been replaced by a more critical observation, more complications of laparoscopy or laparoscopic surgery were not only discovered but also reported. In laparoscopic hernia repair there is a tendency for severe complications when compared to open surgery. There is a controversy on possible side-effects of laparoscopic surgery, e.g., thrombosis, and the increased necessity of prophylaxis for thromboembolic events. Recently a growing number of reports on thromboembolic complications in association with laparoscopic surgery were published. Thrombosis may be caused by detrimental effects of pneumoperitoneum on venous flow (increased abdominal pressure and negative Trendelenburg position) and activation of the haemostatic system. Further risk factors may contribute to the risk to develop venous thrombosis. It is well accepted that varicose veins are associated with an increased risk for the thrombosis. However, the association of varicose veins with complications of laparoscopic surgery is unclear. The possible impact of thrombotic complications makes an analysis of the association of varicose veins or a history of deep vein thrombosis on the development of thrombosis after laparoscopic surgery mandatory. Although this is the first report on ascending thrombophlebitis and thrombosis of the sapheno-femoral junction after laparoscopic surgery, the incidence of deep vein thrombosis or superficial thrombophlebitis after laparoscopic surgery or laparoscopy may be much higher according to the pathophysiological changes during and after these procedures. In many patients venous thrombosis may not be recognized or it appears when the patient is already discharged. CONCLUSION: Laparoscopy and laparoscopic procedures may have an increased risk for the development of thrombosis due to increased abdominal pressure and negative Trendelenburg position. Patients with varicose veins and a history of thromboembolism may aggravate laparoscopy associated risks for the development of thromboembolic complications. Superficial thrombophlebitis in the thigh is not a benign disease entity and may lead to deep vein thrombosis (DVT) and pulmonary embolism (PE). Urgent surgical treatment (high ligation) may be warranted together with low-molecular weight heparin (LMWH) and compressions therapy. Patients with varicose veins and a history of venous thrombosis may not be suitable candidates for laparoscopic surgery. Family practitioners may be confronted with this complication more often since patients are discharged earlier from hospital after laparoscopic interventions due to legislative regulations.

Diverticulitis, Colonic↗
PubMed1996

Primary renal graft thrombosis.

BACKGROUND: Renal allograft thrombosis is a serious complication of kidney transplantation that ultimately leads to graft loss. Its association with acute and hyperacute rejection is well documented; however, in a large proportion of patients the precise cause remains obscure. The exact incidence and the associated risk factors for those episodes of graft thrombosis lacking evidence of rejection have not yet been clearly established. METHODS: All reported episodes of graft thrombosis in 558 consecutive cadaveric kidney transplants performed in a single centre were examined to identify those without histopathological evidence of rejection, i.e. primary renal graft thrombosis. Univariate and multivariate types of analysis were applied to study the possibly related risk factors and any associated morbid event(s) of those episodes. Recipients without reported episodes of primary renal graft thrombosis (n = 493) represented the control group for the 34 identified cases. RESULTS: The calculated incidence of primary renal graft thrombosis was 6% (1.9% arterial, 3.4% venous and 0.7% both), comprising 45% of early (90 days) and 37% of 1-year graft losses in our centre. The multivariate analysis identified five independent risk factors for primary renal graft thrombosis: donor's right kidney P < 0.007, past history of venous thrombosis (renal or extrarenal) P = 0.000, and diabetic nephropathy P = 0.000 of the recipient, technical surgical problems P = 0.000, and recipient's haemodynamic status peri and early postoperatively P < 0.001. Primary renal graft thrombosis was related to the presentation with delayed graft function (DGF) P < 0.0005 and was significantly associated with extrarenal thromboembolic manifestations P < 0.0005. There was no association between primary renal graft thrombosis and recipient's age, sex, number of previous transplants, type of dialysis, pretransplant treatment with erythropoietin, antiplatelet agents, or oral anticoagulants, donor's age, sex, number or graft vessels, warm and cold ischaemia times, site of transplant (R/L iliac fossa) and type of immunosuppressive agent used for induction whether cyclosporin A (CsA) or OKT3. CONCLUSIONS: Primary renal graft thrombosis is an important cause of graft loss that may be accompanied by thrombosis of extrarenal sites and effective, safe prophylactic regimens are needed, especially for those at high risk.

Acute Disease↗
PubMedDate not supplied

Value of assessment of pretest probability of deep-vein thrombosis in clinical management.

BACKGROUND: When ultrasonography is used to investigate deep-vein thrombosis, serial testing is recommended for those who test negative initially. Serial testing is inconvenient for patients and costly. We aimed to assess whether the calculation of pretest probability of deep-vein thrombosis, with a simple clinical model, could be used to improve the management of patients who present with suspected deep-vein thrombosis. METHODS: Consecutive outpatients with suspected deep-vein thrombosis had their pretest probability calculated with a clinical model. They then underwent compression ultrasound imaging of proximal veins of the legs. Patients at low pretest probability underwent a single ultrasound test. A negative ultrasound excluded the diagnosis of deep-vein thrombosis whereas a positive ultrasound was confirmed by venography. Patients at moderate pretest probability with a positive ultrasound were treated for deep-vein thrombosis whereas patients with an initial negative ultrasound underwent a single follow-up ultrasound 1 week later. Patients at high pretest probability with a positive ultrasound were treated whereas those with negative ultrasound underwent venography. All patients were followed up for 3 months for thromboembolic complications. FINDINGS: 95 (16.0%) of all 593 patients had deep-vein thrombosis; 3%, 17%, and 75% of the patients with low, moderate, and high pretest probability, respectively, had deep-vein thrombosis. Ten of 329 patients with low pretest probability had the diagnosis confirmed, nine at initial testing and one at follow-up. 32 of 193 patients with moderate pretest probability had deep-vein thrombosis, three diagnosed by the serial (1 week) test, and two during follow-up. 53 of 71 patients with high pretest probability had deep-vein thrombosis (49 by the initial ultrasound and four by venography). Only three (0.6%) of all 501 (95% CI 0.1-1.8) patients diagnosed as not having deep-vein thrombosis had events during the 3-month follow-up. Overall only 33 (5.6%) of 593 patients required venography and serial testing was limited to 166 (28%) of 593 patients. INTERPRETATION: Management of patients with suspected deep-vein thrombosis based on clinical probability and ultrasound of the proximal deep veins is safe and feasible. Our strategy reduced the need for serial ultrasound testing and reduced the rate of false-negative or false-positive ultrasound studies.

Algorithms↗
PubMed1995

Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men.

BACKGROUND: A specific point mutation in the gene coding for coagulation factor V is associated with resistance to degradation by activated protein C, a recently described abnormality of coagulation that may be associated with an increased risk of venous thrombosis. Whether this mutation also predisposes patients to arterial thrombosis is unknown, as is the value of screening for the mutation in order to define the risk of venous thrombosis among unselected healthy people. METHODS: Among 14,916 apparently healthy men in the Physicians' Health Study who provided base-line blood samples, 374 had myocardial infarctions, 209 had strokes, and 121 had deep venous thrombosis, pulmonary embolism, or both, during a mean follow-up of 8.6 years. We determined whether a mutation at nucleotide position 1691 of the factor V gene was present or absent in these 704 men and in an equal number of matched participants who remained free of vascular disease. RESULTS: The prevalence of heterozygosity for the mutation among men who had myocardial infarctions (6.1 percent, P = 0.9) or strokes (4.3 percent, P = 0.4) was similar to that among men who remained free of vascular disease (6.0 percent). However, the prevalence of the mutation was significantly higher among men who had venous thrombosis, pulmonary embolism, or both (11.6 percent, P = 0.02). In adjusted analyses, the relative risk of venous thrombosis among men with the mutation was 2.7 (95 percent confidence interval, 1.3 to 5.6; P = 0.008). This increased risk was seen with primary venous thrombosis (relative risk, 3.5; 95 percent confidence interval, 1.5 to 8.4; P = 0.004) but not with secondary venous thrombosis (relative risk, 1.7; 95 percent confidence interval, 0.6 to 5.3; P = 0.3), and it was most apparent among older men. Specifically, the prevalence of the mutation among men over the age of 60 in whom primary venous thrombosis developed was 25.8 percent (relative risk, 7.0; 95 percent confidence interval, 2.6 to 19.1; P < 0.001). CONCLUSIONS: In a large cohort of apparently healthy men, the presence of a specific point mutation in the factor V gene was associated with an increased risk of venous thrombosis, particularly primary venous thrombosis. The presence of the mutation was not associated with an increased risk of myocardial infarction or stroke. This mutation appears to be the most common inherited factor thus far recognized that predisposes patients to venous thrombosis.

Aged↗
PubMed1998

Noninvasive diagnosis of deep venous thrombosis. McMaster Diagnostic Imaging Practice Guidelines Initiative.

PURPOSE: To review noninvasive methods for diagnosis of first and recurrent deep venous thrombosis and provide evidence-based recommendations for the diagnosis of deep venous thrombosis in symptomatic, asymptomatic, and pregnant patients. DATA SOURCES: Accuracy (comparison with contrast venography) and management (safety of withholding anticoagulants when results were normal) studies that evaluated tests for diagnosis of deep venous thrombosis were identified from a MEDLINE search, personal files, and bibliographies of reviews and original studies. STUDY SELECTION: Prospective cohort studies (accuracy and management studies) and randomized comparisons (management studies) that satisfied predefined methodologic criteria were included. DATA EXTRACTION: Sensitivity, specificity, and positive and negative predictive values were determined for accuracy studies. Rates of venous thromboembolism during long-term follow-up of patients with normal results were determined for management studies. DATA SYNTHESIS: Data from individual studies were combined under a random-effects model. The accuracy of noninvasive tests was compared, with emphasis on within-study comparisons. Recommendations for diagnosis of deep venous thrombosis were developed by a multidisciplinary group and graded according to the strength of the supporting evidence. Venous ultrasonography is the most accurate noninvasive test for the diagnosis of a first symptomatic proximal deep venous thrombosis. However, neither ultrasonography nor impedance plethysmography is accurate in asymptomatic postoperative patients. Venous ultrasonography is less accurate for symptomatic isolated distal (calf) deep venous thrombosis than for proximal deep venous thrombosis, and the clinical utility of venous ultrasonography of the distal veins is uncertain. Withholding anticoagulant therapy in symptomatic patients with suspected deep venous thrombosis who have normal results on serial venous ultrasonography or impedance plethysmography is safe. Diagnosis of recurrent deep venous thrombosis requires evidence of new thrombus formation, such as a new noncompressible venous segment detected by venous ultrasonography, conversion of a normal result on impedance plethysmography to abnormal, or presence of an intraluminal filling defect on venography. Suspected deep venous thrombosis in pregnant patients can usually be managed with serial venous ultrasonography or impedance plethysmography. In symptomatic patients with a suspected first episode of deep venous thrombosis, clinical assessment and D-dimer testing are complementary to testing with venous ultrasonography and impedance plethysmography. CONCLUSIONS: Patients with suspected deep venous thrombosis can usually be managed with noninvasive testing. However, if the results of this testing are nondiagnostic or are discordant with the clinical assessment, venography should be considered.

Algorithms↗
PubMedDate not supplied

Deep vein thrombosis as a complication of megestrol acetate therapy among nursing home residents.

OBJECTIVES: To describe a cluster of cases of proximal deep vein thrombosis among nursing home residents treated with megestrol acetate, to identify other risk factors for deep vein thrombosis development among these patients, and to alert physicians to this potential complication of megestrol acetate therapy. DESIGN: Retrospective review. SETTING: A 129-bed Maryland nursing home. PARTICIPANTS: Nineteen residents prescribed megestrol acetate between November 1997 July 1998, identified by computerized pharmacy records. MEASUREMENTS: Demographic data (including identification of known risk factors for deep vein thrombosis development) were collected along with information on the indications for megestrol acetate therapy and its duration, diagnostic studies related to detection of deep vein thrombosis and their results, and patient outcomes following diagnosis of deep vein thrombosis. RESULTS: Megestrol acetate was prescribed for 18 nutritionally at-risk patients and one with uterine cancer. Six (32%) patients developed deep vein thrombosis signs and symptoms, and all diagnoses were confirmed as proximal deep vein thromboses with Doppler studies. (No diagnosis of deep vein thrombosis were made among any nursing home patients not being treated with megestrol acetate during the observation period.) All patients diagnosed with deep vein thrombosis were hospitalized and anticoagulated, but none were diagnosed with pulmonary embolus or died. The length [median (range)] of megestrol acetate treatment was similar regardless of whether deep vein thrombosis developed [117 (57-244) versus 143 (2-294) days, respectively, P = 0.83]. Stratification by length of treatment in 50-day increments revealed that most patients who developed deep vein thrombosis did so after 50 days of treatment (P = 0.046). CONCLUSION: A high incidence of deep vein thrombosis was identified among nursing home residents treated with megestrol acetate, even among ambulatory individuals with no other known risk factors. Because the efficacy of megestrol acetate treatment in nursing home residents with weight loss is unproven, the risk of deep vein thrombosis must be considered when prescribing megestrol acetate, and its use to treat nutritionally at-risk nursing home residents should be limited.

Journal Article↗
PubMed2006

Elevated levels of soluble fibrin or D-dimer indicate high risk of thrombosis.

BACKGROUND: Fibrin-related markers such as soluble fibrin (SF) and D-dimer are considered useful for the diagnosis of thrombosis. However, the evidence for diagnosis of thrombosis by fibrin-related markers is not well-established. OBJECTIVE: To evaluate the cutoff values of D-dimer and SF in the diagnosis of thrombosis. PATIENTS AND METHODS: Plasma concentrations of SF and D-dimer were measured in 784 inpatients suspected of having thrombosis between 1 August 2003 and 31 December 2004, and then correlated with thrombosis. RESULTS AND CONCLUSIONS: Plasma concentrations of D-dimer and SF were significantly higher in patients with disseminated intravascular coagulation (DIC), deep vein thrombosis (DVT) and cerebral thrombosis, compared with those in patients without thrombosis. When cutoff values of > 3.0 microg mL(-1) for D-dimer and > 6.0 microg mL(-1) for SF were used for the diagnosis, more than 50% of patients (with the exception of liver transplant patients and postoperative patients) had thrombosis. Receiver operating characteristic analysis showed that SF was more useful than D-dimer for the diagnosis of thrombosis (i.e. DVT and DIC). The cutoff value of D-dimer (7.87 microg mL(-1)) was the same for DVT and DIC, while that of SF was slightly lower for DVT (7.05 microg mL(-1)) than for DIC (8.60 microg mL(-1)). Our findings suggest that high levels of plasma fibrin-related markers reflect high risk for thrombosis.

Aged↗
PubMedDate not supplied

Inhibitors of nitric oxide promote microvascular thrombosis.

BACKGROUND: Microvascular free tissue transfer is a widely utilized method of head and neck reconstruction. Despite advances in the field, reports of experienced microvascular surgeons on large series of free flap procedures reveal that the incidence of free flap failure varies between 5% and 9%. Most cases of free flap failure are initiated by platelet-mediated events that result in thrombosis at the microvascular anastomoses. Recent evidence indicates that nitric oxide (NO) plays a critical role in preventing thrombosis by inhibiting platelet adhesion and aggregation. The role of NO in microvascular anastomotic thrombosis has not been studied. OBJECTIVE: To determine the role of NO in microvascular thrombosis using an in vivo rabbit model. METHODS: An arterial inversion graft (AIG)-induced microvascular thrombosis model was utilized in New Zealand white rabbits. The femoral arteries were used bilaterally to create 3-mm AIGs. Intravenous NO donor, NO inhibitor, or isotonic sodium chloride solution (control) was administered for 1 hour following the completion of the AIG, and vessel patency was then checked using a direct "milking test." Sixteen rabbits (32 AIGs) were used as controls. A potent NO inhibitor, N(w)-nitro-L-arginine methylester (L-NAME), was administered to 13 rabbits (26 AIGs) and L-arginine, a NO precursor/donor, was given to 10 rabbits (20 AIGs). RESULTS: The control animals had a thrombosis rate of 46.9%. The rate of thrombosis in animals exposed to an NO inhibitor (L-NAME) was significantly higher, at 76.9% (P<.05, chi( 2) = 4.23). The L-arginine group did not show a statistical difference with the control in the rate of thrombosis (50.0%). CONCLUSIONS: Nitric oxide plays a role in microvascular anastamotic thrombosis. Intravenous NO inhibitors appear to increase the short-term rate of microvascular thrombosis. L-arginine, an NO precursor, does not appear to produce the opposite effect. Further studies using local NO donors and antagonists as well as more potent NO precursors are needed to further evaluate NO's role in microvascular thrombosis. The results of this study may have applications to human microvascular surgery.

Animals↗
PubMed2005

Incidence, predictors, and outcome of thrombosis after successful implantation of drug-eluting stents.

CONTEXT: Traditionally, stent thrombosis has been regarded as a complication of percutaneous coronary interventions during the first 30 postprocedural days. However, delayed endothelialization associated with the implantation of drug-eluting stents may extend the risk of thrombosis beyond 30 days. Data are limited regarding the risks and the impact of this phenomenon outside clinical trials. OBJECTIVE: To evaluate the incidence, predictors, and clinical outcome of stent thrombosis after implantation of sirolimus-eluting and paclitaxel-eluting stents in routine clinical practice. DESIGN, SETTING, AND PATIENTS: Prospective observational cohort study conducted at 1 academic hospital and 2 community hospitals in Germany and Italy. A total of 2229 consecutive patients underwent successful implantation of sirolimus-eluting (1062 patients, 1996 lesions, 2272 stents) or paclitaxel-eluting (1167 patients, 1801 lesions, 2223 stents) stents between April 2002 and January 2004. INTERVENTIONS: Implantation of a drug-eluting stent (sirolimus or paclitaxel). All patients were pretreated with ticlopidine or clopidogrel and aspirin. Aspirin was continued indefinitely and clopidogrel or ticlopidine for at least 3 months after sirolimus-eluting and for at least 6 months after paclitaxel-eluting stent implantation. MAIN OUTCOME MEASURES: Subacute thrombosis (from procedure end through 30 days), late thrombosis (>30 days), and cumulative stent thrombosis. RESULTS: At 9-month follow-up, 29 patients (1.3%) had stent thrombosis (9 [0.8%] with sirolimus and 20 [1.7%] with paclitaxel; P = .09). Fourteen patients had subacute thrombosis (0.6%) and 15 patients had late thrombosis (0.7%). Among these 29 patients, 13 died (case fatality rate, 45%). Independent predictors of stent thrombosis were premature antiplatelet therapy discontinuation (hazard ratio [HR], 89.78; 95% CI, 29.90-269.60; P<.001), renal failure (HR, 6.49; 95% CI, 2.60-16.15; P<.001), bifurcation lesions (HR, 6.42; 95% CI, 2.93-14.07; P<.001), diabetes (HR, 3.71; 95% CI, 1.74-7.89; P = .001), and a lower ejection fraction (HR, 1.09; 95% CI, 1.05-1.36; P<.001 for each 10% decrease). CONCLUSIONS: The cumulative incidence of stent thrombosis 9 months after successful drug-eluting stent implantation in consecutive "real-world" patients was substantially higher than the rate reported in clinical trials. Premature antiplatelet therapy discontinuation, renal failure, bifurcation lesions, diabetes, and low ejection fraction were identified as predictors of thrombotic events.

Angioplasty, Balloon, Coronary↗
PubMed1979

Effect of implant surface chemistry upon arterial thrombosis.

A series of poly(alpha-amino acid)s with controlled chemical variations were investigated in order to assess the effect of different chemical moieties upon arterial thrombosis. The gross implant surface properties ranged from hydrophobic to hydrophilic ionic and nonionic. The materials were tested by implantation within canine femoral and carotid arteries. Results were compared with the response to the polyurethane Biomer. The changes in implant surface chemistry elicited a range of response that varied from intense thrombosis and rapid vessel occlusion to minimal thrombosis and endothelialization. The results showed that no simple relationship exists between a gross surface property, such as hydrophobicity, and the degree of thrombosis resistance. Some hydrophobic and hydrophilic materials were found to have good thrombosis resistance, while others were found to have poor thrombosis resistance. Leukocytes were shown to play an important role in both initial thrombosis and endothelialization. The major difference between materials that progressed to rapid vessel occlusion and materials that remained patent was the degree of direct leukocyte adherence and spreading on the implant surface prior to extensive platelet aggregation (less than 30 min). It was consistent for both hydrophobic and hydrophilic materials that the lack of direct leukocyte adherence to the implant surface was associated with intense thrombosis and rapid vessel occlusion. Conversely, the presence of numerous leukocytes directly adherent to either hydrophobic or hydrophilic surfaces appeared to have a moderating effect upon thrombosis and vessels with these implants remained patent. In instances when thrombosis was nonocclusive, the surfaces of the thrombi became endothelialized, primarily through the transformation of mononuclear leukocytes into endothelial cells. This article includes a hypothetical model representing the sequence of events and alternative pathways occurring at the blood-material interface, with special attention given to the involvement of leukocytes in arterial thrombosis.

Animals↗
PubMed1994

Effect of a novel thrombin active-site inhibitor on arterial and venous thrombosis.

The effects of a thrombin active-site inhibitor on arterial and venous thrombosis, and thrombin-induced thrombocytopenia were determined in anesthetized rats. Desamino D-Phe-Pro-Arg-aldehyde (BMY 44621) was administered before experimental intervention as a loading i.v. dose plus continuous i.v. infusion. Carotid artery thrombosis was produced by transmural vessel injury and vena cava thrombosis was produced by partial stasis of blood flow combined with endothelial injury. Thrombocytopenia was induced by an i.v. injection of human alpha-thrombin. BMY 44621 inhibited arterial and venous thrombosis in a dose-dependent manner. Its threshold antithrombotic dose for venous thrombosis was half of that for arterial thrombosis. Maximum reductions in thrombus weight were greater for venous (> 90%) compared to arterial (57%) thrombosis and correlated with 2-and 9-fold prolongation of ex vivo thrombin clotting time, respectively. A 40% reduction in platelet counts induced by thrombin injection was abolished by the threshold dose of BMY 44621 for inhibiting venous thrombosis. These experiments demonstrate that thrombin's active-site is an effective target for inhibiting venous and arterial thrombosis, although venous thrombosis is more sensitive to this therapeutic strategy than arterial thrombosis.

Aldehydes↗
PubMed2004

Predictors of and outcomes of early thrombosis following balloon angioplasty versus primary stenting in acute myocardial infarction and usefulness of abciximab (the CADILLAC trial).

We sought to identify the predictors and clinical outcomes of early thrombosis after primary angioplasty and stenting for acute myocardial infarction (AMI). Little is known about the correlates and prognosis of acute and subacute thromboses after percutaneous coronary intervention (PCI) for AMI. We therefore studied the frequency, clinical determinants, and implications of early thrombosis in a large trial of patients who had primary PCI. In the Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications trial, 2,082 patients who had AMI were randomized in a 2 x 2 factorial design to primary stenting or to balloon angioplasty, each with and without abciximab. Early thrombosis occurred in 19 patients (0.9%) at a median of 2 days (range 0 to 23). Maximal balloon diameter was smaller, and aneurysmal and bifurcation lesions were more prevalent in the group with early thrombosis. Early thrombosis occurred in 0.4% of patients who had been randomized to receive abciximab versus 1.5% of control patients (p <0.01) and in 0.5% of patients who had been randomized to undergo stenting versus 1.4% of those who underwent balloon angioplasty (p = 0.04). By multivariate analysis, abciximab use was an independent predictor of no thrombosis (hazard ratio 0.27, 95% confidence interval 0.09 to 0.86, p = 0.026). Within 30 days, 5.3% of patients who had early thrombosis died, 32.9% developed reinfarction, and 89.5% required repeat target vessel revascularization (including bypass surgery in 11.1%). As a result, patients who had versus those who did not have early thrombosis had markedly higher rates of major adverse cardiac events at 30 days (94.7% vs 5.0%, p <0.0001) and at 1 year (94.7% vs 16.9%, p <0.0001). Patients who develop early thrombosis after primary PCI have a very high rate of major adverse cardiac events, including death and reinfarction, and usually require repeat coronary angioplasty or surgery for management. Complex baseline angiographic morphology and smaller maximal balloon diameter are predictors of early thrombosis after primary PCI for AMI. The incidence of early thrombosis after primary angioplasty and stenting is decreased by abciximab use.

Abciximab↗