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At least 19 recordsLinked to original sources
PubMed1997

Thrombosis in the young: epidemiology and risk factors. A focus on venous thrombosis.

Thrombosis occurs most often as myocardial infarction, cerebral infarction or venous thromboembolism, ie, deep-vein thrombosis and pulmonary embolism. The incidence of all types of thrombosis is strongly dependent on age. Among young individuals, up to age 40, venous thrombosis is the most common form of thrombosis. The risk factors for arterial and venous thrombosis differ, and among the latter disorders of hemostasis appear to be more prominent. In children venous thrombosis appears almost exclusively in association with venous catheters, with an exception of the renal vein thrombosis of the newborn, which has an unknown etiology. In young adults, the risk factors for venous thrombosis are essentially the same as in older individuals, excepting oral contraceptives, pregnancy and puerperium which are limited to young women. In young women, most venous thrombotic events can be attributed to oral contraceptives. Venous thrombosis is a multicausal disease: more than one risk factor needs to be present before thrombosis occurs. The younger an individual, the more risk factors are required to precipitate thrombosis: in children often three or four, and in young adults often two or more.

Adolescent↗
PubMed1993

Distribution of thrombosis in patients with symptomatic deep vein thrombosis. Implications for simplifying the diagnostic process with compression ultrasound.

BACKGROUND: Two different diagnostic strategies are used to perform compression (real-time) ultrasound for the diagnosis of clinically suspected deep-vein thrombosis. One is to examine the entire proximal venous system from common femoral to distal popliteal vein; the other is a limited examination of only the common femoral and the entire popliteal vein. The latter strategy, which is less time-consuming and requires less expensive equipment, is based on a strong impression from prospective studies using limited compression ultrasound that proximal vein thrombi always involve the common femoral or popliteal vein. This impression, which is supported by the demonstrated safety at long-term follow-up of not treating patients whose limited compression ultrasound is normal at presentation and then repeated within the next week, has not been tested in a formal study. Therefore, we reviewed a large series of venograms performed in consecutive patients with clinically suspected venous thrombosis to determine the distribution of venous thrombosis in symptomatic patients. METHODS: Venograms were performed using 150 mL of radiographic contrast material. Before the study, a panel of experts agreed on the standardized criteria for the assessment of venograms. Venograms were adjudicated blindly for the presence of deep vein thrombosis and to determine the distribution of proximal vein thrombosis and isolated calf-vein thrombosis, the size of proximal thrombi, and whether they were occlusive or nonocclusive. Subsequently, the duration of symptoms was related to the venographic findings. RESULTS: Five hundred sixty-two venograms from consecutive patients with a first episode of clinically suspected deep vein thrombosis were adjudicated. Of these, 20 (3.6%) were inadequate for interpretation. In the remaining 542, venous thrombosis was demonstrated in 189 instances (prevalence, 35%; 95% confidence interval, 31% to 39%) and were located in the proximal veins in 166 (88%; 95% confidence interval, 82% to 92%) venograms. Isolated calf-vein thrombosis was present in the remaining 23 (12%; 95% confidence interval, 8% to 18%) venograms. Proximal with concurrent calf thrombosis was detected in 164 (99%) of the 166 patients. Proximal thrombi involved only the popliteal vein in 16 (10%); the popliteal and superficial femoral veins in 70 (42%); and the popliteal, superficial, and common femoral vein in eight (5%); whereas thrombi involving the entire proximal deep venous system were detected in 58 (35%) venograms. Isolated thrombosis of the superficial femoral, common femoral, and iliac vein was not observed. Proximal venous thrombi were occlusive in 146 (88%) patients. No relation between the duration of symptoms and the extent or the occlusiveness of venous thrombi could be demonstrated. CONCLUSIONS: Most symptomatic patients have extensive occlusive proximal vein thrombosis at the time of presentation. Thrombi isolated to the superficial femoral or iliac vein were not observed in this large sample of consecutive patients. Our data support the use of the relatively simple, inexpensive, and rapid compression ultrasound method that limits the examination of the proximal veins to the common femoral and popliteal veins.

Analysis of Variance↗
PubMed2002

Late coronary stent thrombosis: early vs. late stent thrombosis in the stent era.

The incidence of coronary stent thrombosis is < 1%-2% in recent studies, with the highest-risk period considered to be the first 30 days following stent implantation. Recently, stent thrombosis after 30 days has been reported in patients undergoing brachytherapy with stenting. We reviewed the incidence of stent thrombosis causing myocardial infarction in nonbrachytherapy patients at our institution between 1 January 1996 and 30 November 1999. A case control methodology was employed with a 1:3 ratio of stent thrombosis to control patients. Of 1,191 patients undergoing coronary stenting, acute (< 24 hr) plus subacute (1-30 days) stent thrombosis occurred in 0.92% (11 of 1,191 patients). A further 0.76% (9 of 1,191 patients) developed late stent thrombosis after 30 days. There were no clinical or angiographic features at the time of the initial procedure that were associated with stent thrombosis as an entire group compared with control group, but early (acute and subacute) stent thrombosis patients had a smaller final stent minimal lumen diameter and longer stent length compared with patients who had late stent thrombosis or controls. Late stent thrombosis occurs in nonbrachytherapy patients and is almost as frequent as early stent thrombosis. Further studies are required to determine whether longer-term poststent pharmacological treatment may decrease or prevent this complication.

Biomarkers↗
PubMed2003

Introduction to thrombosis proficient and cost-effective approaches to thrombosis.

Thrombosis is the most common single cause of death in the United States. More than 2 million people die each year of arterial or venous thrombosis or its consequences, and a similar number experience nonfatal thrombosis-deep vein thrombosis, nonfatal pulmonary embolus, nonfatal cerebrovascular thrombosis, transient cerebral ischemic attacks (40% of patients will have a fatal or nonfatal cerebrovascular thrombosis within 1 year), nonfatal coronary artery thrombosis, retinal vascular thrombosis, and other nonfatal thrombotic episodes. Yet many, if not most, episodes of thrombosis can be prevented by appropriate primary antithrombotic therapy, and most recurrences can be prevented by the appropriate choice of secondary therapy.

Clinical Trials as Topic↗
PubMed1995

International Society on Thrombosis and Haemostasis (ISTH), and International Union of Pure and Applied Chemistry (IUPAC), Clinical Properties and units in the clinical laboratory sciences. V. Properties and units in thrombosis and haemostasis (recommendation 1995). International Society on Thrombosis and Haemostasis (ISTH) and International Union of Pure and Applied Chemistry (IUPAC),and International Federation of Clinical Chemistry (IFCC).

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Chemistry, Clinical↗
PubMed2001

Does the location of thrombosis determine the risk of disease recurrence in patients with proximal deep vein thrombosis?

PURPOSE: To determine if the location of deep vein thrombosis is a predictor of recurrent venous thromboembolism during the initial 3 months of anticoagulant therapy. METHODS: The study population consisted of 1,149 consecutive patients with symptomatic proximal deep vein thrombosis. In all patients, deep vein thrombosis was confirmed by Duplex ultrasound or venography and was classified as popliteal, femoral, or iliofemoral. Patients received initial treatment with unfractionated heparin, enoxaparin, or reviparin for least 4 days, as well as a coumarin derivative, with a target international normalized ratio of 2.0 to 3.0, starting on the 1st or 2nd day of treatment. All patients were followed for 3 months, and all episodes of recurrent venous thromboembolism were confirmed with objective diagnostic tests. RESULTS: The overall rate of recurrent venous thromboembolism during the initial 3 months of anticoagulant therapy was 5.5% (63/1,149). The rate of recurrence in patients with popliteal vein thrombosis was 5.1% (23/453); in patients with femoral vein thrombosis, it was 5.3% (34/645); and in patients with iliofemoral vein thrombosis, it was 11.8% (6/51). Two clinical risk factors were associated with an increased risk of recurrent venous thromboembolism: iliofemoral vein thrombosis (odds ratio [OR] = 2.4; 95% confidence interval [CI]: 0.95, 5.9), and cancer (OR = 2.6; 95% CI: 1.5, 4.4). CONCLUSIONS: Patients with extensive iliofemoral vein thrombosis who receive conventional anticoagulant therapy have a greater than twofold higher risk of developing recurrent venous thromboembolism than patients without iliac vein involvement (i.e., 11.8% vs. 5.2%). Prospective studies are needed to determine whether alternative antithrombotic strategies are warranted in such patients.

Anticoagulants↗
PubMed2002

Normalization rates of compression ultrasonography in patients with a first episode of deep vein thrombosis of the lower limbs: association with recurrence and new thrombosis.

BACKGROUND AND OBJECTIVES: Delayed thrombus regression after a first episode of deep vein thrombosis (DVT) of the inferior limbs has been implicated in the development of the post-thrombotic syndrome. Whether normalization of vein segments involved in the index DVT has prognostic significance with respect to the probability of DVT recurrence or new thrombosis is currently unknown. In this study, we prospectively monitored thrombus regression in consecutive patients with symptomatic and asymptomatic DVT. Factors affecting normalization rates and the relationship between previous normalization and DVT recurrence or new thrombosis were explored. DESIGN AND METHODS: One hundred and seventy-nine patients with a first episode of symptomatic DVT of the lower limbs (38 with cancer) and 104 patients with DVT occurring after hip replacement surgery were serially monitored by real time B-mode compression ultrasonography (C-US) over a period of 12 months (months 1, 3, 6 and 12). C-US normalization of popliteal and femoral venous segments was arbitrarily assigned to be residual thrombus occupying, at maximum compressibility, less than 40% of the vein area in the absence of compression. RESULTS: In patients with no DVT recurrence or new thrombosis, C-US normalization was observed at 12 months in 100% of 99 patients with post-operative DVT, in 59% of 134 cancer-free symptomatic DVT outpatients and in 23.3% of 30 symptomatic DVT outpatients with cancer (p = 0.0001). Independent negative effects on the probability of C-US normalization were observed for younger age (p <0.05), for the outpatient presentation of the index DVT (p 0.017), for DVT involving the entire femoro-popliteal axis (p 0.05), and for the presence of cancer (p 0.05). DVT recurrence or new thrombosis was observed in 5 patients with post-operative DVT (4.8%), in 7 cancer-free patients with symptomatic DVT (5.0%) and in 8 patients with cancer (21.1%). Only 4 of these patients had shown normalization of their index DVT prior to the event. The presence of cancer was the only significant predictor of DVT recurrence and/or new thrombosis occurring within 3 months from the index DVT (OR = 4.90, p = 0.002). The absence of previous C-US normalization was the only predictor of recurrence or new thrombosis occurring after 3 and 6 months from the index DVT (OR 5.26, p 0.027). INTERPRETATION AND CONCLUSIONS: Absence of C-US normalization after a first episode of DVT appears to be a factor favoring recurrence or new thrombosis and may be relevant to the optimal duration of oral anticoagulant treatment.

Adolescent↗
PubMed1975

[Electric thrombosis of the experimental aneurysm--effect of alteration in intraaneurysmal hemodynamics on thrombus formation and progress of thrombosis (author's transl)].

Electric thrombosis may be one of useful method to provide protection against re-bleeding from the intracranial aneurysm which cannot be obliterated by clipping or ligation of its neck without disturbing arterial circulation. However, a better method is required to make the aneurysm to be almost completely thrombosed within one or two hours and to avoide marked damage of its wall, dislodging of the formed thrombus and excessive thrombosis. In this report a method of electric thrombosis of the experimental aneurysm was studied, and effects of hematocrit value and alteration in intraaneurysmal hemodynamics on thrombus formation and progression of thrombosis were investigated. An aneurysm-like vein pouch of 6 to 9 mm in diameter and of 5 to 8 mm in height was made on the common carotid artery of the dog. One week later, patency of the "aneurysm" was confirmed on angiogram. An anodal electrode of a platinum needle of 0.2 mm in diameter was inserted into the "aneurysm" to place the tip of the needle approximately at the center of the sack. Two platinum plates of 3 mm in diameter and of 0.1 mm in thickness were used as the cathodes and were placed externnally on the aneurysm wall. Direct current of 3 mA was applied for 5 or 10 minutes, or current of 5 mA for 5 minutes. Intraaneurysmal pulsating jet and turbulent flows were reduced by occlusion or stenosis of the common carotid. Size of the thrombus immediately after passing current and further progress of thrombosis were evaluated on angiogram and also on plethysmogram of the "aneurysm". Hematocrit value of 45% or more was favorable in producing a thrombus. Although direct current of 3 or 5 mA was desirable to avoid injury of the "aneurysm" wall and to inhibit dislodging of the formed thrombus, only a small thrombus was produced around the anode. Simultaneous occlusion or stenosis of the carotid artery proximally to the "aneurysm" during application of the current markedly promoted thrombus formation. With current application for 5 minutes, 30 to 40% or more of "aneurysm" lumen was occupied by the thrombus in a half of the cases. When the thrombus had reached to approximately 40% of aneurysm "sack" 5 minutes after passing DC current, it progressed to 80% within the following one hour. The most favorable site of the anode for progression of thrombosis was the proximal wall (cardiac side) of "aneurysm". Proximal occlusion or stenosis of the carotid artery promoted remarkably also progress of thrombosis. Excessive thrombosis, dislodging or spontaneous resolution of the formed thrombus was not found throughout one month follow-up. Histologically, the thrombus was organized within one month and covered with the endothel extending from the parent artery.

Animals↗
PubMed1991

[Diagnosis of deep leg vein thrombosis with color-coded duplex sonography and sonographic determination of the duration of the thrombosis].

In a prospective study, 188 patients with suspected deep venous thrombosis were examined by color-coded duplex sonography. In 114 patients the diagnosis of deep venous thrombosis was based on the criteria of 1) compressibility, 2) blood flow changes during compression, and 3) pelvic level during Valsalva maneuver. In all patients the results were compared with data from contrast venography. Venography was performed by an investigator, who was blinded to the prior findings. Sensitivity and specificity of the color-coded duplex sonography in diagnosing deep vein thrombosis were 96% and 97%, respectively. In the other 74 patients, in which the diagnosis of deep vein thrombosis was made by phlebography and/or ultrasound, a follow-up by color-coded duplex sonography was performed to determine the age of thrombosis. Criteria considered to determine the thrombus age included 1) margin of the vessel, 2) echogenicity; and 3) venous diameter. In 20 patients the results were compared to the age of thrombus that had been determined by histologic criteria (group I). In 54 patients the results were compared with the age that had been determined by patient history and symptoms (group II). A significant correlation was found between the age of thrombosis and the venous diameter (p less than 0.001). When thrombosis was less than 10 days old, the venous diameter was at least twice that of the diameter of the accompanying artery. The two other criteria, echogenicity and margin of the venous wall, however, did not prove to be accurate criteria to determine the age of deep venous thrombosis.

Adolescent↗
PubMed1997

[Venous thrombosis of the legs and cancer. Evaluation of risk factors of venous thrombosis in the medical environment].

In medical patients, risk factors of leg venous thrombosis are not well evaluated. Cancer is considered as an important one. The aim of this study was to evaluate the role of intrinsic thrombotic risk (tumor hypercoagulable state) and external thrombotic risk (associate factors). We have made a prospective analysis of thrombotic venous risk factors in two medical populations with leg venous thrombosis: patients with cancer and patients without cancer. Risk of thrombosis depends on the thrombogenic importance of the risk factor and its chronicity or not. We assessed cancer and thromboembolic disease at the time of diagnosis and during a median follow up of 125.2 days. We included 31 consecutive cases of cancer (21 men, 10 women, mean age 63.8 years), and 50 consecutive cases of non cancer patients (32 men, 18 women, mean age 65.5 years), these two populations were not different. The classic risk factors of venous thrombosis were not frequent in cancer patient. Analysis of thrombotic risk showed that 61% of cancer patient group had venous thrombosis without classic thrombotic risk, as compared to 32% in non cancer patient group, showing the direct role of cancer in thrombosis (p < 0.01). The cancer was often aggressive and metastatic adenocarcinoma of various origins. The effect of chemotherapy is not clear, only hormonotherapy seemed to be responsible in two cases. Cancer hypercoagulability, defined by clinical characteristics, is a real risk factor of venous thrombosis but of low frequency. Indeed, the incidence of venous thrombosis in oncologic unit is rare (0.4%). Finally, thromboembolic disease in cancer patients is not different than in no cancer patients, Trousseau's syndrome is unfrequent. Prognosis is poor (40% death with 44.5 days of median survival), and antithrombotic therapy complications are frequent (bleeding 16%, oral anticoagulants resistance 20%).

Aged↗
PubMed2002

[Heparin-induced thrombocytopenia and thrombosis. Thrombosis as an early cardinal symptom of heparin allergy].

Apart from bleeding complications, heparin-induced thrombocytopenia (HIT) type II is the most severe side effect of heparin therapy. It is widely agreed that its most important clinical symptom is thrombocytopenia, with or without thromboembolism.Assuming, unlike other authors, that thrombosis is the leading clinical symptom of HIT type II, we investigated the frequency of an immunological reaction indicative of HIT type II in patients suffering from thrombosis. From January 1999 to December 2000, 77% ( n=6713) of our in-patients received heparin for more than 5 days as thrombosis prophylaxis. When thrombosis was suspected on the grounds of clinical appearances, the patient concerned underwent phlebography, and two different serological tests for anti-heparin antibodies were also carried out. In such cases, patients were immediately switched to hirudin instead of heparin. In 29 out of 101 patients, the clinical suspicion of thrombosis was confirmed. Three patients developed pulmonary embolism. In 4 patients both serological tests revealed the presence of anti-heparin antibodies. Three of the remaining 72 patients with negative phlebography results were found to have antibodies on serological testing. In none of the 7 patients with a confirmed diagnosis of HIT type II was the classical sign of thrombocytopenia was present. Even with thorough clinical and phlebographic examinations, the incidence of HIT type II is only 0.13% in our institution. One of the 7 patients with thrombosis was not thrombocytopenic but did show the typical immunological reaction. Since the incidence of HIT type II is low and thrombocytopenia is not a reliable indicator for HIT II, the need for frequent thrombocyte counts (twice weekly) should be reconsidered.However,patients developing thrombosis while receiving heparin need to be treated for clinically suspected HIT type II until the final diagnosis is made.

Adult↗
PubMed1998

Case-control study of risk of cerebral sinus thrombosis in oral contraceptive users and in [correction of who are] carriers of hereditary prothrombotic conditions. The Cerebral Venous Sinus Thrombosis Study Group.

OBJECTIVE: To investigate whether users of oral contraceptives and in [corrected] carriers of a hereditary prothrombotic condition (factor V Leiden mutation, protein C, S, or antithrombin deficiency) have an increased risk of cerebral sinus thrombosis. DESIGN: Comparison of a prospective series of cases of cerebral sinus thrombosis with population data. SETTING: Neurological teaching hospitals from different regions in the Netherlands (cases) and a representative sample of the non-institutionalised Dutch population (controls). SUBJECTS: 40 women aged 18-54 years with cerebral sinus thrombosis (cases) and 2248 women aged 18-49 years (controls). MAIN OUTCOME MEASURE: Current use of oral contraceptives at the time of the thrombosis (cases) or at the time of the questionnaire (controls). Prevalences of a hereditary prothrombotic condition in patients and in the population with odds ratios. RESULTS: 34 of 40 (85%) women with cerebral sinus thrombosis used oral contraceptives, versus 1007 of 2248 (45%) of the control women; the age adjusted odds ratio was 13 (95% confidence interval 5 to 37). Seven of 36 patients (19%) had a prothrombotic deficiency, versus 7% expected in the population; this corresponds to a threefold to fourfold increase in risk. In women who used oral contraceptives and also carried a prothrombotic defect, the odds ratio for cerebral sinus thrombosis was about 30 relative to women who had neither risk factor. CONCLUSION: The use of oral contraceptives and being a carrier of a hereditary prothrombotic condition increase the risk of and interact in a multiplicative way in the development of cerebral sinus thrombosis.

Adolescent↗
PubMed2002

Fulminate intracardiac thrombosis associated with Budd-Chiari-syndrome and inferior vena cava thrombosis.

The most common cause of edema of the legs and dyspnea is congestive heart failure. Further differential diagnosis such as renal or hepatic failure have to be considered. We report the case of a previous healthy 65-year-old woman who developed dyspnea and massive edema of the legs followed by acute hepatic and renal failure. Imaging studies showed a thrombosis of the inferior vena cava (IVC) caused by a tumor between the right kidney and the IVC. Histological examination revealed a leiomyosarcoma of the IVC. Hepatic failure due to venous outflow obstruction (Budd-Chiari syndrome, BCS) was diagnosed. Coagulation profile showed a complex disorder due to acute hepatic failure. Factor V Leiden and prothrombin gene mutation G20210A could be excluded. The thrombosis extended from the femoral veins up to the right atrium. After 11 days of anticoagulation with heparin platelet counts decreased by more than 50%. Suspecting a heparin-induced thrombocytopenia the patient was placed on recombinant hirudin (lepirudin) for anticoagulation. Hepatic venogram showed a thrombosis of the hepatic vein orifices but not of the hepatic veins. The tumor and the thrombi were removed surgically. When the cardiopulmonary bypass was terminated new intracardiac thrombi occurred. Despite immediate surgical intervention the patient finally died due to right ventricular failure caused by the fulminate intracardiac thrombosis. In conclusion, thrombosis of the IVC may mimic congestive heart failure and may cause BCS. Neoplasms and coagulation disorders may cause thrombosis of the IVC.

Aged↗
PubMed2002

Interleukin 8 and venous thrombosis: evidence for a role of inflammation in thrombosis.

Elevated plasma levels of interleukin 8 (IL-8) were previously shown to be associated with recurrent venous thrombosis. To assess the risk of venous thrombosis, IL-8 plasma concentrations were measured in patients and control subjects of the Leiden Thrombophilia Study (LETS). This population based case-control study included 474 patients with a first deep-vein thrombosis and 474 age- and sex-matched controls. The risk of venous thrombosis for subjects with elevated IL-8 levels (above 90th percentile of controls) compared with subjects with IL-8 levels below the 90th percentile was increased 1.8-fold (95%CI 1.2-2.8). Adjusted for age and sex, the odds ratio was 1.9 (95%CI 1.3-2.8). IL-8 concentrations were weakly correlated with age, male sex, and concentrations of C-reactive protein, factor VIII coagulation activity and homocysteine, but adjustment for these factors did not substantially affect the association between IL-8 and venous thrombosis. Our results suggest that IL-8 is a risk factor for venous thrombosis.

Adolescent↗
PubMed2003

Use of elastic compression stockings after deep venous thrombosis: a comparison of practices and perceptions of thrombosis physicians and patients.

Daily long-term use of elastic compression stockings (ECS) by patients with deep venous thrombosis (DVT) may help to prevent the post-thrombotic syndrome (PTS). However, the effectiveness of ECS in clinical practice is difficult to predict, since the practices and perceptions of patients and thrombosis physicians regarding ECS have not been documented. The objectives were to survey DVT patients and thrombosis physicians on their practices and perceptions regarding use of ECS after DVT, and to evaluate whether physician perceptions are supported by patient responses. Two surveys were conducted. The first was sent to 38 Canadian thrombosis physicians. The second was administered to 80 DVT patients attending Thrombosis Clinic at one of two Canadian university-affiliated hospitals. Most physicians believed that ECS were useful in preventing PTS and in managing venous symptoms. However, there was a lack of consensus regarding the optimal timing of initiation of ECS, duration of therapy, and compression strength, and only one-third routinely prescribed ECS to asymptomatic patients to prevent PTS. Most DVT patients who were prescribed ECS purchased them, 87% wore them daily, and most reported that ECS relieved swelling and symptoms. Physicians underestimated the degree of patient compliance with ECS, but correctly identified the main reasons for non-compliance. There is a lack of consensus among thrombosis physicians regarding ECS use after DVT. Patients with DVT are willing to comply with ECS therapy and most find them to be helpful. Our findings suggest that long-term study of the optimal use of ECS after DVT is both necessary and feasible.

Adult↗
PubMed2001

Long-term clinical course of proximal deep venous thrombosis and detection of recurrent thrombosis.

Symptomatic proximal deep vein thrombosis of lower extremities carries a high risk for recurrent venous thromboembolism that persists for many years. This risk is dependent on readily identifiable risk factors, being low after a trauma or a surgical intervention and higher in all the other patient categories. Moreover, postthrombotic sequelae will develop in one of every three patients, this risk being strongly related to the development of ipsilateral thrombosis. Although the optimal duration of anticoagulation in patients who experience an episode of proximal vein thrombosis is unknown, it seems reasonable to administer a short-term course of coumarin drugs to patients with thrombosis associated with transient risk factors, whereas a longer course (6 to 12 months) should be considered in patients with idiopathic thrombosis and in those with permanent risk factors. Indefinite anticoagulant therapy is a clinical judgement in the individual patient. The management of patients who develop clinical manifestations suggestive of recurrent ipsilateral venous thrombosis still represents a challenge for clinicians. Recent data suggest that these patients can be safely managed with the use of serial compression ultrasonography.

Clinical Trials as Topic↗
PubMed2002

Safety and efficacy of only 2 weeks of ticlopidine therapy in patients at increased risk of coronary stent thrombosis: results from the Antiplatelet Therapy alone versus Lovenox plus Antiplatelet therapy in patients at increased risk of Stent Thrombosis (ATLAST) trial.

BACKGROUND: Controversy exists regarding the frequency of late stent thrombosis among patients treated with intracoronary stents and the most appropriate duration of treatment with a thienopyridine that is required to prevent this complication. METHODS: We analyzed the frequency of stent thrombosis and other ischemic events in the Antiplatelet Therapy alone versus Lovenox plus Antiplatelet therapy in patients at increased risk of Stent Thrombosis (ATLAST) trial. In the ATLAST trial, 1102 patients at increased risk of stent thrombosis (ST-elevation myocardial infarction within 48 hours, diffuse distal disease, a large amount of thrombus, acute closure, residual dissection, etc) were randomly assigned to receive either enoxaparin (40 or 60 mg given every 12 hours for 14 days) or placebo; all patients received aspirin (325 mg daily) and ticlopidine (250 mg twice daily) for only 14 days. RESULTS: The primary end point, the 30-day combined incidence of death, nonfatal myocardial infarction, and urgent revascularization, was reached in 2.3% of patients (1.8% of patients taking enoxaparin vs 2.7% of patients taking placebo; P =.295). However, during the 15th through 30th days, the frequency of ischemic events was only 0.73%, and only 0.27% (3/1102) of patients had possible stent thrombosis (95% CI 0.06, 0.77). CONCLUSION: The frequency of stent thrombosis and other adverse ischemic events in the 15th through 30th days after stent placement in even high-risk stent patients treated with ticlopidine for only 2 weeks is low whether or not enoxaparin is administered.

Coronary Thrombosis↗