Lungenembolie Development Mechanism

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Original Article. Dabigatran versus Warfarin in the Treatment of Acute Venous Thromboembolism. Sam Schulman, M.D., Clive Kearon, M.D., Ajay K. .

N Lungenembolie Development Mechanism J Med ; The direct oral thrombin inhibitor dabigatran has a predictable anticoagulant effect and may be an alternative therapy to warfarin for patients who have acute venous thromboembolism. Full Text of Background In a Lungenembolie Development Mechanism, double-blind, noninferiority trial involving patients with acute venous thromboembolism who were initially given parenteral anticoagulation therapy for a median of 9 days interquartile range, 8 to 11we compared oral dabigatran, administered at a dose of mg twice daily, with warfarin that was dose-adjusted to achieve an international normalized ratio of 2.

The primary outcome was the 6-month incidence of recurrent symptomatic, objectively confirmed venous thromboembolism and related deaths. Safety end points included bleeding events, Behandlung von Krampfadern Joghurt coronary syndromes, other adverse events, and results of liver-function tests. Full Text of Methods A total of 30 of the patients randomly assigned to receive dabigatran 2, Lungenembolie Development Mechanism.

The hazard ratio with dabigatran was 1. Major bleeding episodes occurred in 20 patients assigned to dabigatran 1.

The numbers of deaths, acute coronary syndromes, and abnormal liver-function tests were similar in the two groups. Adverse events leading Lungenembolie Development Mechanism discontinuation of the study drug occurred in 9. Full Text of Results For the treatment of acute venous thromboembolism, a fixed dose of dabigatran is as effective as warfarin, has a safety profile that is similar to that of warfarin, and does not require laboratory monitoring.

Full Text of Discussion Venous thromboembolism affects 1 to 2 adults per annually and is the third most common cause of vascular death after myocardial infarction and stroke. Dabigatran etexilate hereafter termed dabigatran is an orally available, potent, direct inhibitor of thrombin.

It is rapidly converted by ubiquitous esterases to the active drug, Lungenembolie Development Mechanism, is administered in fixed doses without the need for coagulation monitoring, is excreted by the kidney, and has a half-life of 12 to 17 hours. In the RE-COVER study, a double-blind, double-dummy, randomized trial, we compared 6 months of treatment with dabigatran, at a fixed dose of mg twice daily, with dose-adjusted warfarin therapy, Lungenembolie Development Mechanism, after initial parenteral anticoagulation, Lungenembolie Development Mechanism.

The study was funded, designed, and conducted, and the data analyzed, by Boehringer Ingelheim in conjunction with the steering committee, whose members vouch for the accuracy and completeness of the data and the analyses in this report. The members of the steering committee wrote the manuscript and made the decision to submit it for publication. Patients were recruited from clinical centers in 29 countries.

Patients 18 years of age or older who had acute, symptomatic, Lungenembolie Development Mechanism, objectively verified proximal deep-vein thrombosis of the legs or pulmonary Lungenembolie Development Mechanism and for whom 6 months of anticoagulant therapy was Lungenembolie Development Mechanism to be an Lungenembolie Development Mechanism treatment were potentially eligible.

There were no weight restrictions, Lungenembolie Development Mechanism. All patients provided written informed consent, and the institutional review board at each participating clinical center approved the study. Before randomization, the diagnosis of venous thromboembolism was established with the use of compression ultrasonography or venography of leg veins and ventilation—perfusion lung scanning, angiography, or spiral computed tomography Lungenembolie Development Mechanism pulmonary arteries, Lungenembolie Development Mechanism.

Additional baseline examination of the initially nonexamined leg or legs with the use of compression ultrasonography and, in case of symptomatic deep-vein thrombosis, examination of the pulmonary arteries with the use of perfusion lung scanning or spiral computed tomography were Lungenembolie Development Mechanism to be performed within 72 hours after randomization. We used a computer-generated randomization scheme with variable block sizes, stratified according to presentation pulmonary embolism Ösophagusvarizen Empfehlungen deep-vein thrombosis without Lungenembolie Development Mechanism pulmonary embolism and the presence or absence of active cancer.

Staff members at the clinical centers called an interactive voice-response system that Lungenembolie Development Mechanism assigned subjects to one of the supplied medication kits, Lungenembolie Development Mechanism. The treatment-group assignment was concealed from all the investigators and their staff at the coordinating center and the clinical centers and from the clinical monitors. Patients were assigned in a 1: Initial treatment with an approved parenteral anticoagulant generally unfractionated heparin administered intravenously or low-molecular-weight heparin administered subcutaneously was usually started before random assignment.

Warfarin or a placebo that looked identical to warfarin was generally started on the day of random assignment and was adjusted to achieve an INR of 2. Administration of dabigatran or a placebo that looked identical to dabigatran was initiated, and the parenteral anticoagulant was stopped, once the parenteral Lungenembolie Development Mechanism had been given for at least 5 days and the true or sham INR was recorded as 2.

The first dose of dabigatran was given within 2 hours before the time that the next dose of initial parenteral therapy would have been due or at the time of discontinuation of intravenous unfractionated heparin, Lungenembolie Development Mechanism.

Patients were assessed at 7 days and then monthly until 6 months and were told to contact their study site immediately if symptoms developed that were suggestive of venous thromboembolism or bleeding.

An additional follow-up visit was scheduled for 30 days after completion of the study, unless the patient had discontinued the study drug before 6 months, Lungenembolie Development Mechanism, had started open-label anticoagulant therapy, or had been enrolled in another trial.

Symptoms suggestive of Lungenembolie Development Mechanism venous thromboembolism were evaluated with Lungenembolie Development Mechanism use of the same diagnostic methods that had been used for the initial diagnosis. Bleeding was defined as major if it was clinically overt and if it was associated with a fall in the hemoglobin level of at least 20 g per liter, resulted in the need for transfusion of 2 or more units of red cells, involved a critical site, or was fatal.

Other adverse events, results of liver-function tests and other laboratory measures, occurrence of acute coronary syndromes, and adherence quantified by capsule counts were routinely assessed. All suspected outcome events and deaths were classified by central adjudication committees, whose members were unaware of the treatment assignments.

The trial was designed to determine whether 6 months of dabigatran therapy was as effective as 6 months of warfarin therapy i. A sample size of patients, with in each group, and an expected Lungenembolie Development Mechanism of 46 events satisfied these requirements, Lungenembolie Development Mechanism.

No formal interim analyses were planned or performed. The data and safety monitoring board monitored safety and efficacy end points. The primary analysis for efficacy was a comparison between the groups of the time to the first occurrence of the composite end point of symptomatic venous thromboembolism or death associated with venous thromboembolism in the 6 months after random assignment, as assessed by the hazard ratio calculated with the use of the Cox model and the difference in risk calculated with the use of Kaplan—Meier estimates.

Both summary statistics were adjusted for the initial presentation i. If noninferiority was established by both criteria, testing for superiority Lungenembolie Development Mechanism dabigatran was to be performed.

We analyzed efficacy according to a modified intention-to-treat principle, since patients who did not receive any study drug were excluded from all analyses, as was prespecified in the protocol. For safety analyses, including bleeding episodes, events were considered from the time of the first intake of the study drug to 6 days after the last intake of the study drug; these analyses were performed on the basis of the patient's actual treatment with the study drug.

The 6-day period after the last intake of the study drug was not included in the analysis if patients started open-label anticoagulant therapy or if they were enrolled in the RE-MEDY study ClinicalTrials. All safety analyses and secondary Lungenembolie Development Mechanism analyses were predefined. From April through Novembera total of patients were randomly assigned to a study group; Seven patients in the dabigatran group and 18 in the warfarin group did not receive any study medication 4 did not meet the inclusion criteria for venous thromboembolism, 11 met the exclusion criteria, 5 withdrew consent, 4 never took the study drug, and 1 had another reason.

A total of patients in the dabigatran group and in the warfarin group were included in the analysis of efficacy.

One patient who was assigned to receive dabigatran mistakenly received warfarin during the entire Lungenembolie Development Mechanism this patient did not have any outcome event and was included as part of the warfarin group in the safety analysis.

There were no significant differences between the groups in baseline characteristics Table 1 Table 1 Characteristics of the Patients and Treatments. Parenteral anticoagulation was given for a mean of 10 days in both treatment groups. The details of the treatment given are shown in Table 1. The Lungenembolie Development Mechanism number of INR values obtained in the warfarin group over the course of 6 months was The study drug was stopped before 6 months in patients The observation time for the assessment of efficacy was shorter than 6 months in patients 7.

Although it was intended that all patients who stopped the study drug owing to an adverse event or who were considered to show nonadherence would complete 6 months of follow-up, this did not always occur.

After completion of 6 Lungenembolie Development Mechanism in this trial, patients in the dabigatran group and patients in the warfarin group gave additional informed consent and were randomly assigned a second time to receive treatment with dabigatran or warfarin as extended secondary prophylaxis, as part of the double-blind RE-MEDY study, Lungenembolie Development Mechanism. The investigators suspected that recurrent venous thromboembolism had occurred or that a death had been related to recurrent venous thromboembolism in patients in the dabigatran group and patients in the warfarin group.

After central adjudication, the primary outcome for efficacy was confirmed in 30 patients in the dabigatran group 2. The difference in risk was 0. The results for the components of the primary end point are shown in Table 2 Table 2 Efficacy and Bleeding Outcomes.

There was no significant difference in efficacy in predefined subgroups see the Supplementary Appendix, Lungenembolie Development Mechanism. Since noninferiority was established, we tested for superiority and found that it was not reached.

A total of 20 patients in the dabigatran group 1. The hazard ratio with dabigatran for major bleeding at 6 months was 0. The sites of major bleeding events in the dabigatran group were gastrointestinal nine eventsurogenital fiveintraarticular oneintramuscular oneor other sixand the sites in the warfarin group were urogenital six eventsgastrointestinal fiveintraarticular fourintracranial threeintramuscular threeor other four ; some patients had bleeding at more than one site.

INR values were not obtained when bleeding occurred, in order Lungenembolie Development Mechanism avoid unblinding of the treatment assignment. A total of 71 patients in the dabigatran group 5. The relative risk Lungenembolie Development Mechanism bleeding with dabigatran as compared with warfarin was similar among the subgroups data not shown.

The only type of bleeding that showed a trend to higher incidence in the dabigatran group was gastrointestinal hemorrhage Table 2. There were patients in the dabigatran group 9, Lungenembolie Development Mechanism. The number of patients who died, had an acute coronary syndrome, or had an elevation of the alanine aminotransferase level or the aspartate aminotransferase level exceeding three times the upper limit of normal while taking the study drug did not differ significantly between the treatment groups Table 3 Table 3 Adverse Events during the Double-Dummy Phase and during the Total Period of Treatment.

A combination of an alanine aminotransferase level exceeding Lungenembolie Development Mechanism times the upper limit of normal and bilirubin exceeding twice the upper limit of normal was seen in two patients in the dabigatran group of whom one had pancreatic cancer and the other had cholangitis and four patients in the warfarin group of whom three had Lungenembolie Development Mechanism cancer and one had uterine cancer with liver metastases. There were no significant differences between the two treatment groups in the frequency of any adverse events Table 3 except for dyspepsia 2.

Lungenembolie Development Mechanism this large, double-blind trial involving patients with acute venous thromboembolism, Lungenembolie Development Mechanism, we compared 6 months of treatment with dabigatran, administered at a dose of mg twice daily, with warfarin therapy, Lungenembolie Development Mechanism, after initial treatment with parenteral anticoagulation.

We showed that dabigatran is noninferior to Lungenembolie Development Mechanism when warfarin is dose-adjusted to achieve and maintain an INR in the range of 2.

Venous thromboembolism or related deaths occurred in 30 patients in the dabigatran group as compared with 27 patients in the warfarin group.

Dabigatran is an effective anticoagulant agent because direct thrombin inhibitors suppress thrombus growth by inhibiting both fibrin-bound and free thrombin, which converts fibrinogen to fibrin. The rates of bleeding with dabigatran were similar to or lower than those with warfarin. There were 20 Lungenembolie Development Mechanism bleeding events in the dabigatran group as compared with 24 in the warfarin group, and there were fewer episodes of nonmajor bleeding with dabigatran than with warfarin.

These findings are consistent with data on bleeding from the Randomized Evaluation of Long-Term Anticoagulation Therapy trial RE-LY; NCT8 in which open-label dabigatran and warfarin therapies were compared in patients with atrial fibrillation, Lungenembolie Development Mechanism. In the RE-LY trial, major bleeding and intracranial bleeding were less frequent among patients receiving dabigatran at a dose of mg twice daily than among those receiving warfarin, and in both the RE-LY trial and the current study, the incidence of nonmajor bleeding was reduced with dabigatran.

Clinically relevant nonmajor bleeding is an important factor to consider, since its management is time-consuming and costly 16 and since bleeding is the most important reason for the perception of decreased health and quality of life among patients treated with warfarin.

In trials of the only previously available oral direct thrombin inhibitor, ximelagatran, noninferiority with respect to warfarin was achieved in the treatment of recurrent venous thromboembolism, and rates of major bleeding Lungenembolie Development Mechanism similar in both treatment groups, Lungenembolie Development Mechanism. The mechanism for increased dyspepsia among patients receiving dabigatran therapy is currently unknown.

None of the other adverse events differed significantly between the treatments. Therefore, additional studies should be performed that involve patients whose baseline characteristics differ markedly from this population.

A limitation of the study is that the first dose of dabigatran, which has a rapid onset of effect, was given only after initial parenteral anticoagulation therapy had been administered for a median of 9 days interquartile range, 8 to Thus, Lungenembolie Development Mechanism, there are no data to support the use of dabigatran monotherapy for acute venous thromboembolism.

We chose to treat patients in the dabigatran group with initial parenteral anticoagulation, because treatment of acute venous thromboembolism with ximelagatran alone appeared to be associated with a higher early rate of recurrent venous thromboembolism than did treatment with enoxaparin and warfarin.

Our trial provides data to support dabigatran as a fixed-dose oral treatment for acute deep-vein thrombosis and pulmonary embolism. For patients and health care providers, dabigatran is a far more convenient drug than warfarin because it has Lungenembolie Development Mechanism known interactions with foods and minimal interactions with other Blutegel als Behandlung für Krampfadern and therefore does not require routine blood-coagulation testing.


Lungenembolie Development Mechanism

N Engl J Med ; Comments open through May 30, Extending Lungenembolie Development Mechanism prevents recurrences but is associated with increased bleeding.

The benefit of aspirin for the prevention of recurrent venous thromboembolism is unknown. Full Text of Background In this multicenter, investigator-initiated, double-blind study, patients with first-ever unprovoked venous thromboembolism who had completed 6 to 18 months of oral anticoagulant treatment were randomly assigned to aspirin, mg daily, or placebo for 2 years, with the option of extending the study treatment.

The primary efficacy outcome was recurrence of venous thromboembolism, and major bleeding was the primary safety outcome. Full Text of Methods Venous thromboembolism recurred in 28 of the patients who received aspirin and in 43 of the patients who received placebo 6.

During a median treatment period of One patient in each treatment group had a major bleeding episode, Lungenembolie Development Mechanism. Adverse events were similar in the two groups. Full Text of Results Aspirin reduced the risk of recurrence when given to patients with unprovoked venous thromboembolism who had discontinued anticoagulant treatment, with no apparent increase in the risk of major bleeding.

Full Text of Discussion The risk of recurrence of venous thromboembolism persists for many years after anticoagulant treatment is withdrawn. The role of aspirin in the Grundstück von trophischen Geschwüren am Bein prevention of venous thromboembolism has been evaluated in various clinical settings.

A potential benefit from antiplatelet therapy in the secondary prevention of venous thromboembolism first became evident with Lungenembolie Development Mechanism results of a randomized study involving only 39 patients, Lungenembolie Development Mechanism. The aim of the Aspirin for the Prevention of Recurrent Venous Thromboembolism the Warfarin and Aspirin [WARFASA] study was to assess the clinical benefit of aspirin for the prevention of recurrence after a course of treatment with vitamin K antagonists in patients with unprovoked venous thromboembolism.

Patients older than 18 years of age were eligible for the study if they had been treated for 6 to 18 months with vitamin K antagonists with a target international normalized ratio [INR] of 2. Venous thromboembolism was considered to be unprovoked when it occurred in the absence of any known risk factor for this event.

The main exclusion criteria can be found in the Supplementary Appendixavailable with the full text of this article at NEJM.

Eligible patients were randomly assigned to aspirin, mg once daily, Lungenembolie Development Mechanism placebo for 2 years, with the option of extending the study treatment.

Randomization occurred within 2 weeks after vitamin K antagonists had been withdrawn. All suspected study outcome events were assessed by a central, independent adjudication committee whose members were unaware of the group assignments and who reviewed the imaging results. The primary efficacy outcome was symptomatic, objectively confirmed recurrence of venous thromboembolism, defined Lungenembolie Development Mechanism the composite of deep-vein thrombosis or nonfatal or fatal pulmonary embolism.

Pulmonary embolism was considered to be the cause of death if it was confirmed on autopsy or if death was preceded by a diagnosis of either pulmonary embolism objectively confirmed on computed tomography or lung scanning or deep-vein thrombosis objectively confirmed on compression ultrasonography and whenever the cause could not be attributed to an alternative diagnosis, Lungenembolie Development Mechanism.

Secondary efficacy outcomes included nonfatal myocardial infarction, unstable angina, stroke, Lungenembolie Development Mechanism, transient ischemic attack, acute ischemia of the lower limbs, Lungenembolie Development Mechanism, and death from any Lungenembolie Development Mechanism. The principal safety outcome was major bleeding. An overt bleeding event was defined as major if it was fatal, occurred in a critical location intracranial, intraspinal, intraocular, retroperitoneal, intraarticular, pericardial, or intramuscular [leading to a compartment syndrome]or was associated with a decrease in the hemoglobin level of at least 2.

Clinically relevant, nonmajor bleeding, defined as any overt bleeding that required a medical intervention and did not meet any of the criteria for major bleeding, was a Lungenembolie Development Mechanism safety outcome. Patients were reexamined every 3 months during the first year after randomization and every 6 months thereafter. Patients were instructed to report to the study center immediately if they had symptoms suggestive of recurrent venous thromboembolism or bleeding complications.

In cases of suspected recurrence, objective testing was required, Lungenembolie Development Mechanism. The study was designed by the members of the steering committee. The protocol and amendments were approved by the institutional review board or ethics committee at each study center. During the course of the study, two substantial protocol amendments were made and submitted to the ethics committees in May and December The first of these amendments reflected the change to an event-driven design, Lungenembolie Development Mechanism, and the second reflected the change of the primary study end point to venous thromboembolism only.

These changes were made so that the study design would be consistent with that of contemporary trials of extended treatment for venous thromboembolism i. The study was performed in accordance with the protocol and with the provisions of the Declaration of Helsinki and local regulations. The protocol and statistical analysis plan are available at NEJM. Written informed consent was obtained from all patients before randomization.

The steering committee had final responsibility for verification and analyses of the data. The writing committee wrote the manuscript and vouches for the accuracy and completeness of the reported data.

All authors contributed to the interpretation of the results, approved the final version of the manuscript, Lungenembolie Development Mechanism made the decision to submit the manuscript for publication, Lungenembolie Development Mechanism. The study was supported by a grant-in-aid from Bayer HealthCare. Aspirin and placebo tablets were supplied by Bayer HealthCare. Bayer played no role in the design of the study, in data collection or analysis, or Lungenembolie Development Mechanism manuscript preparation.

With an expected event rate of 8. The primary efficacy analysis, which Lungenembolie Development Mechanism all outcome events occurring Lungenembolie Development Mechanism randomization to the end of the Krampfadern Behandlung zum Forum, was performed according to a modified intention-to-treat principle, with all patients who received at least one dose of the assigned study drug after randomization included in the analysis, Lungenembolie Development Mechanism.

Event rates are reported as proportions of patients per year. Hazard ratios, confidence intervals, and P values were calculated with the use of Cox proportional-hazards models and SPSS statistical software, version The safety analysis included all patients who received at least one dose of the study drug. Bleeding events were included in the analyses if they occurred during the period of administration of the study drug or within 2 days after its discontinuation.

From May through Augusta total of patients were randomly assigned to a study group; patients received aspirin, received placebo, and 1 patient, who was assigned to the placebo group, did not receive the study drug Figure 1 Figure 1 Enrollment and Randomization. Adverse events were presumed to be drug-related. VTE denotes venous thromboembolism. The median period during which the patients participated in the study was The study drug was discontinued prematurely in 16 patients given aspirin and in 15 patients given placebo Figure 1, Lungenembolie Development Mechanism.

Since the end of the study was event-driven, the duration of treatment was shorter than the intended 2 years for 10 patients in the aspirin group 4. The median duration of the study treatment was Three patients in the aspirin group 1. There were no significant between-group differences in baseline characteristics of the patients Table 1 Table Lungenembolie Development Mechanism Demographic and Clinical Characteristics of the Patients, According to Study Group.

A recurrence of venous thromboembolism occurred in 71 patients 8, Lungenembolie Development Mechanism. A recurrence in the form of pulmonary embolism was more common among the patients who entered the study because of prior pulmonary embolism than among those who entered because of deep-vein thrombosis The primary prespecified outcome, recurrence of venous thromboembolism, occurred in 28 of the patients who received aspirin, Lungenembolie Development Mechanism, as compared with 43 of the patients who received placebo 6.

Panel A shows the cumulative risk of recurrent venous thromboembolism during the entire study period, and Panel B shows the risk during treatment. Panel C shows the results of an analysis of risk during the study period after adjustment for age, sex, Lungenembolie Development Mechanism, index event pulmonary embolism or deep-vein thrombosisand duration of anticoagulant therapy. While taking the study drug, 23 patients in the aspirin group had a recurrence, as compared with 39 patients in the placebo group 5.

Exploratory, post hoc subgroup analyses revealed that 11 of 83 patients in the aspirin group who entered the study because of pulmonary embolism had a recurrent event, as compared with 16 of 67 patients in the placebo group 6.

Among the patients who entered the study because of deep-vein thrombosis, 17 of in the aspirin group and 27 of in the placebo group had a recurrent event 6.

An analysis adjusted for age, sex, index event pulmonary embolism or deep-vein thrombosisand duration of initial anticoagulant treatment confirmed that aspirin treatment reduced the risk of recurrence adjusted hazard ratio, 0.

Independent risk factors for recurrent venous thromboembolism included an age of more than 65 years hazard ratio, 2. No association was found between recurrent venous Lungenembolie Development Mechanism and prior anticoagulant therapy lasting for 6 months, as compared with a more extended duration hazard ratio, 1. There were two episodes of nonfatal major bleeding: Clinically relevant, Lungenembolie Development Mechanism, nonmajor bleeding occurred in three patients who were randomly assigned to aspirin gingival bleeding in one patient and cutaneous hematomas in two patients and in three patients who were randomly assigned to placebo musculoskeletal bleeding after trauma in two and hemorrhagic gastritis in one.

Death occurred in six patients in the aspirin group 1. Sudden death occurred in two patients one in each groupand both deaths were adjudicated as being the result of pulmonary embolism. In addition, four patients died from cancer and five from other causes. Arterial events occurred in eight patients in the aspirin group and in five patients in the placebo group 1. Five patients had an adverse event that was Lungenembolie Development Mechanism to be due to the study treatment and led to discontinuation of the drug.

These events were gastric pain in three patients one in the aspirin group and two in the placebo groupa cutaneous reaction in one aspirin-treated Lungenembolie Development Mechanism, and renal failure in another Lungenembolie Development Mechanism patient. An indication for antiplatelet therapy other than an acute arterial event occurred in five patients in the aspirin group and in three patients in the placebo group, and an indication for anticoagulant therapy other than recurrent venous thromboembolism occurred in three patients and in two patients in the two groups, respectively.

This benefit is achieved with no apparent increase in the risk of major bleeding. Patients with unprovoked venous thromboembolism are at high risk for recurrence after oral anticoagulant treatment is withdrawn. Our study shows that aspirin therapy is a potential alternative to extended oral anticoagulant treatment for the long-term secondary prevention of venous thromboembolism. The reduction in the risk of recurrence of venous thromboembolism that was observed with aspirin treatment in our study is consistent with the reduction shown in previous studies evaluating aspirin for the primary prevention of venous thromboembolism.

The efficacy of aspirin for primary or secondary prevention of venous thromboembolism is biologically plausible because of the involvement of platelets in the formation of venous thrombi and the increased levels of markers of platelet 21,22 and endothelial 23 activation in patients with venous thromboembolism.

As compared with placebo, aspirin was not associated with an increase in the rate of major bleeding, which was about 0. We used the dose of aspirin recommended for the secondary prevention of cardiovascular or cerebrovascular events.

In two studies of a low-intensity warfarin regimen for extended treatment of venous thromboembolism, Lungenembolie Development Mechanism, the rates of major bleeding were 0. Since patients were excluded from our study if they had cancer, clinically significant thrombophilia, or a bleeding event during the period of anticoagulant treatment, the results are not applicable to these groups.

However, we estimate that a substantial proportion probably the majority of patients with an initial episode of venous thromboembolism would be eligible for aspirin therapy as secondary prevention. The oral thrombin inhibitor dabigatran 28,29 and the oral factor Xa inhibitor rivaroxaban 30 were recently evaluated for the extended treatment of Lungenembolie Development Mechanism thromboembolism.

An advantage of these agents over vitamin K antagonists is that they do not require laboratory monitoring and dose adjustments. As expected, the reduction in the risk of recurrence is lower with aspirin than with these Lungenembolie Development Mechanism oral agents.

All the available antithrombotic strategies for extended treatment of venous thromboembolism have been compared with placebo. The place of aspirin among these strategies remains to be defined in future studies, Lungenembolie Development Mechanism. However, aspirin is low in cost and its side effects are well known, since its safety has been assessed over the years in millions of patients.


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Original Article. Dabigatran versus Warfarin in the Treatment of Acute Venous Thromboembolism. Sam Schulman, M.D., Clive Kearon, M.D., Ajay K. .
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Original Article. Dabigatran versus Warfarin in the Treatment of Acute Venous Thromboembolism. Sam Schulman, M.D., Clive Kearon, M.D., Ajay K. .
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Original Article. Dabigatran versus Warfarin in the Treatment of Acute Venous Thromboembolism. Sam Schulman, M.D., Clive Kearon, M.D., Ajay K. .
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Original Article. Dabigatran versus Warfarin in the Treatment of Acute Venous Thromboembolism. Sam Schulman, M.D., Clive Kearon, M.D., Ajay K. .
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Original Article. Dabigatran versus Warfarin in the Treatment of Acute Venous Thromboembolism. Sam Schulman, M.D., Clive Kearon, M.D., Ajay K. .
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