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Trevor Baglin

Publications and source records attributed to Trevor Baglin.

9 recordsLinked to original sources
PubMed2006

Platelet-dependent thrombography: a method for diagnostic laboratories.

The thrombin-platelet feedback loop was examined at low concentration tissue factor using calibrated automated thrombography in combination with the elimination of contact factor activation by corn trypsin inhibitor. The results indicated that, when contact factor activation was eliminated, the thrombin-platelet feedback loop was a major determinant of thrombin generating capacity and that platelets had a greater role in regulating the propagation of thrombin generation than its initiation. This method has potential application to the measurement of platelet-dependent thrombin generation in clinical diagnostic laboratories and hence the investigation of patients with apparent hypo- or hypercoagulable phenotypes.

Adult↗
PubMed2005

Narrative review: aspirin resistance and its clinical implications.

Aspirin is currently the most cost-effective drug for the secondary prevention of cardiovascular disease, but treatment failures are relatively common. Several factors have been linked to these recurrent vascular events in patients prescribed aspirin, including smoking, drug interactions, nonadherence, comorbid conditions, and aspirin resistance. The term aspirin resistance has been used to describe not only an absence of the expected pharmacologic effects of aspirin on platelets but also poor clinical outcomes, such as recurrent vascular events, in patients treated with aspirin. Aspirin resistance is perhaps more precisely understood as the phenomenon of measurable, persisting platelet activation that occurs in patients prescribed a therapeutic dose of aspirin and may underlie an unknown proportion of aspirin treatment failures. Key challenges for future research are to standardize a definition of aspirin resistance and to compare whether different measures of platelet activation, either alone or in combination, independently predict cardiovascular events. These challenges must be met before researchers conduct studies to assess the clinical utility of testing on patient outcomes and cost-effective prescribing.

Aspirin↗
PubMed2005

The measurement and application of thrombin generation.

It is the capacity to generate thrombin, and the enzymatic work that thrombin does, that determines blood coagulability. Therefore, measurement of the enzymatic work potential of thrombin provides a method for quantifying the composite effect of the multiple factors that determine coagulation capacity. The application of measurement of thrombin generation to clinical decision making has been hampered by numerous technical difficulties and pitfalls, many of which have now been overcome. Technical advances now permit rapid, reproducible measurement. A review of clinical studies performed to date indicates the need to appreciate the precise methodology used in each case and the need to consider standardisation in future studies. Applying thrombin generation measurement to clinical decision making will require up-to-date estimates of risks relating to the disorder and the intended therapeutic intervention. Ultimately management studies will be required if the clinical utility of measurement of thrombin generation is to be proven.

Antithrombin III↗
PubMed2003

Incidence of recurrent venous thromboembolism in relation to clinical and thrombophilic risk factors: prospective cohort study.

BACKGROUND: Stratification for risk of recurrence after a first episode of venous thromboembolism (VTE) would affect the duration of anticoagulant therapy. We aimed to determine the incidence of recurrence of VTE in relation to clinical risk factors and standard laboratory testing for heritable thrombophilic defects. METHODS: We established a database to prospectively follow-up a cohort of unselected patients who had had a first episode of objectively proven VTE. We excluded patients with malignant disease and antiphospholipid syndrome. All patients were offered testing for heritable thrombophilia. FINDINGS: At 2 years, the cumulative recurrence rate in 570 patients was 11%. Incidence was lowest after surgery-related VTE (0%) and highest after unprecipitated VTE (19.4%) (p<0.001). 85% of patients were tested for heritable thrombophilic defects. Recurrence rates were not related to presence or absence of laboratory evidence of heritable thrombophilia (hazard ratio 1.50 [95% CI 0.82-2.77]; p=0.187). In patients with a first event that was unprecipitated or was associated with a non-surgical trigger, recurrence rates did not differ in patients with or without thrombophilia (1.34 [0.73-2.46]; p=0.351). INTERPRETATION: In unselected patients who have had a first episode of VTE, testing for heritable thrombophilia does not allow prediction of recurrent VTE in the first 2 years after anticoagulant therapy is stopped. However, assessment of clinical risk factors associated with the first episode of VTE does predict risk of recurrence. Patients with postoperative VTE have a very low rate of recurrence.

Adult↗
PubMed2003

Oral anticoagulant therapy in subjects with congenital or acquired thrombophilia.

Thrombophilia testing is now commonplace. However, testing for heritable thrombophilia does not predict outcome in response to oral anticoagulant therapy. At present there is no conclusive evidence that recurrence on treatment with warfarin with a target International Normalized Ratio of 2.5 is greater in patients with laboratory evidence of heritable thrombophilia compared with those without. Similarly, there is no conclusive evidence that patients with laboratory evidence of heritable thrombophilia are more likely to suffer an earlier recurrence once treatment is stopped. Therefore, the management of patients with familial thrombotic disease and patients with laboratory evidence of heritable thrombophilia should be influenced by their personal and family history rather than the results of laboratory investigations. There is no doubt that the relative risk of thrombosis is increased in affected family members of thrombosis-prone families but this translates to a relatively low absolute risk per year, and long-term primary prophylaxis with oral anticoagulant therapy is not justified in the majority. Evidence of antiphospholipid syndrome is associated with an increased risk of recurrent venous thromboembolism, but there is still uncertainty as to the optimal intensity and duration of oral anticoagulant therapy after an episode of arterial or venous thrombosis in patients with detectable antiphospholipid activity.

Administration, Oral↗
PubMedDate not supplied

Management of thrombophilia: who to screen?

Testing for laboratory evidence of heritable thrombophilia is now common. This practice undoubtedly arose in response to association studies, which revealed the influence of heritable thrombophilic defects on the development of VTE. Now that high quality clinical outcome studies are being reported it is becoming apparent that despite association, testing has limited predictive value for the majority of unselected symptomatic patients. Clearly, there is a difference between the ability of a test to explain why one individual is more likely to suffer a thrombosis than another and the ability of the same test to predict which patients who have already had thrombosis are likely to suffer a recurrence. In the absence of grade A recommendations, it is inevitable that practice will vary. Decisions will be influenced by local resources, competing demands for clinical and laboratory services and not least the professional interest of the haematologist. If thrombophilia testing is performed there is a strong case for selecting patients for testing as in most cases decisions regarding intensity and duration of anticoagulant therapy can be made purely in relation to clinical criteria.

Humans↗