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Introduction: The national Venous Thromboembolism (VTE) Prevention Programme in England was launched in 2010 and incorporates standardised guidance on risk assessment (RA) and thromboprophylaxis (TP) with a requirement for root cause analysis of all episodes of hospital associated thrombosis (HAT), defined as any VTE occurring whilst an inpatient or within 90 days of discharge. We previously reported findings of root cause analysis for HAT over 2010 - 2012, demonstrating that achieving a 90% risk assessment rate resulted in a significant reduction in the incidence of HAT. We update our findings on the impact of implementation of the national programme on the incidence of HAT, proportion of potentially preventable HAT episodes, and mortality from hospital-associated pulmonary embolism (PE). As appropriate TP only reduces the risk of VTE by two-thirds, we also looked at risk factors for TP failure. Methods: We examined HAT data collected from the root cause analysis programme at King's College Hospital from April 2011 to March 2015. Further data were gathered through retrospective review of patient notes. VTE risk factors for HAT attributed to TP failure were compared to a "non-HAT" group, (patients who received appropriate TP and did not develop HAT) drawn from VTE prevention audit data from 2013-2014. Episodes of HAT that developed following inadequate prescription or administration of either anticoagulant or mechanical TP were deemed as "potentially preventable" episodes. Results: Across the four-year study period there were 725 episodes of HAT, giving an incidence of 3.28 episodes per 1000 hospital admissions. There was no significant change in incidence from 2011-2015. The median age of the cohort was 64 years (IQR = 27 years). 56.7% (n = 411) of the HAT episodes were deep vein thromboses, of which 54.7% (n = 225) involved the proximal vasculature. PE accounted for 41.7% (n = 302) episodes, of which 10.9% (n = 33) were fatal events. HAT developed following medical, surgical or obstetric admission in 43.3% (n = 314), 54.6% (n = 396) and 2.1% (n = 15) respectively. VTE risk factors were present in 97.9% (n = 710) of patients with HAT with concomitant bleeding risk factors in 37.1% (n = 269). Consistently, the most common outcome of root cause analysis was TP failure (47.6% overall, n = 345) with no significant trend across the study period; 19.7% (n = 143) of episodes were attributed to inadequate anticoagulant TP, 26.1% (n = 189) to contraindication to anticoagulant TP, 4.4% (n = 32) to contraindication to all forms of TP, and 2.2% (n = 16) episodes were unexpected (HAT occurring in a patient without identifiable VTE risk factors). There has been a significant reduction in the proportion of potentially preventable HAT episodes from 38.2% (n = 66) in 2011-2012 to 20.3% (n = 39) in 2014-2015 (p < 0.001). Furthermore, the proportion of fatal PE reduced over the study period from 16.0% (n = 12) of HAT in 2011-2012 to 6.3% (n = 5) of HAT in 2014-2015 (p = 0.049). The audit of VTE prevention practice over 2013/14 included 515 patients, of which 423 (82.1%) received appropriate TP and did not develop HAT. Compared to this group, patients with HAT attributed to TP failure had more risk factors (3.1 vs. 2.7, p < 0.002), were more likely to be over 60 years of age (59.4% vs. 42.3%, p = 0.01), or to have had orthopaedic surgery(6.7% vs. 1.8%, p = 0.001). Discussion: Implementation of a comprehensive VTE prevention programme incorporating root cause analysis of HAT has led to a significant fall in the proportion of HAT that were potentially preventable with a corresponding reduction in mortality attributed to PE. However, there has been no change in the overall incidence of HAT with a rise in cases associated with TP failure. Further research is required to optimise TP in high VTE risk groups. Disclosures Arya: Bayer plc: Research Funding.

The direct oral anticoagulants (DOACs) are revolutionising the management of acute venous thromboembolism (VTE). Although favourable short term outcomes have been demonstrated with these agents, there is a growing need to improve our understanding of biological and clinical predictors of longer-term outcomes with all DOACs. In addition to reducing the need for dual anticoagulant coverage, the use of oral rivaroxaban, has accelerated the implementation of outpatient and early discharge treatment protocols for VTE, in particular for pulmonary embolism (PE). Although clinical trials provide evidence of efficacy and safety, there is a need for ongoing assessment of outcomes in unselected populations treated in routine 'real-world' clinical practice. As for most drugs, conditions requiring special attention include advanced age, impaired renal or liver function, extremes of body weight, presence of multiple co-morbidities, and the need for concomitant therapies. Such conditions commonly co-exist, particularly in elderly patients. In clinical practice patients aged 80 years or older and requiring anticoagulation are becoming increasingly common. In addition, trials do not report long-term adverse outcomes after VTE; aside from bleeding, currently there are no long-term data that assess the impact of the DOACs as part of a single-drug treatment algorithm on long-term recurrence. The FIRST registry will assess long-term outcomes of patients with acute VTE treated with rivaroxaban from diagnosis - our hypothesis is that the long-term outcomes for such patients will be favourable due to consistent anticoagulation intensity, particularly during the acute phase of thrombosis. There are currently no data describing post-thrombotic syndrome (PTS) or chronic thromboembolic pulmonary hypertension (CTEPH) incidence rates in patients treated with DOACs. Patients enrolled onto the FIRST registry will be followed up for five years with primary end-points defined as incidence of long-term sequelae (PTS and CTEPH, defined clinically) and secondary endpoints including recurrence, bleeding and anticoagulation related satisfaction and adherence scores. Analysis of these data may also contribute to improved risk stratification strategies to identify patients who have the greatest risk of adverse bleeding events, recurrence and long-term VTE-related morbidity. Recruitment is currently underway at 20 UK hospitals, with a target of 1500 patients, to be achieved by summer 2017. Disclosures No relevant conflicts of interest to declare.

This study examines histomorphometric features in chorionic villi obtained by chorionic villus sampling (CVS) at 11-14 weeks of gestation from 124 ongoing pregnancies (38 with trisomy 21, 14 with trisomy 18, 11 with trisomy 13 and 61 chromosomally normal controls). In the trisomy 21 group there was an inverse relationship between fetal nuchal translucency thickness (NT) and villus diameter and number of capillaries per villus cross-section. In about half of the cases there was perivillous fibrinoid present, and the amount of this increased with gestation. Compared to the chromosomally normal group, in trisomy 18 the villus diameter was smaller and the number of capillaries per villus cross-section was reduced. In the trisomy 21 group, villi had an increased percentage of two layered trophoblast present and an increased proportion of villus capillaries with nucleated red blood cells present. In all three trisomies, but particularly in trisomies 18 and 13, both the amount of basophilic stippling of the basement membrane and the proportion of cases with stippling was increased. These results provide data on the possible mechanisms of increased fetal NT and on abnormal placental development in fetal trisomies.

Abstract 363 The national Venous Thromboembolism (VTE) Prevention Programme in England incorporates standardised guidance on risk assessment (RA) and thromboprophylaxis (TP) with a requirement for root cause analysis of all episodes of hospital associated thrombosis (HAT), defined as any VTE occurring whilst an inpatient or within 90 days of discharge. We previously reported findings of root cause analysis for HAT from 2010. We present updated findings from combined census of VTE RA and the root cause analysis programme at King's College Hospital, London over a 24 month period. A principal change in VTE RA process was the phased introduction of prompted electronic RA in 2011. Census data collection of RA identified a significantly higher median monthly RA rate in 2011 of 93.9% (IQR 92.3 – 94.5) compared to 85.8% (IQR 72.0–90.4; P=0.001) in 2010. The root cause analysis programme for HAT identified 192 episodes in 2011 compared to 236 events in 2010. The median number of events per month was significantly lower at 1.2 per 1000 admissions (IQR 0.8 to 1.4) in 2011 compared to 1.5 per 1000 admissions (IQR 1.3 – 1.8; P=0.023) in 2010. There was no significant difference in type of admission preceding HAT between 2010 and 2011 (medical 55.5% vs 47.4%, surgical 42.4% vs 49.5% and obstetric 2.1% vs 3.1% respectively). The proportion of HAT presenting as PE was lower in 2011 (36.7%) compared to 2010 (46.7%, P=0.07). The proportion of fatal PE was non-significantly lower in 2011 at 6.2% (n=12) compared to 2010 (7.3%, n=17). There was no significant difference in 90 day mortality between 2010 and 2011 (21.2% vs 19.3%). Root cause analysis was completed for 65.3% and 89.0% of HATs in 2010 and 2011 respectively. Of investigated episodes, RA was completed for 85.4% in 2011 compared to 43.9% (P Disclosures: No relevant conflicts of interest to declare.

Abstract 675 The national Venous Thromboembolism (VTE) Prevention Programme in England incorporates standardised guidance on risk assessment (RA) and thromboprophylaxis (TP) with a requirement for root cause analysis of all episodes of hospital associated thrombosis (HAT), defined as any VTE occurring whilst an inpatient or within 90 days of discharge. We report findings from audit of root cause analysis of HAT over 12 months at King's, a major London tertiary centre with 900 beds and an estimated 53 000 admissions per annum. 239 episodes of HAT were identified associated with surgical, medical and obstetric admission accounting for 101 (42.3%), 133 (55.6%) and 5 (2.1%) cases respectively. The estimated incidence of HAT is 4.5 per 1000 admissions. The mean age of patients with HAT was 62.7 (+/− 16.8) years, with males accounting for 53.6% of the cohort. HAT manifested as deep vein thrombosis in 121 (50.6%) and pulmonary embolism in 128 (49.6%). The median time to diagnosis of HAT following admission was 16 days (IQR 7–30). 171 (67.4%) of HAT occurred prior to discharge. Of the 78 (31.7%) events occurring post discharge, 60 (76.9%) required readmission for management of HAT and 2 (2.6%) represented with fatal events. HAT was associated with mortality in 51 cases (21.3%), with death directly attributable to PE in 16 (6.7%). The estimated incidence of HAT associated with fatal PE is 0.3 per 1000 admissions. Of note, autopsy was undertaken in 12/51 with PE identified as the primary cause of death in 11/12 (2/12 had known/suspected VTE prior to death). The five remaining patients with PE as the primary cause of death had the diagnosis made on clinical suspicion alone in four cases and radiological imaging in one case. The remaining deaths were attributed to other causes in 25, with 15 having unknown cause of death as certification occurred in the community (10 with known advanced malignancy at discharge). Root cause analysis has been completed for 149 (62.3%) of HAT episodes. Of these, 43.9% had RA undertaken on admission to hospital. Retrospective RA revealed 91.0% of patients were at high risk for VTE with 33.1% also at high risk of bleeding. 72% were prescribed anticoagulant TP. Anticoagulant prophylaxis was prescribed for 30/49 (61.2%) medical, 33/36 (91.7%) surgical and 3/4 (75%) obstetric HAT cases with a high VTE risk and low bleeding risk. Of those with a high bleeding risk, 8/23 (34.8%) and 15/27 (55.6%) medical and surgical patients respectively received anticoagulant TP for part of their admission. Mechanical TP was prescribed for 41/63 (65.1%) surgical, all obstetric (4) HAT cases and 5/15 (33.3%) medical patients in whom mechanical TP was indicated and appropriate. HAT was attributed to inadequate TP in 51 (32.5%), contraindication to chemical TP in 23 (14.6%), contraindication to all TP in 11 (7.0), TP failure in 43 (27.4%), line associated in 20 (12.7%), and was considered unexpected in 9 (5.7%) patients without any risk factors for VTE. Inadequate TP resulted from failure to prescribe in 17 (33.3%), unexplained delay in initiation in 8 (15.7%), unexplained missed doses in 7 (13.7%), inadequate duration of TP in 5 (9.8%) or inferior agent or dose in 9 (17.6%) cases with a combination of the above in 5 (9.8%) cases. Mortality associated with inadequate TP was 21.6% with death directly attributable to PE of 5.9%. TP remains underused in cases of HAT, with lowest rates associated with medical admission. At our centre, improved RA and TP could reduce the annual incidence of HAT by an estimated 21%. Further research is required to improve risk assessment and thromboprophylactic strategies to address unexpected events and those arising despite optimal TP. Disclosures: No relevant conflicts of interest to declare.

Abstract 4211 Platelet size is thought to reflect reactivity; Mean platelet volume (MPV) was recently reported as a possible predictor for VTE, but it is not clear whether ethnic origin impacts on this risk factor. King's serves an ethnically diverse community and to assess whether MPV is a predictor of VTE in our population, we conducted a retrospective analysis of consecutive patients referred to our DVT service between January 2007 and October 2009. Patients with a confirmed first lower limb DVT (provoked n=153, unprovoked n=110) were included as subjects and controls (n=151) were derived from consecutive patients referred with objective exclusion of a DVT and no previous history of VTE, active cancer or surgery in the previous 6 weeks. All patients had a full blood count at presentation analysed on an automated analyser (using optical light scatter for MPV) within 4 hours of collection. There was no difference in mean age (54.7 vs 54.8), smoking status or ethnic group (51% vs 52.3% white, 38.4% vs 33.8% black and 10.6% vs 13.9% other) between subjects and controls respectively. Males accounted for 47.5% of subjects and 27.2% of controls. DVTs were unprovoked in 41.8% with 13.7% associated with surgery, 7.6% cancer, 10.6% pregnancy or hormone therapy. The remainder (25.1%) were secondary to cast, trauma, immobilisation or travel. Mean MPV was significantly higher in subjects than controls (8.17 vs 7.79, p=0.001) with a more marked difference in those with unprovoked DVT compared with controls (8.28 vs 7.79, p 9.18 (90th centile) was 1.26 (95% CI 1.08– 4.76, p=0.01) and increased to 1.59 (1.18-2.1, p=0.008) in those with unprovoked DVT. Relative risk associated with platelet count Disclosures: No relevant conflicts of interest to declare.

Abstract 3825 The national Venous Thromboembolism prevention programme in England emphasises reducing hospital-associated thrombosis by ensuring adequate prophylaxis, but this is problematic in stroke patients due to poor uptake of pharmacological prophylaxis and lack of evidence for mechanical measures. Our prospective study aimed to develop clinical and laboratory predictors of thrombosis in patients after acute stroke. Participants were recruited within 48 hours of admission to the Acute Stroke Centre at King's College Hospital London UK, between June 2009 and June 2010. 142 participants were recruited with complete data available from 86 participants. Racial distribution was as follows: 75% Caucasian, 19% African/Caribbean, 6% Asian. Mean age was 69 years (SD15) and 45/86 (52%) were female. 73 strokes were ischaemic and 13 haemorrhagic. In the ischaemic stroke group, 33 of 73 (45%) were thrombolysed as per National stroke strategy. Baseline demographic data and clinical evaluation using the NIH Stroke Scale (NIHSS) and Barthel Index (BI) were recorded. Analysis of prothrombotic markers was performed including D-dimer (DD), Clauss fibrinogen (CFIB) and thrombin generation (TG) measured by calibrated automated thrombography (CAT). The TG assay measured kinetics in platelet poor plasma including lag time (LT) - time taken to generate 10nM of thrombin; time to peak (TTP) - time in reach maximum TG; peak thrombin generation (PTG)- maximum thrombin concentration; and endogenous thrombin potential (ETP) - area under the curve (expressed in nmol/L of thrombin). In the second week all laboratory tests were repeated and lower limb compression ultrasound scan (CUSS) performed. 18/86 (20.9%) had objectively confirmed DVT (5 proximal and 13 distal). 4 DVTs (2 proximal and 2 distal) occurred in patients with haemorrhagic stroke, and 14 DVTs (3 proximal and 11 distal) occurred in patients with ischaemic stroke. Both BI (p=0.02) and body mass index (p=0.05) but not NIHSS (p=0.13) were associated with DVT. TG assay parameters and CFIB were not associated with the risk of DVT. Elevated DD was significantly associated with DVT development both at baseline (DD 2425 ng/ml vs 1010 ng/ml, p=0.0010) and at week 2 (DD 2770 ng/ml vs 830 ng/ml, P Disclosures: No relevant conflicts of interest to declare.

Abstract 434 Budd-Chiari Syndrome (BCS) is a group of disorders resulting from obstruction to hepatic venous outflow; myeloproliferative disorder (MPD) accounts for 10-40% of cases. We previously described latent MPD in 58.5% of patients with idiopathic BCS, detected with allele-specific PCR for the JAK2V617F mutation and proposed its use as a screening tool for occult MPD. A predisposing germline JAK2 haplotype (designated 46/1) has since been described as a strong genetic risk factor for MPD and may further characterise latent MPD in BCS. We studied 28 patients with BCS (23 from our original cohort; female n=16, mean age 30.3 years, SD 10) presenting between 1985 and 2008; 14 with the JAK2V617F mutation. Genomic DNA was obtained from archived bone marrow films, fractionated and unfractionated peripheral blood or bone marrow leucocytes. Skin biopsy or CD3+ cells were used as a source of constitutional DNA. DNA was analysed by pyrosequencing for 2 SNPs (rs12340895, rs12343867) which tag the 46/1 JAK2 haplotype. The 46/1 haplotype was detected in 16/28 (57.1%) subjects; 50% of those with the JAK2V617F mutation and 64.3% of those without it. The prevalence in those lacking the JAK2V617F mutation is significantly higher than the frequency in the Wellcome Trust Case Control Consortium cohort of 24% (P=0.0023). 3/28 subjects had previously diagnosed JAK2V617F positive Polycythemia Vera (PV) and all had the 46/1 haplotype, resulting in a prevalence of 36.4% in those with JAK2V617F positive latent MPD. Age at presentation of BCS was significantly lower in those with the 46/1 haplotype (26.4 years compared to 34.8 years, P=0.03). This difference remained significant in those lacking the JAK2V617F mutation (24.0 years compared to 37.6 years, P=0.024) but was not seen in those with the JAK2V617F mutation (P=0.547). There was no difference in presenting clinical features, haematological parameters or treatment between those with and without the 46/1 haplotype. Overall survival in 26/28 patients was 76.9% (median 90 months, range 2 days to 266 months). 17/28 subjects underwent OLT of which 14/17 (11/12 with 46/1 haplotype) are alive at a median of 90 months post transplant (range 9-266 months). 3/17 patients developed post-OLT veno-occlusive disease, all with the JAK2V617F mutation and 2/3 with the 46/1 haplotype. Overt MPD has not developed in any patient without the JAK2V617F mutation; repeat JAK2 mutational analysis was undertaken in 3/14 (2/3 with 46/1 haplotype) and none have acquired the mutation at a mean of 54 months. 19/28 cases were genotyped using SNP markers (Affymetrix SNP6); 3/19 have acquired uniparental disomy (aUPD) on 9p overlapping the JAK2 gene. As TET2 has been postulated as a ‘pre-JAK2' aberration, we sequenced the complete TET2 gene using massively parallel high throughput sequencing (Roche 454); 2/15 patients samples were positive for TET2 mutations. One of our cases had a familial history of PV; the patient, his father and uncle all have JAK2V617F positive PV and were heterozygous for the 46/1 haplotype in DNA extracted from a skin biopsy. 2/3 were homozygous for both the 46/1 haplotype and JAK2V617F mutation in bone marrow granulocytes with SNP6 array data confirming aUPD on 9p. JAK2V617F was detected in cultured in vitro colonies from all 3 family members. All 3 affected family members had normal cytogenetics and normal TET2 gene. 3 unaffected siblings were heterozygous for the 46/1 haplotype both in peripheral blood, CD3+ cells and granulocytes but negative for JAK2V617F mutation and lacked aUPD on 9p. We have found a highly significant prevalence of the 46/1 haplotype in our cohort of BCS, as well as in family members of a patient with JAK2V617F positive BCS and PV. The 46/1 haplotype was detected in patients with idiopathic BCS with and without the JAK2V617F mutation, suggesting a predisposition to idiopathic BCS independent of JAK2V617F mutation acquisition and latent MPD. The prevalence and lower age of presentation in those with the 46/1 haplotype lacking the JAK2V617F mutation supports an alternate, as yet unknown, mechanism predisposing to BCS. The presence of the 46/1 haplotype in unaffected relatives of our JAK2V617F BCS patient suggests that additional germline variation may predispose to or protect from acquisition of JAK2V617F positive disease. Alternatively the 46/1 haplotype may directly confer a cellular growth advantage via increased responsiveness of JAK2 to cytokine stimulation. Disclosures: No relevant conflicts of interest to declare.

We report five cases of clonal lymphocytosis with striking monocytoid features, immunophenotype and clinical features distinct from chronic lymphocytic leukaemia (CLL), splenic marginal zone lymphoma (MZL) also known as splenic lymphoma with villous lymphocytes (SLVL) and mantle cell lymphoma (MCL). We believe these cases to represent a unique leukaemic variant of monocytoid MZL. All cases presented with marked peripheral blood lymphocytosis, no smear cells and monocytoid morphology with voluminous sometimes vacuolated cytoplasm. Immunophenotyping confirmed clonal lymphocytosis with strong light chain restriction, positivity for CD19 and CD20, absent or weak expression of CD10, CD22, CD23 and FMC7 and variable but weak CD5 expression. Bone marrow trephine biopsies revealed marked hypercellularity with a non-nodular diffuse lymphoid infiltrate. Cytogenetic analysis in cases 1 and 5 was normal, and fluorescent in-situ hybridisation (FISH) for abnormalities associated with CLL (11q23, trisomy 12, 13q14 and 17p13) and MCL (t11,14) were negative. Case 1: A 70 year old male presented with symptoms of anaemia, generalised lymphadenopathy, splenomegaly and leucocytosis. He progressed through chlorambucil and prednisolone but responded to oral fludarabine. He has been successfully retreated with fludarabine on relapse and remains alive, more than six years post diagnosis. Case 2: A 79 year old female was admitted with abdominal pain and vomiting. Investigation revealed marked leucocytosis with grossly abnormal liver function tests. This patient’s condition deteriorated rapidly and she died before intervention was possible, ten days post presentation. Case 3: An 87 year old female presented with an incidental finding of lymphocytosis and isolated splenomegaly. Six months following her presentation she developed anaemia, thrombocytopenia and progressive lymphocytosis. Her disease progressed through chlorambucil and cyclophosphamide but responded to fludarabine. She unfortunately died of a cerebrovascular accident, eighteen months after diagnosis. Case 4: A 72 year old female presented with B symptoms, axillary lymphadenopathy and massive splenomegaly. She developed progressive B symptoms and rapid doubling of her white cell count, necessitating initiation of treatment. Despite an initial partial response to chlorambucil and prednisolone, her disease continued to progress and was refractory to multiple lines of chemotherapy. She died six years after her initial presentation. Case 5: An 84 year old presented with mild anaemia and leucocytosis and had clinical splenomegaly. He was managed with supportive therapy only and died of unrelated causes. Summary: The clinical presentation of these cases mimics that of CLL. The morphology of the peripheral blood lymphocytes is, however, markedly different. Patients are typically elderly with a high white cell count, marked splenomegaly and heavy marrow infiltration. Marker analysis is distinct from typical CLL and extranodal features at presentation are atypical of SLVL and nodal MZL. FISH results in two cases were also atypical for CLL. The clinical behaviour is distinct with resistance to alkylating agents but sensitivity to purine analogues. We believe that these unique cases represent an as yet undescribed leukaemic variant of monocytoid MZL probably currently classed and treated as atypical CLL.

Background: There is increasing recognition that menstruating women prescribed anticoagulants experience heavy menstrual bleeding. Objectives: The aim of this study is to report the extent of bleeding in menstruating women after commencing anticoagulants and the impact it has on their quality of life. Methods: Women aged 18 to 50, initiated on anticoagulant therapy, were approached to take part in the study. In parallel, a control group of women was also recruited. Women were asked to complete the menstrual bleeding questionnaire and a pictorial blood assessment chart (PBAC) during their next 2 menstrual cycles. Differences between the control and anticoagulated group were compared. Significance was considered at < .05. Ethics committee approval: REC reference: 19/SW/0211. Results: Fifty-seven women in the anticoagulation and 109 women in the control group returned their questionnaires. Women in the anticoagulated group reported an increase in the median length of their menstrual cycle from 5 to 6 days after commencing anticoagulation, compared to 5 days for women in the control group (P < .05). Anticoagulated women reported significantly higher PBAC scores as compared to the control group (P < .05), with two-thirds of women in the anticoagulation group reporting heavy menstrual bleeding. Women in the anticoagulation group reported worsening quality of life scores following the initiation of anticoagulation, compared with women in the control group (P < .05). Conclusion: Heavy menstrual bleeding occurred in two-thirds of women commencing anticoagulants, who completed a PBAC, which had negative impact on their quality of life. Clinicians commencing anticoagulation therapy should be mindful of this, and recognized measures should be taken to help minimize this problem for menstruating individuals.

Background Anticoagulant therapy is prescribed for millions of patients worldwide for the prevention and treatment of both arterial and venous thrombosis. Historically, only vitamin K antagonists have been available for clinicians to prescribe. The anticoagulation landscape is changing. The recent availability of the novel oral anticoagulants overcome many of the disadvantages associated with vitamin K antagonists. However the lack of formal monitoring and clinic follow-up is a concern for clinicians, as medication adherence is being assumed, which is known to decline in patients prescribed medications for chronic conditions. The switching study is a programme of work investigating the association between medication adherence and patient’s beliefs about anticoagulation therapy (warfarin and subsequently novel oral anticoagulants), together with beliefs about their illness and anticoagulation related quality of life. Methods/design The anticoagulation database at King’s College Hospital will be interrogated and two groups of patients will be identified; those with a time in therapeutic range on warfarin of ≥75 % and those