Pulmonary hypertension is a severe clinical condition characterized by molecular and anatomic changes in pulmonary circulation. It is associated with increased pulmonary vascular resistance, which leads to right-sided heart failure if left untreated and, ultimately, death. Treatment of patients with pulmonary arterial hypertension (PAH) involves a complex strategy that takes into consideration disease severity, general and supportive measures, and combination drug regimens. Abnormalities of blood coagulation factors, anti-thrombotic factors, and the fibrinolytic system may contribute to a prothrombotic state in patients with idiopathic PAH. These physiologic changes, in concert with the presence of non-specific risk factors for venous thromboembolism such as heart failure and immobility, are thought to be the basis for oral anticoagulation in PAH. Several observational studies provide helpful information in favor of anticoagulation use in idiopathic PAH but not in other pulmonary hypertension etiologies. Guideline recommendations are based on the lack of prospective comparative trials in this regard. For that reason, large differences exist in the use of anticoagulants in different countries and centers. More studies should be carried out to clarify the risks and the potential benefits of anticoagulant use in a heterogeneous population of patients who are already at considerable life risk.
BackgroundClinical guidelines recommend anticoagulation for patients with atrial fibrillation (AF) at high risk of stroke; however, studies report 40% of this population is not anticoagulated.ObjectiveTo evaluate a population health intervention to increase anticoagulation use in high-risk patients with AF.MethodsWe used machine learning algorithms to identify patients with AF from electronic health records at high risk of stroke (CHA2DS2-VASc risk score ≥2), and no anticoagulant prescriptions within 12 months. A clinical pharmacist in the anticoagulation service reviewed charts for algorithm-identified patients to assess appropriateness of initiating an anticoagulant. The pharmacist then contacted primary care providers of potentially undertreated patients and offered assistance with anticoagulation management. We used a stepped-wedge design, evaluating the proportion of potentially undertreated patients with AF started on anticoagulant therapy within 28 days for clinics randomised to intervention versus usual care.ResultsOf 1727 algorithm-identified high-risk patients with AF in clinics at the time of randomisation to intervention, 432 (25%) lacked evidence of anticoagulant prescriptions in the prior year. After pharmacist review, only 17% (75 of 432) of algorithm-identified patients were considered potentially undertreated at the time their clinic was randomised to intervention. Over a third (155 of 432) were excluded because they had a single prior AF episode (transient or provoked by serious illness); 36 (8%) had documented refusal of anticoagulation, the remainder had other reasons for exclusion. The intervention did not increase new anticoagulant prescriptions (intervention: 4.1% vs usual care: 4.0%, p=0.86).ConclusionsAlgorithms to identify underuse of anticoagulation among patients with AF in healthcare databases may not capture clinical subtleties or patient preferences and may overestimate the extent of undertreatment. Changing clinician behaviour remains challenging.
Appropriate timing of bivalirudin discontinuation as a bridge to warfarin is complicated, as bivalirudin may cause a falsely prolonged international normalized ratio (INR). The purpose was to evaluate patient and medication characteristics associated with differences in INR prolongation caused by bivalirudin. Adult patients receiving bivalirudin as a bridge to warfarin in 2014 were retrospectively evaluated. Patients were excluded if they had known thrombophilia or inappropriate INR monitoring after discontinuation of bivalirudin. Data recorded included indication for bivalirudin use, bivalirudin dosing, and coagulation assays. Univariate analysis was performed to determine variables associated with a larger change in INR when discontinuing bivalirudin. Variables with P < .3 were included in multivariate analysis. In total, 50 patient admissions were included in the analysis. Patients with ventricular assist devices represented the majority of the patient population (74%). The most common INR goals were 2.0 to 3.0 and 2.5 to 3.5. The mean initial weight-based bivalirudin rate was 0.076 mg/kg/h, and the mean increase in INR when starting bivalirudin was 0.6. The mean final weight-based bivalirudin rate was 0.13 mg/kg/h, and the mean change in INR after stopping bivalirudin was 0.8. On multivariate analysis, factors associated with a larger change in INR after stopping bivalirudin included higher serum creatinine ( P = .033), greater change in INR after initiation of bivalirudin ( P = .028), and higher final bivalirudin rate ( P < .001). The change in INR when starting or stopping bivalirudin appears to be patient specific and dose related. A nomogram was developed to predict the ideal timing of bivalirudin discontinuation. Prospective evaluation of the nomogram is under way.
Bivalirudin may cause a falsely prolonged international normalized ratio (INR) that complicates the discontinuation of bivalirudin when used as a bridge to warfarin. To prospectively validate our novel bivalirudin to warfarin transition nomogram, adult patients who received bivalirudin as a bridge to warfarin between July 2015 and June 2016 were prospectively evaluated, utilizing our predictive nomogram. The major outcome of our analysis was the correlation between the predicted change in INR upon bivalirudin discontinuation based on the nomogram, and the actual change in INR upon bivalirudin discontinuation. The major outcome was analyzed using the Pearson's correlation test. A Pearson's correlation coefficient >0.6 was considered to be a strong correlation. Bivalirudin was used as a bridge to warfarin in 29 patients. The majority of patients (86%) included in the analysis had a ventricular assist device. The median initial bivalirudin rate was 0.07 mg/kg/h and the mean increase in INR when starting bivalirudin was 0.6. The mean final weight-based bivalirudin rate was 0.08 mg/kg/h and the mean change in INR after stopping bivalirudin was 0.7. The Pearson correlation coefficient between the predicted change in INR upon bivalirudin discontinuation and the actual change in INR upon bivalirudin discontinuation was 0.86 (p < 0.001). After bivalirudin discontinuation, 68% of patients had a therapeutic INR. The results of this prospective analysis successfully validated our novel bivalirudin to warfarin transition nomogram. There was a very strong correlation between the predicted change and actual change in INR upon bivalirudin discontinuation.
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