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In a series of patients with venous thromboembolism who had been treated with anticoagulation for at least 3 months, d -dimer testing was performed 1 month after the discontinuation of anticoagulation. Patients with an abnormal d -dimer level were randomly assigned either to resume or to stop anticoagulation. The group resuming anticoagulation had a significantly lower rate of subsequent venous thromboembolism and major bleeding. Patients with an abnormal D-dimer level were randomly assigned either to resume or to stop anticoagulation. The group resuming anticoagulation had a significantly lower rate of subsequent venous thromboembolism and major bleeding. Even though long-term treatment with vitamin K antagonists is highly effective in the prevention of a recurrence after a first episode of unprovoked venous thromboembolism, the optimal duration of such therapy is still uncertain. 1 – 4 Since the risk of recurrence is greatest in the first 6 to 12 months after the initial episode and gradually diminishes thereafter, 5 the benefit of an extended course of anticoagulation may be offset over time by the risk of clinically important bleeding. 1 – 4 , 6 , 7 Earlier prospective studies involving patients with venous thromboembolism 8 – 10 showed that the d-dimer level after anticoagulation had a highly predictive . . .

This chapter about antithrombotic therapy for venous thromboembolic disease is part of the seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: Evidence Based Guidelines. Grade 1 recommendations are strong and indicate that the benefits do, or do not, outweigh risks, burden, and costs. Grade 2 suggests that individual patients' values may lead to different choices (for a full understanding of the grading see Guyatt et al, CHEST 2004; 126:179S-187S). Among the key recommendations in this chapter are the following: for patients with objectively confirmed deep vein thrombosis (DVT), we recommend short-term treatment with subcutaneous (SC) low molecular weight heparin (LMWH) or, alternatively, IV unfractionated heparin (UFH) [both Grade 1A]. For patients with a high clinical suspicion of DVT, we recommend treatment with anticoagulants while awaiting the outcome of diagnostic tests (Grade 1C+). In acute DVT, we recommend initial treatment with LMWH or UFH for at least 5 days (Grade 1C), initiation of vitamin K antagonist (VKA) together with LMWH or UFH on the first treatment day, and discontinuation of heparin when the international normalized ratio (INR) is stable and > 2.0 (Grade 1A). For the duration and intensity of treatment for acute DVT of the leg, the recommendations include the following: for patients with a first episode of DVT secondary to a transient (reversible) risk factor, we recommend long-term treatment with a VKA for 3 months over treatment for shorter periods (Grade 1A). For patients with a first episode of idiopathic DVT, we recommend treatment with a VKA for at least 6 to 12 months (Grade 1A). We recommend that the dose of VKA be adjusted to maintain a target INR of 2.5 (INR range, 2.0 to 3.0) for all treatment durations (Grade 1A). We recommend against high-intensity VKA therapy (INR range, 3.1 to 4.0) [Grade 1A] and against low-intensity therapy (INR range, 1.5 to 1.9) compared to INR range of 2.0 to 3.0 (Grade 1A). For the prevention of the postthrombotic syndrome, we recommend the use of an elastic compression stocking (Grade 1A). For patients with objectively confirmed nonmassive PE, we recommend acute treatment with SC LMWH or, alternatively, IV UFH (both Grade 1A). For most patients with pulmonary embolism (PE), we recommend clinicians not use systemic thrombolytic therapy (Grade 1A). For the duration and intensity of treatment for PE, the recommendations are similar to those for DVT.

Background Circulating microRNAs (miRNAs) emerge as novel biomarkers in cardiovascular diseases. Diagnosing acute pulmonary embolism (PE) remains challenging due to a diverse clinical presentation and the lack of specific biomarkers. Here we evaluate serum miRNAs as potential biomarkers in acute PE. Methods We enrolled 30 patients with acute, CT (computed tomography)-angiographically confirmed central PE and collected serum samples on the day of emergency room admission (1st day) and from 22 of these patients 9 months thereafter. For comparison, we examined serum samples from patients with acute non ST-segment elevation myocardial infarction (NSTEMI, n = 30) and healthy individuals (n = 12). Results We randomly selected 16 out of 30 PE patients and screened sera from the acute (1st day) and chronic stages (9 months) for 754 miRNAs using microarrays and found 37 miRNAs to be differentially regulated. Across all miRNAs, miRNA-1233 displayed the highest fold change (FC) from acute to chronic stage (log 2 FC 11.5, p < 0.004). We validated miRNA-1233 by real-time quantitative polymerase chain reaction (RT-qPCR). In acute PE (1st day) we found elevated levels of miRNA-1233 in comparison to NSTEMI (log 2 FC 5.7, p < 0.0001) and healthy controls (log 2 FC 7.7, p < 0.0001). miRNA-1233 differentiated acute PE from NSTEMI patients and healthy individuals with 90 and 90 % sensitivity, and 100 and 92 % specificity [area under the curve (AUC) 0.95, p < 0.001 and 0.91, p < 0.001], respectively. Conclusions This is the first report that identifies a miRNA that allows distinguishing acute PE from acute NSTEMI and healthy individuals with high specificity and sensitivity.

Among patients with a low clinical pretest probability of pulmonary embolism and a d -dimer level of less than 1000 ng per milliliter (twice the usual threshold used to rule out the disorder), the need for diagnostic imaging was reduced from 51.9% to 34.3% of patients, without increasing the risk of missing the diagnosis of pulmonary embolism.

Purpose Current guidelines recommend the use of low molecular weight heparin (LMWH) for most haemodynamically stable patients with pulmonary thromboembolism (PTE), however, it is not clear whether LMWH is preferable to unfractionated heparin (UFH) for the treatment of massive PTE. We aimed to compare the use of LMWH versus UFH after thrombolytic treatment in the management of acute massive PTE for hemorrhage and hospital mortality. Methods The study, a randomized, single center, parallel design trial, included the patients who had confirmed the diagnosis of massive PTE according to clinical findings and computerized thorax angiography and no contraindication to the treatment between January 2011 and October 2013. After thrombolytic treatment, the patients assigned to therapy with LMWH or UFH. Any hemorrhage, major hemorrhage, and hospital mortality were assessed. Results A total of 121 patients, 71 female (58.7 %) and 50 male (41.3 %), who had massive PTE with an average age 62.6 ± 15.7 (ranges 22–87) were included for analyses in the study. They were allocated to either LMWH ( n  = 60) or UFH ( n  = 61) group. Although the occurrence of any adverse event (21.7 vs 27.9 %) and each individual type of adverse event were all lower in the LMWH group compared to UFH group (6.7 vs 11.5 %, 3.3 vs 9.8 %, and 15.0 vs 19.7 % for death, major hemorrhage, and any hemorrhage, respectively), the differences were not statistically significant. Conclusions Our findings suggest that LMWH might be a better option in the management of the patients with massive PTE. Multi-center larger randomized controlled trials are required to confirm our results.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its associated clinical syndrome COVID-19 are causing overwhelming morbidity and mortality around the globe and disproportionately affected New York City between March and May 2020. Here, we report on the first 100 COVID-19-positive autopsies performed at the Mount Sinai Hospital in New York City. Autopsies revealed large pulmonary emboli in six cases. Diffuse alveolar damage was present in over 90% of cases. We also report microthrombi in multiple organ systems including the brain, as well as hemophagocytosis. We additionally provide electron microscopic evidence of the presence of the virus in our samples. Laboratory results of our COVID-19 cohort disclose elevated inflammatory markers, abnormal coagulation values, and elevated cytokines IL-6, IL-8, and TNFα. Our autopsy series of COVID-19-positive patients reveals that this disease, often conceptualized as a primarily respiratory viral illness, has widespread effects in the body including hypercoagulability, a hyperinflammatory state, and endothelial dysfunction. Targeting of these multisystemic pathways could lead to new treatment avenues as well as combination therapies against SARS-CoV-2 infection.

Objective: Association of ABO blood type with occurrence of pulmonary embolism (PE) has been demonstrated, and association of blood type with disease mortality and morbidity has recently been reported. Presently described was a retrospective study of mortality and morbidity according to blood group. Methods: Blood type and medical data of 230 patients with confirmed PE was abstracted from medical records. Two control groups were used for data analysis; the 1st included blood donors (Control 1), the 2nd included hospital staff born in the same region (Control 2). Results: In PE patients, blood group A was the most common phenotype (46.1%), followed by blood groups O (25.2%), B (20.4%), and AB (8.2%). Among the control groups, no significant difference was found in distribution of A vs non-A (36.4% vs 36.6%, respectively) or O vs non-O (66.6% vs 66.4%, respectively) blood groups. Blood group A was significantly more prevalent than non-A in patients with PE, compared to both control groups (p=0.002 and 0.03, respectively), and blood group O was significantly less prevalent than non-O in patients with PE, compared with both control groups (p=0.009 and 0.04, respectively). No significant difference was found in PE patients regarding in-hospital and midterm (6–36 months follow-up) mortality (p=0.36 and 0.15, respectively) based on blood groups. Conclusion: Blood group A was significantly more common, and blood group 0 significantly less common, in patients with PE. No association was found regarding blood type and in-hospital outcome or midterm mortality.

Objective To examine the effect of balloon pulmonary angioplasty (BPA) on chronic thromboembolic pulmonary hypertension (CTEPH) in patients with inoperable disease or persistent pulmonary hypertension after pulmonary endarterectomy. Design Observational cohort study. Setting Referred patients with inoperable or persistent CTEPH. Patients Twenty consecutive CTEPH patients (10 females), aged 60±10 years. Interventions BPA. Main outcome measures Right heart catheterisation, functional capacity (cardiopulmonary exercise testing (CPET) and NYHA class) and blood sampled biomarkers N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin T examined at the time of diagnosis and repeated in all patients 3 months after the last BPA. Results Seventy-three catheterisations were performed with 18.6±6.1 BPAs per patient on segmental and subsegmental arteries. Two deaths occurred following the first BPA, with an overall 10% periprocedural death rate. Reperfusion oedema complicated seven procedures. Comparisons before and after BPA showed significant haemodynamic improvements, including decreased mean pulmonary artery pressure (mPAP) (45±11 mm Hg vs 33±10 mm Hg; p<0.001) and increased cardiac output (4.9±1.6 L/min vs 5.4±1.9 L/min; p=0.011). Reduced right ventricular strain was indicated by significantly lower plasma levels of NT-proBNP and troponin T. Significant improvement in functional capacity was evident as assessed by NYHA class (3.0±0.5 vs 2.0±0.5; p<0.001) and CPET (13.6±5.6 mL/kg/min vs 17.0±6.5 mL/kg/min; p<0.001). Seventeen patients (85%) were alive after 51±30 months of follow-up. Conclusions BPA may offer an alternative form of treatment in selected CTEPH patients. While prognostic markers such as haemodynamics, functional capacity and biomarkers improve, significant periprocedural complications must be recognised. Randomised trials are warranted.

Not all patients with acute pulmonary embolism (PE) have a high risk of an adverse short-term outcome. This prospective cohort study aimed to develop a multimarker prognostic model that accurately classifies normotensive patients with PE into low and high categories of risk of adverse medical outcomes. The study enrolled 848 outpatients from the PROTECT (PROgnosTic valuE of Computed Tomography) study (derivation cohort) and 529 patients from the Prognostic Factors for Pulmonary Embolism (PREP) study (validation cohort). Investigators assessed study participants for a 30-day complicated course, defined as death from any cause, hemodynamic collapse, and/or adjudicated recurrent PE. A complicated course occurred in 63 (7.4%) of the 848 normotensive patients with acute symptomatic PE in the derivation cohort and in 24 patients (4.5%) in the validation cohort. The final model included the simplified Pulmonary Embolism Severity Index, cardiac troponin I, brain natriuretic peptide, and lower limb ultrasound testing. The model performed similarly in the derivation (c-index of 0.75) and validation (c-index of 0.85) cohorts. The combination of the simplified Pulmonary Embolism Severity Index and brain natriuretic peptide testing showed a negative predictive value for a complicated course of 99.1 and 100% in the derivation and validation cohorts, respectively. The combination of all modalities had a positive predictive value for the prediction of a complicated course of 25.8% in the derivation cohort and 21.2% in the validation cohort. For normotensive patients who have acute PE, we derived and validated a multimarker model that predicts all-cause mortality, hemodynamic collapse, and/or recurrent PE within the following 30 days.

Venous thromboembolism (VTE) is categorized by the U.S. Surgeon General as a major public health problem. VTE is relatively common and associated with reduced survival and substantial health-care costs, and recurs frequently. VTE is a complex (multifactorial) disease, involving interactions between acquired or inherited predispositions to thrombosis and VTE risk factors, including increasing patient age and obesity, hospitalization for surgery or acute illness, nursing-home confinement, active cancer, trauma or fracture, immobility or leg paresis, superficial vein thrombosis, and, in women, pregnancy and puerperium, oral contraception, and hormone therapy. Although independent VTE risk factors and predictors of VTE recurrence have been identified, and effective primary and secondary prophylaxis is available, the occurrence of VTE seems to be relatively constant, or even increasing.