Journal of thrombosis and haemostasis : JTH
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J. Thromb. Haemost. · Feb 2016
LetterShock, acute disseminated intravascular coagulation and microvascular thrombosis: is 'shock liver' the unrecognized provocateur of ischemic limb necrosis?
For unknown reasons, a small minority of critically ill patients with septic or cardiogenic shock, multiorgan failure, and disseminated intravascular coagulation develop symmetrical acral (distal extremity) limb loss due to microvascular thrombosis ('limb gangrene with pulses'). Case reports have described preceding 'shock liver' in some critically ill patients who developed such a picture of ischemic limb necrosis. ⋯ We hypothesize that shock liver is the key predisposing risk factor underlying ischemic limb necrosis in the majority of patients who develop this complication in the setting of acute disseminated intravascular coagulation complicating septic or cardiogenic shock. As shock liver precedes onset of limb ischemia by several days, therapeutic intervention may be possible.
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J. Thromb. Haemost. · Jan 2016
Multidetector computed tomographic pulmonary angiography in patients with a high clinical probability of pulmonary embolism.
ESSENTIALS: When high probability of pulmonary embolism (PE), sensitivity of computed tomography (CT) is unclear. We investigated the sensitivity of multidetector CT among 134 patients with a high probability of PE. A normal CT alone may not safely exclude PE in patients with a high clinical pretest probability. In patients with no clear alternative diagnosis after CTPA, further testing should be strongly considered. ⋯ A normal multidetector CTPA result alone may not safely exclude PE in patients with a high clinical pretest probability.
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J. Thromb. Haemost. · Jan 2016
Comorbid risks of deep vein thrombosis and pulmonary thromboembolism in patients with chronic pancreatitis: a nationwide cohort study.
ESSENTIALS: Risks of deep vein thrombosis (DVT) and pulmonary embolism (PE) in chronic pancreatitis (CP) are unclear. We conducted a nationwide cohort study to evaluate the risks of DVT and PE in CP patients. 17 778 patients with CP and 71 106 without CP were followed for 86 740 and 429 116 person-years, respectively. Patients with CP had a 2.95-fold increased rate of DVT and a 4.51-fold increased rate of PE. ⋯ The risks of DVT and PE are significantly higher in CP patients than in the general population.
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J. Thromb. Haemost. · Jan 2016
Replication of a genetic risk score for venous thromboembolism in whites but not in African Americans.
ESSENTIALS: There is little prospective information on genetic risk scores to predict venous thromboembolism (VT). Community based cohort followed a median of 22.6 years for VT occurrence. A 5-SNP risk score identified whites at risk of VT, but not African Americans. The utility of genetic risk scores for VT is yet to be established. ⋯ Higher values for a five-SNP genetic risk score helped identify white adults at risk of VTE. The genetic risk score did not identify future VTE occurrence in African Americans.
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J. Thromb. Haemost. · Jan 2016
Observational StudyDerivation of a clinical prediction score for chronic thromboembolic pulmonary hypertension after acute pulmonary embolism.
Essentials Predicting chronic thromboembolic pulmonary hypertension (CTEPH) after pulmonary embolism is hard. We studied 772 patients with pulmonary embolism who were followed for CTEPH (incidence 2.8%). Logistic regression analysis revealed 7 easily collectable clinical variables that combined predict CTEPH. Our score identifies patients at low (0.38%) or higher (10%) risk of CTEPH. ⋯ Introduction Validated risk factors for the diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH) after acute pulmonary embolism (PE) are currently lacking. Methods This is a post hoc patient-level analysis of three large prospective cohorts with a total of 772 consecutive patients with acute PE, without major cardiopulmonary or malignant comorbidities. All underwent echocardiography after a median of 1.5 years. In cases with signs of pulmonary hypertension, additional diagnostic tests to confirm CTEPH were performed. Baseline demographics and clinical characteristics of the acute PE event were included in a multivariable regression analysis. Independent predictors were combined in a clinical prediction score. Results CTEPH was confirmed in 22 patients (2.8%) by right heart catheterization. Unprovoked PE, known hypothyroidism, symptom onset > 2 weeks before PE diagnosis, right ventricular dysfunction on computed tomography or echocardiography, known diabetes mellitus and thrombolytic therapy or embolectomy were independently associated with a CTEPH diagnosis during follow-up. The area under the receiver operating charateristic curve (AUC) of the prediction score including those six variables was 0.89 (95% confidence interval [CI] 0.84-0.94). Sensitivity analysis and bootstrap internal validation confirmed this AUC. Seventy-three per cent of patients were in the low-risk category (CTEPH incidence of 0.38%, 95% CI 0-1.5%) and 27% were in the high-risk category (CTEPH incidence of 10%, 95% CI 6.5-15%). Conclusion The 'CTEPH prediction score' allows for the identification of PE patients with a high risk of CTEPH diagnosis after PE. If externally validated, the score may guide targeting of CTEPH screening to at-risk patients.