https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1538-7836.2008.02981.x

D-Dimer for venous thromboembolism diagnosis: 20 years later.

This New Frontiers article reviews the epidemiology, pathophysiology, diagnosis, treatment, and prevention of pulmonary embolism (PE) in 2 parts. In this first section we summarize the mechanisms of right ventricular dysfunction, arterial hypoxemia, and other abnormalities of gas exchange. For diagnosis, we streamline and expedite the work-up. For the second part we provide a contemporary approach to risk stratification to determine which patients may warrant intervention beyond use of heparin and warfarin alone. We conclude with an overview of contemporary concepts in optimizing prophylaxis. PE is a common cardiovascular and cardiopulmonary illness with an incidence in the United States that exceeds 1 per 1000 and a mortality rate 15% in the first 3 months after diagnosis. 1 This makes PE possibly as deadly an illness as acute myocardial infarction. Nevertheless, the lay public has not been well educated about PE. Consequently, early detection and prompt presentation for medical evaluation have lagged far behind the public awareness of acute coronary syndromes and stroke. Although discussion of the etiology of PE has classically focused on acquired and inherited causes of hypercoagulability, there is also an association between atherosclerotic disease and spontaneous venous thrombosis.2 The most common reversible risk factor for PE is obesity, an increasing pandemic in our society. Other common reversible risk factors include cigarette smoking and hypertension. Nevertheless, public fascination with PE has centered on long-haul air travel, a rare cause of venous thromboembolism. 3 PE also occurs in the context of illness attributable to surgery, trauma, immobilization, cancer,4 oral contraceptives,5 pregnancy, and postmenopausal hormone replacement therapy, 6 as well as medical conditions such as pneumonia and congestive heart failure. Genetic predisposition to venous thrombosis is being increasingly recognized, 7 and twin studies have demonstrated the important contribution of an inherited prothrombotic state. 8 Increased levels of clotting factors and activation peptides contribute to the risk of PE. Deficiencies of anticoagulant factors also increase thrombotic risk.9 Pathophysiology

Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis.

GRADE Guidelines 28: Use of GRADE for the assessment of evidence about prognostic factors: rating certainty in identification of groups of patients with different absolute risks

Clinical outcome studies have shown that it is safe to withhold anticoagulant therapy in patients with suspected pulmonary embolism (PE) who have a negative D-dimer result and a low pretest probability (PTP) either using a PTP model or clinical gestalt. It was the objective of the present study to assess the safety of the combination of a negative VIDAS D-dimer result in combination with a non-high PTP using the Wells or Geneva models to exclude PE. A systematic literature search strategy was conducted using MEDLINE, EMBASE, the Cochrane Register of Controlled Trials and all EBM Reviews. Seven studies (6 prospective management studies and 1 randomised controlled trial) reporting failure rates at three months were included in the analysis. Non-high PTP was defined as "unlikely" using the Wells' model, or "low/intermediate" PTP using either the Geneva score, the Revised Geneva Score, or clinical gestalt. Two reviewers independently extracted data onto standardised forms. A total of 5,622 patients with low/intermediate or unlikely PTP were assessed using the VIDAS D-dimer. PE was ruled out by a negative D-dimer test in 2,248 (40%, 95% confidence intervals [CI] 38.7 to 41.3%) of them. The three-month thromboembolic risk in patients left untreated on the basis of a low/intermediate or unlikely PTP and a negative D-dimer test was 3/2,166 (0.14%, 95% CI 0.05 to 0.41%). In conclusion, the combination of a negative VIDAS D-dimer result and a non-high PTP effectively and safely excludes PE in an important proportion of outpatients with suspected PE.

VIDAS D-dimer in combination with clinical pre-test probability to rule out pulmonary embolism. A systematic review of management outcome studies.

Proposals for the measurement of anti-beta2-glycoprotein I antibodies. Standardization group of the European Forum on Antiphospholipid Antibodies.

Accuracy of D-dimer/fibrinogen ratio to predict pulmonary embolism: a prospective diagnostic study.

Potential role of d-dimer to rule in pulmonary embolism: reply to a rebuttal

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Accuracy of D-dimer/fibrinogen ratio to predict pulmonary embolism: a prospective diagnostic study.

Potential role of d-dimer to rule in pulmonary embolism: reply to a rebuttal