D-dimer is a typical degradation product of cross-linked fibrin and its plasma levels are detectable at levels >0.5 pg/ml fibrinogen equivalent units in nearly all patients with venous thromboembolism28. Despite being nonspecific, since elevated plasma levels can be found in intravascular activation of the coagulation system and secondary fibrinolysis (i.e., various forms of malignancies, infections, renal disease, resent trauma and surgery, disseminated intravascular coagulation, postfibrinolysis), it can be used effectively mainly due to its high negative predictive value to exclude deep venous thromboembolism and pulmonary embolism28-30.
Recently, elevated plasma levels of D-dimer were found in a small series of patients who experienced aortic dissection31 and in patients treated with en-dovascular graft for aortic dissection repair32. The authors suggested that this finding could be explained by the extrinsic pathway of the coagulation cascade at the site of the aortic vessel wall injury by tissue factor. They also observed that the extent of the dissection correlates with the absolute degree of D-dimer elevation. Since aortic dissection is associated with disorders of the coagulation system not only in acute stages but also in the later stages which are associated with DIC, not only D-dimer but also other coagulopathic markers should be occasionally examined to rule out this condition33. More recently, Eggebrecht and associates have showed that D-dimers are highly elevated in acute aortic dissection34. In this study, all acute AD patients showed highly elevated D-dimer values that were similar to the levels of patients affected by pulmonary embolism (2,238 ± 1,765 |g/l vs. 1,531 ± 837 |g/l, p = 0.15) but significantly higher than in chronic AD, AMI, or patients presenting with chest pain (p < 0.001).
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