AorticDissection.com-Does the D-Dimer Test Reall Work?

Here's another great article on the D-Dimer testing and results in detecting for an aortic dissection.

Our data show that D-Dimer measurement has a high sensitivity in diagnosing AAD. Moreover, D-Dimer levels significantly correlate with the extension of the disease and are higher in patients with patent false lumen than in patients with intramural hematoma. Overall, a positive link between D-Dimer and in hospital-mortality was observed.

 

Until recently, laboratory tests played a minor role when assessing AAD but were considered to be useful to exclude other diseases.[2] Elevations of C-reactive protein and leukocytosis have been described in AAD and may result from systemic inflammatory response.[21] Additionally, lactate dehydrogenase may be raised when the celiac artery is involved in the dissection and may reflect visceral ischemia.[2] In our study, none of these markers at presentation were predictive of the diagnosis of AAD. Suzuki et al.[21] investigated the reliability of smooth muscle myosin heavy chain plasma levels in a series of 37 patients with AAD and reported a sensitivity and a specificity of 90% and 97%, respectively. However, smooth muscle myosin heavy chain is unavailable for routine practice. Recently, positive D-Dimer levels have been described in AAD[12,14] in two small series (24 and 16 patients). Both found that D-Dimer had a 100% sensitivity to detect AAD and that D-Dimer level correlated with the time elapsed between onset of symptoms and blood testing.[12,14] In a significantly larger series (94 patients), we have observed a sensitivity of 99%. Only one patient with a localized intramural hematoma had a normal D-Dimer (i.e., <400 ng/mL). Since data regarding the precise hour of symptoms onset were not available in the majority of the charts, we were unable to evaluate the relationship between D-Dimer levels and the duration of symptoms. However, in several patients we observed levels above the upper limit of the assay (20,000 ng/mL) as soon as 3 hrs after the beginning of symptoms, suggesting a very early increase of this biomarker in AAD.

In patients with AAD, D-Dimer was influenced by the anatomical extension and by the type of the dissection. The number of aortic segments involved in the dissection correlated with D-Dimer levels. This suggests that D-Dimer increases proportionally to the surface of contact between the bloodstream and the thrombogenic components of the false lumen. Furthermore, the lower level of D-Dimer observed in intramural hematoma compared with patent false lumen also supports this hypothesis.

D-Dimer measurement is currently used in the diagnosis of venous thromboembolic disease, where it shows low specificity and very high sensitivity when a cutoff of 400 ng/mL is chosen.[6] In our study, 66% of patients in the control group showed elevated D-Dimer. This figure is in accordance with large trials evaluating D-Dimer in venous thromboembolic disease,[22,23] in which the proportion of positive Sta-Liatest D-DI test among controls ranged from 56% to 68%, leading to a low specificity. Similarly, in our study, D-Dimer measurement had a low specificity (34%).

Our data indicate that the D-Dimer test has a high sensitivity and a low specificity at the usual threshold of 400 ng/mL for the diagnosis of AAD. We chose a low diagnostic threshold for the test, as in thromboembolic disease, since the cost of missing a diagnosis is high in AAD. Therefore, by using this threshold of 400 ng/mL, we showed that the D-Dimer test might consistently contribute, when negative, in the ruling out of AAD, since the negative likelihood ratio of the test is 0.03.

Of note, we observed that 38% patients with AAD ( Table 3 ) showed very high D-Dimer concentrations (>12,000 ng/mL) and in 28% D-Dimer was >20,000 ng/mL. Therefore, the positive likelihood of aortic dissection increased when D-Dimer was in the highest values (>12,000 ng/mL; positive likelihood ratio = 12). Consequently, in case of a high D-Dimer elevation, physicians should be aware of the possibility of AAD, even if the clinical presentation is nonevocative, and they should not only consider venous thromboembolic disease.

The mortality rate (23.4%) observed in patients with AAD in this study is similar to previous reports.[24,25] We found a significant relationship between D-Dimer and in-hospital mortality. These results confirm a not significant trend observed in a previous study that included a lower number of patients.[14] Since mortality rate is higher in Stanford A than in Stanford B, this relation might be the consequence of higher D-Dimer level in patients with Stanford A and might reflect the higher frequency of complications when the ascending aorta is involved. Furthermore, false lumen patency, which triggers the coagulation cascade and therefore possibly enhances D-Dimer level, is also known to be associated with a poorer prognosis,[26,27] and might be involved in the relationship between D-Dimer and mortality. Overall, D-Dimer has been reported as a marker of risk for both multiple organ failure and death in critically ill patients,[28] which may account for the higher mortality rate observed in patients presenting with the highest levels. Therefore, it is possible that patients with a D-Dimer level in the higher range are presenting with extensive forms of aortic dissection and thus have an increased risk of unfavorable outcome.

Study Limitations

The retrospective design of this study is the principal limitation of these findings. The control group was limited to matched patients and did not include all patients admitted for acute chest pain in our institution. However, we report the largest series of patients yet published with aortic dissection and D-Dimer testing. The immunoturbidimetric test was used for D-Dimer testing. Our results should not be extended to other D-Dimer assays.

source: http://www.medscape.com/viewarticle/530783_4

 

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