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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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