Apart from the possibility of micro-clots in the sample, does a decreased PT/APTT signify a hypercoagulable state in the body, therefore being at a higher risk of thrombotic event?
a quick look to your question suggests a link between shortened APTT and an increase in coagulation factors (VIII, IX, XI, II, and fibrinogen). There's a publication in blood about the risk of VTE and shortened APTT as well. it's in blood 104: 3631-34
Given that the tests PT and APTT measure the hypocoagulable responses due to the effects of warfarin or heparin respectively, any decrease in the PT and APTT may or may not be reflective of a hypercoagulable states. Although, the hypercoagulable responses can be measured by thrombelastography or ROTEM, PT and APTT tests are not designed to measure hypercoagulable effects.
As per your question, the possibility or the presence of microclots itself could be suggestive of a procoagulant state. In addition to the possibility of microclots and evidence of a shortened PT or APTT is suggestive of a hypercoagulable state. As mentioned earlier since PT and APTT tests are not designed to measure hypercoagulable states, the degree of shortening of PT and APTT may not correlate with the severity of a hypercoagulable state. Hence, a better measure of hypercoagulable state may be TEG which would show shortening of the r-time, decrease in k-time, increase in the angle and an increased MA suggestive of a hypercoagulant state. However, in case of TEG the degree of shortening of the r-time may correlate with the severity of a hypercoagulable state. Other markers of activation of coagulation may may corroborate the hypercoagulable effects.
Many thanks for the answers. Possibly the PT and APTT can be utilised as an initial screening tests for hypercoagulable states, and proceed with other tests such as factor assay levels and thromboelastography. Therefore having a cost worth approach before proceeding to more complex tests for patients having such shortened PT/APTT.
Unfortunately the most comon cause of "short" PT and APTT is collection artefact. You should never assume collection is always perfect. Another cause is use of agents lke Novoseven. Of vital imprtance are relevant clinical notes from the clinician and collectors who are wiling to tell you when they thought there was a issue with collection.
Which definition of hypercoagulable state is used to assess the question? PT and APTT do not measure total fibrinogen turnover, but only the first part of the propagation phase.
To add to the comments about sample integrity and elevated FVIII, an elevated fibrinogen can shorten APTT, and there is also an extremely rare FIX variant, FIX Padua, with a gain of function mutation that shortens APTT and is associated with thrombosis. FIX levels can be >700%.
The problem with clinicians is that they would not admit a collection problem, otherwise they would not send the sample. I would rather check and compare previous results, if not possible request a repeat sample.
High levels of factor VIII have been known to cause shortened APTT results. Fibrinogen levels and TEG will be more suited towards detecting a hypercoagulable state. However is TEG useful in a clinical laboratory or like here, it is a point of care apparatus? Possibly the best approach is to compare previous PT/APTT results of patients suffering from repetitive thromboembolic events.
Hypercoagulability is usually tested with other tests not PT or APTT, although shorter APTT is associated with increased risk of VTE (depends on the reagent). TEG would not be my first choice though. Thrombin generation, D-dimer etc. are more sensitive to hypercoagulation than TEG.
The problem with D-dimer is the low specificity due to the multifactorial causes for elevated results. I would prefer the use of D-dimer to exclude VTE.
the most common reason for short aPTT is sampling problem that activate coagulation cascade as partial. however, other reasons such as DIC and hypercoagulate state can also cause short aPTT.
The coagulation tests such as PT and APTT etc are basically designed to measure the hypocoagulable effect and not the hypercoagulable states. Hence a shorter result may not be signify hypercoagulable effect. If at all you want to measure the hypercoagulable effects, you may rely on other tests such as Thrombelastography, ROTEM, F1.2, TAT, D-Dimer and platelet microparticles, and P-selectin-expression etc.