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Use of a Fixed Activated Partial Thromboplastin Time Ratio to Establish a Therapeutic Range for Unfractionated Heparin
Shannon M. Bates, MDCM;
Jeffrey I. Weitz, MD;
Marilyn Johnston, ART;
Jack Hirsh, MD;
Jeffrey S. Ginsberg, MD
Arch Intern Med. 2001;161:385-391.
Background The commonly recommended therapeutic range for patients receiving unfractionated
heparin of 1.5 to 2.5 times the control activated partial thromboplastin time
(aPTT) is not universally applicable. It has been suggested that the therapeutic
range for each aPTT reagent should be based on plasma heparin levels. We sought
to identify an aPTT ratio that corresponds to therapeutic anti–factor
Xa heparin levels for combinations of several reagents and coagulometers that
are commonly used.
Methods Citrated plasma was collected from 126 unselected patients receiving
unfractionated heparin. Four automated coagulometers and 6 commercial aPTT
reagents were used to measure the aPTT. Plasma anti–factor Xa levels
were measured by means of a commercially available assay. The relationship
between the aPTT results and anti–factor Xa heparin levels for each
reagent-coagulometer combination was determined by linear regression analysis,
and the aPTT results corresponding to therapeutic anti–factor Xa heparin
levels were calculated.
Results For all reagent-coagulometer combinations studied, an aPTT ratio of
1.5 resulted in anti–factor Xa heparin levels considerably below the
lower limit of the therapeutic range. When the aPTT was performed on any of
the coagulometers assessed with the use of Actin (Dade Diagnostics, Aguada,
Puerto Rico) and IL Test (Instrumentation Laboratories, Fisher Scientific,
Unionville, Ontario) reagents, aPTT ratios necessary to achieve therapeutic
anti–factor Xa heparin levels approximated 2.0 to 3.5.
Conclusion For laboratories that cannot perform heparin levels, the use of less
responsive reagents and any of the coagulometers studied, along with target
aPTT ratio between 2.0 and 3.5, appears to be a reasonable alternative.
From the Department of Medicine, McMaster University (Drs Bates, Weitz,
Hirsh, and Ginsberg), and Hamilton Civic Hospitals Research Centre (Drs Weitz,
Hirsh, and Ginsberg and Ms Johnston), Hamilton, Ontario.
Corresponding author and reprints: Shannon M. Bates, MDCM, Thromboembolism
Unit, HSC 3W15, McMaster University Medical Centre, 1200 Main St W, Hamilton,
Ontario, Canada L8N 3Z5 (e-mail: batesm{at}mcmaster.ca).
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