Feedback from David K. Cundiff, MD
Sent 6/25/07 updated 8-19-07
The justification for calling for further large-scale RCTs
with low dose heparin and aspirin or low dose heparin alone versus aspirin
comes from subgroup analyses of death at the end of the treatment: “Compared
with aspirin alone, the combination of low-dose UFH and aspirin was associated
with a marginally significant reduced risk of 'any recurrent stroke' and a
marginally significant reduced risk of death at 14 days.” A possible cause for
the favorable non-significant trend in these outcomes with low dose heparin and
aspirin during treatment only is rebound hypercoagulability causing increased
adverse events after the 14th day. Rebound hypercoagulability clearly occurs on
withdrawal of warfarin1, 2 and has been considered with an heparinoid (Lomoparan (Org
10172).3 Clinically significant rebound hypercoagulability due to
heparin or LMWHs has not been ruled out.
Given the
absence of benefit with low dose heparin added to aspirin, the safety of this
combination raises concerns about the recommendation of conducting further
research with anticoagulants. The authors correctly point out that there was
not a statistically significant increase in major extracranial or intracranial
hemorrhage (OR: 1.82 (0.87-3.81) and 1.46 (0.72 – 2.97), respectively).
However, when these two categories of major hemorrhage are combined, there is a
borderline statistically significant increase in major bleeding (OR: 1.63 (0.98
– 2.72), P< 0.06), which represents 6.2 (95% CI: 0.1 – 16.8) additional
major bleeds per 1000 patients by adding the low dose heparin. Risk of bleeding
in clinical practice is probably greater than in closely monitored RCTs.
The review should be updated to reflect the status of the ongoing studies as of 2002. One of the co-authors of this review, Dr. Sandercock, was an author of the RAPID RCT, published in 2005.4 Asian stroke patients reported by Wong and colleagues had no benefit with LMWH over aspirin.5
Since adding low dose heparin to aspirin does
not improve clinical outcomes at the end of followup and does add to the
bleeding risk, the implications for research should say that further trials of
any anticoagulants in acute ischemic stroke would be unethical and any ongoing
such studies should be stopped.
1. Cundiff
DK. Commentary - Insufficient Evidence Supporting Low-Intensity Warfarin for
Venous Thromboembolism (VTE) Prophylaxis. Medscape General Medicine™. 07/02/2003;http://www.medscape.com/viewarticle/457570.
2. Palareti
G, Legnani C, Guazzaloca G, et al. Activation of blood coagulation after abrupt
or stepwise withdrawal of oral anticoagulants--a prospective study. Thromb Haemost. 1994;72(2):222-226.
3. Hoek
JA, Nurmohamed MT, Hamelynck KJ, et al. Prevention of deep vein thrombosis
following total hip replacement by low molecular weight heparinoid. Thrombosis & Haemostasis. 1992;67(1):28-32.
4. Chamorro
A, Busse O, Obach V, et al. The rapid anticoagulation prevents ischemic damage
study in acute stroke--final results from the writing committee. Cerebrovasc Dis. 2005;19(6):402-404.
5. Wong
KS, Chen C, Ng PW, et al. Low-molecular-weight heparin compared with aspirin
for the treatment of acute ischaemic stroke in Asian patients with large artery
occlusive disease: a randomised study. Lancet
Neurol. 2007;6(5):407-413.