The retrospective analysis by Blacker et al [1] outlines the inherent risks in suspending anticoagulation,
prior to a procedure, in patients with AF. Inclusion of data on those AF
patients not previously anticoagulated might have served as a better
control than relying on “theoretical risk” from earlier studies. I prospectively collected preliminary data from a single hospital
over a nine-month period in 2002.
Of patients hospitalized with ischemic stroke, 21 had stopped taking
their anticoagulant prior to presentation. Thirteen of these had AF and
all 13 were originally anticoagulated to prevent cardiac embolic stroke.
Remarkably, five of these 13 had stroke within 30 days, indeed
all five within just 10 days, of stopping their anticoagulant. The
remaining eight of these 21 patients might be considered controls, as they
had been prescribed anticoagulants for other reasons (e.g., DVT prophylaxis).
Here, stroke followed within 30 days in only one case. Those patients with
AF most likely to suffer an early stroke were those who had had a
previous, often distant, stroke. Surprisingly, old age, hypertension and
diabetes failed to identify those at greatest risk – but this is a small
sample.
Such dramatic early clustering of events has not previously been
reported in patients with AF who were unprotected by anticoagulation, even
after recent stroke. This raises the possibility of “rebound
hypercoagulability”. It is instructive to look for evidence that might
support this phenomenon in the earlier major trials of anticoagulation for
patients with NVAF. Only those trials using higher target INRs reported a
similar experience, possibly because bleeding as a complication of
treatment, and hence the need to suspend anticoagulation, was more
frequent. Of patients initially assigned to anticoagulant therapy, two of
six developed an ischemic stroke within five days [2], and three of 11
within seven days [3], of stopping their anticoagulant. Two of four cases
[4], and one of six [5] occurred during temporary discontinuation of
treatment.
With increasing use of anticoagulants in patients with NVAF, and the
frequency with which these are temporarily suspended in this elderly
population, the easily overlooked problem may be far greater than we
imagine. Further confirmation of this association may help promote use of
lower target INRs to reduce the risk of bleeding, may prevent unnecessary
suspension of anticoagulation for certain benign procedures, and encourage
use of perioperative heparin, where appropriate.
References
1). Blacker DJ, Wijdicks EFM, McClelland RL. Stroke risk in
anticoagulated patients with atrial fibrillation undergoing endoscopy.
Neurology 2003; 61: 964-968.
2). Stroke Prevention in Atrial Fibrillation Investigators. Stroke
prevention in atrial fibrillation study. Final results. Circulation 1991;
84: 527-539.
3). Stroke Prevention in Atrial Fibrillation Investigators. Adjusted-dose
warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-
risk patients with atrial fibrillation: Stroke prevention in atrial
fibrillation 111 randomised clinical trial. Lancet 1996; 348: 633-638.
4). Petersen P, Boysen G, Godtfredsen J, Andersen E, Andersen B. Placebo
-controlled, randomised trial of warfarin and aspirin for prevention of
thromboembolic complications in chronic atrial fibrillation. The
Copenhagen AFASAK Study. Lancet 1989; 1: 175-179.
5). Connolly SJ, Laupacis A, Gent M, Roberts RS, Cairns JA, Joyner C.
Canadian atrial fibrillation anticoagulation (CAFA) study. J Am Coll
Cardiol 1991; 18: 349-355.