"Evidence-based" recommendations for
warfarin prescription in patients with history of ischemic
stroke limit its use to prevention of
stroke due to
atrial fibrillation.
Warfarin is also prescribed by the authors to prevent
thrombosis in
stroke patients with
thrombophilia and potential cardiac or arterial source for
thromboembolism. These potential conditions, in the face of
thrombophilia, include, but may not be limited to,
dilated cardiomyopathy, decreased left ventricular function, atrial septal
aneurysm with or without
patent foramen ovale (PFO), PFO with evidence of pelvic or lower extremity
deep venous thrombosis or with clear
thrombophilia, spontaneous echocardiographic contrast, intracardiac or intra-arterial
thrombus, intra-aortic arch
thrombus, high degree of
stenosis of large- and medium-sized cerebrovascular arteries, and arterial dissection. Commonly diagnosed thrombophilic states in our population currently include
protein S or C deficiency,
antiphospholipid antibodies, and less commonly ATIII
deficiency, factor V Leiden mutation, G20210A PT mutation, and
plasminogen activator inhibitor-1 mutation. Thrombophilic states often occur in combination. The occurrence of combined arterial, cardiac, and thrombophilic sources of
thromboembolism poignantly describes the complexity of causation of ischemic
stroke in any one patient. Our practice of treating the complex interaction of thromboembolic sources is based on scientific evidence, which is not arbitrarily limited to probability-based statistics.
Warfarin is well known in the clinical setting to interact with many different contextual factors of the individual patient, making its dosing and response unique to that patient. We have shown why the indications for
warfarin use and its dosing cannot be directly extrapolated to the individual patient from the results of large, double-blind, randomized trials. In practice, the unique patient and his or her context must be considered by the expert physician who makes the therapeutic decision. The context includes, but is not limited to, known pathologies that contribute to
thrombus formation according to the accepted pathophysiologic model of
thrombosis based on Virchow's triad of altered flow, endothelium, and blood components.