Intermittent pneumatic compression after stroke

www.thelancet.com/neurology Vol 13 December 2014 1163 Acute stroke often causes immobility, which predisposes to deep vein thrombosis and pulmonary embolism and these can be fatal or disabling. Low-dose subcutaneous anticoagulation with heparins and heparinoids reduces the risk of venous thromboembolism, but the benefi t is off set by haemorrhagic complications. Even targeting anticoagulation to patients at high risk of venous thromboembolism and low risk of bleeding does not add value because patients at high risk of venous thromboembolism (eg, increased severity of stroke) are also at high risk of bleeding. Application of graduated compression stockings to the legs is a physical method for the prevention of deep vein thrombosis in patients undergoing surgery, but it was ineff ective in immobile patients with acute stroke in the CLOTS (Clots in Legs Or sTockings after Stroke) trials 1 and 2. Intermittent pneumatic compression (IPC) is another physical method for the prevention of deep vein thrombosis in patients undergoing surgery. In 2013, according to the results of the CLOTS 3 trial, IPC, through U-shaped or J-shaped association between outcome of acute stroke (defi ned as death or dependency) and ontreatment blood pressure change—ie, large decreases or increases in blood pressure were associated with worse outcomes of acute stroke, although cognitive outcomes were not assessed. In fact, in rare cases or very small trials of acute stroke caused by large vessel stenosis, in which acute cognitive defi cits are due to regional hypoperfusion beyond the infarct, temporary blood pressure elevation (with fl uids or pressors) has resulted in improvement in cognitive function. Such cases of large vessel stenosis might represent the low end of the J-shaped association— ie, patients who have a poor outcome with a reduction in blood pressure after acute stroke. The absence of an identifi ed link between blood pressure and cognition in the SPS3 trial has several possible explanations. The intervention might not have aff ected cognition because there was no signifi cant reduction in subsequent stroke. Alternatively, the intervention might have been started too late—it might be necessary to treat blood pressure before clinically signifi cant small vessel disease (before stroke) to prevent cognitive decline. Or, it might be too soon (ie, the followup too short) for eff ects on cognition to be identifi ed. Neuroprotective eff ects of blood pressure lowering on cognitive function, especially in the context of small vessel disease, might only be realised many years from the start of the intervention. Finally, a J-shaped or U-shaped association between blood pressure change and cognition might be identifi ed by additional analyses, although such associations are more likely to be identifi ed after acute strokes caused by large vessel stenosis than after acute lacunar strokes (as investigated in SPS3). So, despite the negative results of this study, investigators should continue to measure cognitive outcomes of stroke, and continue to investigate positive long-term eff ects of lowering blood pressure, preferably before, but also after lacunar stroke.