Key points are not available for this paper at this time.
OBJECTIVE: To explore the relationship between hypoperfusion, embolism, and brain infarction. DESIGN: We studied 4 situations in which brain infarction is related to hypoperfusion: extracranial and intracranial occlusive vascular disease, reduced functional vascular reserve in patients with carotid artery occlusive disease, reduced collateral blood flow in patients given thrombolytic treatment, and cardiac surgery. We reviewed results of emboli monitoring using transcranial Doppler ultrasonography. RESULTS: Hypoperfusion is strongly linked to brain ischemia and infarction. The evidence includes close correlation of (1) the severity of arterial stenosis with brain infarction; (2) impaired functional blood flow reserve in patients with carotid artery disease and subsequent brain infarction; (3) reduced collateral blood flow with poor prognosis after thrombolysis; and (4) stroke-related neurologic deficits after cardiac surgery to hypoperfusion during surgery. Microembolization is common in patients with severe symptomatic carotid artery stenosis and during and after cardiac surgery. CONCLUSIONS: Hypoperfusion and embolism often coexist and their pathophysiological features are interactive. Arterial lumenal narrowing and endothelial abnormalities stimulate clot formation and subsequent embolization. Reduced perfusion limits the ability of the bloodstream to clear or wash out emboli and microemboli and reduces available blood flow to regions rendered ischemic by emboli that block supply arteries. The brain border zones are a favored destination for microemboli that are not cleared. We posit that impaired washout is an important but neglected concept that intertwines hypoperfusion, embolization, and brain infarction.
Caplan et al. (Sun,) studied this question.