Like the sea storm's pummeling effects in eroding a coastline, elevated blood pressures immediately after the onset of acute ischemic strokes might similarly be expected to batter impaired and vulnerable brain cells.1,2 But the issue of whether or not to lower elevated blood pressures acutely, an old debate, is not simply endothelial pounding; rather, the problem engages the crucial complexities of ensuring adequate blood flow to ischemically compromised tissue, the so-called ischemic penumbra3 menacingly threatened by infarction. Justification and rationale for not treating hypertension in acute ischemic strokes to optimize blood flow are fourfold: (1) occurrence of altered autoregulation of cerebral blood flow in patients who were hypertensive prior to their stroke; (2) impaired autoregulation caused by strokes; (3) the hazards of inducing "watershed" infarction with hypotensive therapy; and (4) extension of ischemic damage in strokes that initially only partially occlude a major artery.
1. Chronic hypertension, the