Hypertension in Acute Ischemic Strokes

An overview of acute hypertensive response following intracerebral hemorrhage: implifications for clinical practice

“…In the meta-analysis of Koch et al [52] , INTERACT, INTERACT-2, ADAPT, Gong et al [66] , ATACH-2 trials, intensive BP lowering (target SBP < 140 mmHg or MAP < 110 mmHg) showed no effects on 24 h neurologic improvement and 3-month functional outcome, and only attenuated hematoma growth in patients age ≤ 62 years with hematoma volume ≤ 15 mL received treatment within 6 h after symptom onset [70] . In the meta-analysis including Koch et al [55] , INTERACT, INTERACT-2, ICH-ADAPT, ATACH-2 trials, no obvious benefit of intensive BP lowering was observed and the rate of renal failure was higher with intensive treatment [driven predominantly by the trial with lowest SBP target (110-139 mmHg)] [71] .…”

An overview of acute hypertensive response following intracerebral hemorrhage: implifications for clinical practice

“…In the meta-analysis of Koch et al [52] , INTERACT, INTERACT-2, ADAPT, Gong et al [66] , ATACH-2 trials, intensive BP lowering (target SBP < 140 mmHg or MAP < 110 mmHg) showed no effects on 24 h neurologic improvement and 3-month functional outcome, and only attenuated hematoma growth in patients age ≤ 62 years with hematoma volume ≤ 15 mL received treatment within 6 h after symptom onset [70] . In the meta-analysis including Koch et al [55] , INTERACT, INTERACT-2, ICH-ADAPT, ATACH-2 trials, no obvious benefit of intensive BP lowering was observed and the rate of renal failure was higher with intensive treatment [driven predominantly by the trial with lowest SBP target (110-139 mmHg)] [71] .…”

Influence of acute blood pressure on short- and mid-term outcome of ischemic and hemorrhagic stroke

“…Thus, in absence of reliable evidence, opinions on what to do about BP in acute stroke are diverging, with the obvious consequence that the effectiveness of the two opposite approaches of BP intensive lowering and BP raising have been both advocated. Proponents of active treatment focus on the risk that high BP may increase blood-brain barrier disruption and induce infarct-related edema, rebleeding in intracerebral hemorrhage or hemorrhagic conversion of a cerebral infarct [11,21]. In contrast, opponents point at the risk for reduction of cerebral perfusion pressure in the ischemic penumbra [27], with a risk of watershed or extended infarction following hypotensive therapy [18], and for induction of cerebral ischemia in critically perfused or hypometabolic regions of the brain adjacent to a cerebral hematoma [12], although imaging studies failed to identify any such adverse effect [6,19].…”

U‐shaped relationship between mortality and admission blood pressure in patients with acute stroke

“…The most common causes of death in our patients with admission BP‐values >130 mmHg was neurological damage due to extensive brain oedema as shown on repeated brain CT scans. It remains unclear whether oedema formation after ischaemic or haemorrhagic stroke leads to higher BP‐values or BP rises in order to maintain sufficient cerebral perfusion pressure [23, 24].…”

An overview of acute hypertensive response following intracerebral hemorrhage: implifications for clinical practice

“…In the meta-analysis of Koch et al [52] , INTERACT, INTERACT-2, ADAPT, Gong et al [66] , ATACH-2 trials, intensive BP lowering (target SBP < 140 mmHg or MAP < 110 mmHg) showed no effects on 24 h neurologic improvement and 3-month functional outcome, and only attenuated hematoma growth in patients age ≤ 62 years with hematoma volume ≤ 15 mL received treatment within 6 h after symptom onset [70] . In the meta-analysis including Koch et al [55] , INTERACT, INTERACT-2, ICH-ADAPT, ATACH-2 trials, no obvious benefit of intensive BP lowering was observed and the rate of renal failure was higher with intensive treatment [driven predominantly by the trial with lowest SBP target (110-139 mmHg)] [71] .…”

Influence of acute blood pressure on short- and mid-term outcome of ischemic and hemorrhagic stroke

“…Thus, in absence of reliable evidence, opinions on what to do about BP in acute stroke are diverging, with the obvious consequence that the effectiveness of the two opposite approaches of BP intensive lowering and BP raising have been both advocated. Proponents of active treatment focus on the risk that high BP may increase blood-brain barrier disruption and induce infarct-related edema, rebleeding in intracerebral hemorrhage or hemorrhagic conversion of a cerebral infarct [11,21]. In contrast, opponents point at the risk for reduction of cerebral perfusion pressure in the ischemic penumbra [27], with a risk of watershed or extended infarction following hypotensive therapy [18], and for induction of cerebral ischemia in critically perfused or hypometabolic regions of the brain adjacent to a cerebral hematoma [12], although imaging studies failed to identify any such adverse effect [6,19].…”

U‐shaped relationship between mortality and admission blood pressure in patients with acute stroke

“…The most common causes of death in our patients with admission BP‐values >130 mmHg was neurological damage due to extensive brain oedema as shown on repeated brain CT scans. It remains unclear whether oedema formation after ischaemic or haemorrhagic stroke leads to higher BP‐values or BP rises in order to maintain sufficient cerebral perfusion pressure [23, 24].…”

An overview of acute hypertensive response following intracerebral hemorrhage: implifications for clinical practice

“…In the meta-analysis of Koch et al [52] , INTERACT, INTERACT-2, ADAPT, Gong et al [66] , ATACH-2 trials, intensive BP lowering (target SBP < 140 mmHg or MAP < 110 mmHg) showed no effects on 24 h neurologic improvement and 3-month functional outcome, and only attenuated hematoma growth in patients age ≤ 62 years with hematoma volume ≤ 15 mL received treatment within 6 h after symptom onset [70] . In the meta-analysis including Koch et al [55] , INTERACT, INTERACT-2, ICH-ADAPT, ATACH-2 trials, no obvious benefit of intensive BP lowering was observed and the rate of renal failure was higher with intensive treatment [driven predominantly by the trial with lowest SBP target (110-139 mmHg)] [71] .…”

Influence of acute blood pressure on short- and mid-term outcome of ischemic and hemorrhagic stroke

“…Thus, in absence of reliable evidence, opinions on what to do about BP in acute stroke are diverging, with the obvious consequence that the effectiveness of the two opposite approaches of BP intensive lowering and BP raising have been both advocated. Proponents of active treatment focus on the risk that high BP may increase blood-brain barrier disruption and induce infarct-related edema, rebleeding in intracerebral hemorrhage or hemorrhagic conversion of a cerebral infarct [11,21]. In contrast, opponents point at the risk for reduction of cerebral perfusion pressure in the ischemic penumbra [27], with a risk of watershed or extended infarction following hypotensive therapy [18], and for induction of cerebral ischemia in critically perfused or hypometabolic regions of the brain adjacent to a cerebral hematoma [12], although imaging studies failed to identify any such adverse effect [6,19].…”

U‐shaped relationship between mortality and admission blood pressure in patients with acute stroke

“…The most common causes of death in our patients with admission BP‐values >130 mmHg was neurological damage due to extensive brain oedema as shown on repeated brain CT scans. It remains unclear whether oedema formation after ischaemic or haemorrhagic stroke leads to higher BP‐values or BP rises in order to maintain sufficient cerebral perfusion pressure [23, 24].…”