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Akinci et al. Vessel Plus 2021;5:56 https://dx.doi.org/10.20517/2574-1209.2021.20 Page 5 of 20

considering that the most common cause of ICH is chronic hypertension, we can infer that previous studies
mostly examined patients who developed ICH on the basis of chronic hypertension.

Apart from not considering history of previous hypertension, there is also the problem that the definition
“SBP ≥ 140 mmHg” does not consider the relationship between the degree of pretreatment BP and outcome.
Studies showed that the relationship between acute hypertensive response and hematoma enlargement and
[37]
mortality is evident at higher SBPs. In the retrospective study by Dandapani et al. , patients with SBP >
196 mmHg on admission had a higher mortality rate than those with SBP ≤ 196 mmHg (44% vs. 18%).
[19]
Similarly, according to the study by Kazui et al. , SBP ≥ 200 mmHg on admission independently
predisposed to hematoma expansion. In the Intensive Blood Pressure Reduction in Acute Cerebral
Haemorrhage trial (INTERACT), the most significant attenuation of hematoma expansion with early
intensive BP treatment was observed in patients with SBP ≥ 181 mmHg on admission . Thus, the
[38]
definition “a SBP of ≥ 140 mmHg” may provide a uniform standard for measuring prevalence but does not
define therapeutic thresholds for antihypertensive treatment [39,40] .

MANAGEMENT OF ACUTE HYPERTENSIVE RESPONSE
Reducing increased BP following an ICH, which has been found to be associated with hematoma
enlargement, perihematomal edema, and poor outcomes, has been recognized as a potential strategy . On
[17]
the other hand, due to the possibility that acute hypertension might be a protective response to increased
ICP, there were concerns about the potential risk of worsening perihaematomal ischaemia from aggressive
early BP reduction especially in the setting of chronic hypertension, which raises the lower limit of the CBF
autoregulation curve . U- or J-shaped associations between BP levels and poor outcome have been
[41]
[42]
demonstrated for ischemic stroke . For ICH, the results were variable in different studies. A prospective
study reported higher mortality rates in patients with SBP > 220 mmHg or < 120 mmHg compared with
patients with SBP 141-160 mmHg . In a retrospective chart review with 105 spontaneous ICH patients,
[43]
[44]
rapid MAP decline within the first 24 h was associated with increased mortality . However, in a brain
oxygenation positron emission tomography study with 19 acute ICH patients, researchers found no
evidence for ischemia in the periclot zone of hypoperfusion 5 to 22 h after the onset of bleeding . Studies
[45]
suggested that reduced metabolism (hibernation) and preserved autoregulation in the perihematoma region
led to the tolerance of BP lowering [46,47] . In large phase III, multicentre, prospective, randomised, controlled
trials, lowering of SBP to < 140 mmHg in the acute phase has been found safe [48,49] . However, the effect of BP
lowering for special groups continues to be investigated in clinical trials. Antihypertensive Treatments for
Spontaneous Intracerebral Hemorrhage in Patients with Cerebrovascular Stenosis (ATICHST) is a recent
clinical trial designed to investigate the effects of intensive BP reduction (< 140 mmHg) in spontaneous ICH
[50]
patients with cerebrovascular stenosis (constituting 20% to 54% of ICH patients) . Patients with 30%-70%
stenosis in the anterior or posterior circulation in computed tomography (CT) angiography and with a SBP
between 150-220 mmHg will be included. With this ongoing study, it is aimed to understand whether
intensive SBP lowering in the presence of cerebrovascular stenosis increases the risk of ischemia and
infarction.

CURRENT GUIDELINE RECOMMENDATIONS FOR ELEVATED BP IN SPONTANEOUS ICH
The main issues related to the management of acute hypertensive response can be considered to consist of
treatment threshold, and time window, type of antihypertensive drug and routes of administration, and
target BP. Which of these do the current guidelines clarify?