Nearly one-third of patients with intracerebral
hemorrhage (ICH) have acute punctate infarcts on the diffusion-weighted
imaging (DWI) sequence of magnetic resonance imaging (MRI) scans in the
first week after symptom onset.1
These DWI lesions portend poor long-term prognoses and are
independently associated with 2-fold higher odds of major disability or
death.2 From a mechanistic standpoint, underlying cerebral small-vessel disease is purported to cause DWI lesions.2
Whether intensive blood pressure (BP) lowering contributes to these
lesions is highly contested. Several prior studies have shown a
significant relationship between the magnitude of BP reduction in the
first 24 hours and the occurrence of DWI lesions.3
In contrast, a pooled, individual patient–level meta-analysis of 1750
patients showed that admission BP, and not change in BP, was
independently associated with DWI lesions.4
More recently, intensive systolic BP (SBP) control did not result in
DWI lesions compared with liberal SBP management in a post hoc analysis
of the INTERACT2 trial (Intensive Blood Pressure Reduction in Acute
Cerebral Hemorrhage Trial).5
Additionally, in the ICHADAPT trial (Intracerebral Hemorrhage Acutely
Decreasing Arterial Pressure Trial), intensive (SBP <150 mm Hg) vs
liberal (SBP <180 mm Hg) BP control did not lead to significant
reduction in blood flow in the perihematomal or watershed border zones
in patients with an acute ICH, indicating that acute BP reduction does
not result in ischemia in these patients.6
Given these conflicting findings, the role of BP management after acute
ICH, particularly in the context of incident DWI lesions, remains
poorly understood.
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