Ischemia in Intracerebral Hemorrhage Is Associated With Leukoaraiosis and Hematoma Volume, Not Blood Pressure Reduction

Abstract

Background and Purpose— Diffusion-weighted imaging (DWI) lesions have been identified both inside and outside the perihematoma region. We tested the hypotheses that larger hematoma volumes and blood pressure reduction are associated with DWI lesions. Methods— Hematoma and perihematoma edema volumes were measured using planimetric techniques in 117 intracerebral hemorrhage (ICH) patients who underwent DWI. Perihematoma and remote DWI lesion volumes were measured using apparent diffusion coefficient thresholds for moderate (<730×10 −6 mm/s) and severe (<550×10 −6 mm/s) ischemia. Acute blood pressure change over the first 24 hours was calculated. Results— The median (interquartile range) time to magnetic resonance imaging was 2 (1–5) days. Median hematoma volume was 9.8 (2.6–23.0) mL, and median perihematoma edema volume was 7.0 (2.9–18.6) mL. A small portion of the perihematoma region contained tissue below the thresholds for moderate (8.0 [2.9–14.5]%) and severe ischemia (1.1 [0.3–3.5]%). Ischemic perihematoma tissue volumes were correlated with hematoma volumes ( R =0.52, P <0.001), but not maximal systolic blood pressure drop at 24 hours ( R =−0.09, P =0.38). Remote DWI lesions were found in 17 (14.5%) patients (mean volume=0.44±0.3 mL). Patients with remote DWI lesions had higher rates of antiplatelet use ( P =0.01), prior ICH ( P =0.03), lobar ICH (0.04), and larger leukoaraiosis volumes ( P =0.02). Maximal systolic blood pressure drop at 24 hours was similar in patients with (−20.5 [−55, −10] mm Hg) and without remote DWI lesions (−27 [−46, −13] mm Hg, P =0.96). Conclusions— Small DWI lesions within and outside the perihematoma region are common in primary ICH. Perihematoma DWI lesions were independently associated with larger hematoma volumes. Remote DWI lesions may be an epiphenomenon associated with the underlying microvascular pathogenesis. These data do not support a hemodynamic mechanism of ischemic injury after primary ICH.