Abstract

Background: : Intake of omega-3 polyunsaturated fatty acids, such as EPA, has been reported to have protective effects on various diseases including ischemic stroke. However, there have been few studies concerning the effect of omega-3 polyunsaturated fatty acids on hemorrhagic stroke. We studied associations of serum levels of EPA with stroke subtypes including primary ICH Methods: We have examined serum EPA and arachidonic acid (AA) levels in routine practice since 2009. To calibrate the EPA values, we calculated EPA/AA ratio. A total of 212 consecutive acute stroke patients and 27 control subjects were included. The patients 40 years old or younger were excluded. Ischemic stroke subtypes were determined based on TOAST criteria. Primary ICH was classified into lobar or nonlobar types, according to the region of the brain in which it occurred. Results: Of all the 157 ischemic stroke patients (female 47, mean age 72.9 years), 62 were classified with cardioembolic stroke (CES), 25 large-artery atherosclerotic (LAA), 22 small-vessel disease (SVD), and 48 other/undetermined causes (O/U). Of all the 55 ICH patients (female 23, mean age 71.0), 34 patients had nonlobar type, and 21 had lobar one. There were no significant intergroup differences in the mean EPA/AA ratio (p=0.525) among CES (EPA/AA= 0.67±0.42), LAA (0.70±0.30), SVD (0.65±0.45), O/U (0.62±0.38), nonlobar ICH (0.51±0.30), lobar ICH (0.64±0.33), and control (0.60±0.42) groups. However, the EPA/AA ratio of the nonlobar ICH group was considerably low. The EPA/AA ratio of the nonlobar ICH group was significantly (p=0.033) lower than that of the whole other groups (0.65±0.39) and significantly (p=0.003) lower than that of the entire ischemic stroke groups (0.67±0.40). Although the significant differences between the nonlobar ICH and the whole ischemic groups were also observed in systolic and diastolic blood pressure (195±37/107±25 mmHg vs 159±35/82±19 mmHg, p<0.001), multiple linear regression analyses showed the association between the EPA/AA and nonlobar ICH was independent from the blood pressure. Conclusions: Although the strongest risk factor for nonlobar ICH is hypertension, low EPA/AA ratio might play a role in the development of nonlobar ICH.

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