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Summary: In an attempt to determine the presence of hypertension in stroke patients and its relationship with hyperinsulinaemia, a case-control study was carried out in the outpatients clinic, Department of Neurology, Sardjito General Hospital, Yogyakarta. Patients included in the study were those who had survived a stroke at least 3 months after the first attack. the exclusion criteria included: diabetes mellitus, renal failure, heart failure, malignancy, myocardial infarction, current antihypertensive and hypolidaemic treatment. Controls were selected from non-stroke patients at the same department matching for sex and age. During the study 51 stroke patients (39 male and 12 female, aged 58.7 ± 10.3 years) and 51 controls (40 male and 11 female, aged 58.6 ± 9.8 years). There were no significant differences in baseline clinical characteristics; namely, smoking, body mass index, blood sugar and blood lipids except triglyceride (169 ± 61 vs 141 ± 60 P<0.05) of cases and controls. Although there was no significant difference of fasting plasma insulin levels (9.3 ± 8.3 vs 8.3 ± 2.6 mU/L, P= >0.05), significantly higher levels of postprandial insulin (94.8 ± 86.7 vs 55.2 ± 49.1 mU/L, P<0.05) were found in cases than controls. There were a significantly higher levels of blood pressure, both systolic (160 ± 24 vs 131 ± 11 mmHg, P<0.05) and diastolic (101 ± 13 vs 79 ± 4 mmHg, P<0.05), and more frequent hypertension defined as BP ± 140/90 mmHg (72.5 vs 2.0%, P<0.05) in cases than controls. No significant difference of plasma insulin levels (94.9 ± 82.3 vs 94.3 ± 119.2 mU/L, P>0.05) between hypertensive and normotensive stroke patients. However, significantly higher levels of insulin (94.3 ± 119.2 mU/L vs 55.2 ± 49.1 mU/L, P<0.05) were found in normotensive stroke patients than controls. the relationship between 2 h post-prandial blood sugar levels and post-prandial insulin levels was positive and nearly significant relationship (r=0.62, P=0.05). the relationship between mean arterial pressure (MAP) and post-prandial insulin levels of the whole patients (cases and controls) were poor but significant (r = 0.22, P<0.05). the relationship between MAP and post-prandial insulin levels are poor and not significant both in stroke patients (r = 0.00, P>0.05) and controls (r = 0.17, P>0.05). the slope of both curves in both scattered diagrams seemed to be slightly different. We conclude that hypertension and post prandial hyperinsulinaemia may play a role in the genesis of stroke, while hyperinsulinaemia may an independent factor.  相似文献   
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