BACKGROUND: Hyperhomocysteinemia has been shown to be a mild independent risk factor for premature atherosclerosis, and there is evidence of an increased rate of peripheral vascular occlusive disease, myocardial infarction, and stroke. OBJECTIVE: To evaluate clinical, biochemical, and neurophysiological findings in patients with ischemic stroke with and without hyperhomocysteinemia. SUBJECTS: One hundred twenty-five consecutive patients with a history of stroke and 60 healthy control subjects. METHODS: Patients were divided into those with and those without hyperhomocysteinemia, which was defined as blood levels beyond the mean total plasma homocysteine level plus 2 SDs of the healthy control group. History, symptoms, cause, patterns of infarction, biochemical data, continuous and transcranial Doppler sonography, and event-related potentials were recorded in all patients. RESULTS: Twenty-seven patients had hyperhomocysteinemia. Compared with the 98 patients without hyperhomocysteinemia, they had an increased rate of hypertension (odds ratio, 3.5; 95% confidence interval, 1.0-12.6), an increased level of uric acid (P < .007), an increased hematocrit (P < .02), a higher rate of microangiopathy (odds ratio, 2.8; 95% confidence interval, 1.1-7.2), and a trend to a higher rate of multiple infarction. Furthermore, the P3 latency of the event-related potential was significantly increased in hyperhomocysteinemia (P < .004). CONCLUSIONS: Hyperhomocysteinemia is probably an independent risk factor for stroke, with a prevalence of about 20% in all patients with a history of stroke; however, additional factors (eg, hypertension, hyperuricemia) may have an enhancing effect. There are significant differences in stroke patterns between patients with and without hyperhomocysteinemia, with a higher rate of lesions typical of cerebral microangiopathy and a trend to multiple infarctions in the former. Impairment of cognitive processing as measured by visual event-related potential is more pronounced in hyperhomocysteinemia.
BACKGROUND:Hyperhomocysteinemia has been shown to be a mild independent risk factor for premature atherosclerosis, and there is evidence of an increased rate of peripheral vascular occlusive disease, myocardial infarction, and stroke. OBJECTIVE: To evaluate clinical, biochemical, and neurophysiological findings in patients with ischemic stroke with and without hyperhomocysteinemia. SUBJECTS: One hundred twenty-five consecutive patients with a history of stroke and 60 healthy control subjects. METHODS:Patients were divided into those with and those without hyperhomocysteinemia, which was defined as blood levels beyond the mean total plasma homocysteine level plus 2 SDs of the healthy control group. History, symptoms, cause, patterns of infarction, biochemical data, continuous and transcranial Doppler sonography, and event-related potentials were recorded in all patients. RESULTS: Twenty-seven patients had hyperhomocysteinemia. Compared with the 98 patients without hyperhomocysteinemia, they had an increased rate of hypertension (odds ratio, 3.5; 95% confidence interval, 1.0-12.6), an increased level of uric acid (P < .007), an increased hematocrit (P < .02), a higher rate of microangiopathy (odds ratio, 2.8; 95% confidence interval, 1.1-7.2), and a trend to a higher rate of multiple infarction. Furthermore, the P3 latency of the event-related potential was significantly increased in hyperhomocysteinemia (P < .004). CONCLUSIONS:Hyperhomocysteinemia is probably an independent risk factor for stroke, with a prevalence of about 20% in all patients with a history of stroke; however, additional factors (eg, hypertension, hyperuricemia) may have an enhancing effect. There are significant differences in stroke patterns between patients with and without hyperhomocysteinemia, with a higher rate of lesions typical of cerebral microangiopathy and a trend to multiple infarctions in the former. Impairment of cognitive processing as measured by visual event-related potential is more pronounced in hyperhomocysteinemia.
Authors: J J Connors; D Seidenwurm; J C Wojak; R W Hurst; M E Jensen; R Wallace; T Tomsick; J Barr; C Kerber; E Russell; G M Nesbit; A J Fox; F Y Tsai Journal: AJNR Am J Neuroradiol Date: 2000-03 Impact factor: 3.825