Key result
Patients with lacunar infarctions showed lower cerebrovascular reactivity to L-arginine compared to healthy controls, but similar to those with risk factors.
Why the study?
Does L-arginine infusion reveal impaired cerebrovascular reactivity in patients with lacunar infarctions compared to healthy controls and patients with cardiovascular risk factors?
Observational (n=62)
Does L-arginine infusion reveal impaired cerebrovascular reactivity in patients with lacunar infarctions compared to healthy controls and patients with cardiovascular risk factors?
Cerebrovascular reactivity to L-arginine is impaired in patients with cardiovascular risk factors, but patients with lacunar infarctions do not show additional impairment compared to those with risk factors alone.
Answers are grounded in this paper and cite their sources.
Impaired reactivity ties to risk factors, not lacunar infarcts themselves; leaves open diagnostic utility of L-arginine testing.
BACKGROUND: It is well known that endothelial dysfunction plays an important role in the pathogenesis of many cardiovascular disorders. The aim of this study was to test the hypothesis that specific, marked endothelial dysfunction of cerebral arteries is present in patients with lacunar cerebral infarctions. METHODS: Cerebrovascular reactivity to L-arginine, which reveals the function of the cerebral endothelium, was investigated in patients with lacunar infarctions (20 patients, 11 male and 9 female, aged 60.9 +/- 7.3 years), 21 age- and gender-matched asymptomatic patients with similar cardiovascular risk factors (all patients had arterial hypertension) and 21 age- and gender-matched healthy controls. The mean arterial velocity (vm) in both middle cerebral arteries was measured by transcranial Doppler sonography during a 15-min baseline period, a 30-min intravenous infusion of L-arginine and a 15-min interval after L-arginine infusion. Arterial blood pressure, heart rate and CO2 were measured continuously. RESULTS: The measured vm increase during L-arginine infusion in the patients with lacunar infarctions (13.4 +/- 9.1%) was significantly lower compared to the healthy controls (20.5 +/- 9.9%) but similar to that obtained in the patients with cardiovascular risk factors (11.5 +/- 8.9%). CONCLUSIONS: Our results showed that cerebrovascular reactivity to L-arginine, which demonstrates cerebral endothelial function, is significantly impaired in patients with cardiovascular risk factors. Importantly, we found that patients with lacunar infarctions do not show any additional impairment of cerebral endothelial function.
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Oblak et al. (2005) conducted an observational in Lacunar infarctions (n=62). Lacunar infarctions vs. Healthy controls and asymptomatic patients with cardiovascular risk factors was evaluated on Mean arterial velocity (vm) increase during L-arginine infusion. Patients with lacunar infarctions showed lower cerebrovascular reactivity to L-arginine compared to healthy controls, but similar to those with risk factors.
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