Key result
Essential hypertensive patients with microalbuminuria had a higher prevalence of cerebral ischemic lacunae compared to those without (82% vs 27%; OR 12; 95% CI 1.58-91.13; P=0.03).
Why the study?
Is microalbuminuria associated with increased subclinical cerebrovascular damage and carotid IMT in untreated essential hypertensive patients?
Observational (n=22)
Is microalbuminuria associated with increased subclinical cerebrovascular damage and carotid IMT in untreated essential hypertensive patients?
Effect estimate: OR 12 (95% CI 1.58-91.13)
Absolute Event Rate: 82% vs 27%
p-value: p=0.03
Microalbuminuria is associated with subclinical cerebrovascular damage and increased carotid IMT in untreated essential hypertension, suggesting its utility as an early marker for higher cardiovascular risk.
Microalbuminuria was associated with cerebral lacunae in untreated hypertension; leaves open its role in cerebrovascular risk stratification.
Microalbuminuria (Mi) is a marker of hypertensive and atherosclerotic organ damage in essential hypertension (EH) and has been showed to have a powerful prognotic value for cerebral and cardiovascular morbidity and mortality. An association between carotid intima-media thickness (IMT) and increased urinary albumin excretion (UAE) has been reported in patients with EH suggesting a linkage between Mi and atherosclerotic stroke mechanism(s). We therefore investigated the relationship between Mi, carotid artery changes and asymptomatic cerebrovascular damage in two groups of untreated essential hypertensive patients, with (HtAlb+, n=11) and without (HtAlb-, n=11) Mi. The study groups, selected among participants in a large epidemiological trial, were carefully matched for several potentially confounding variables and were free from neurologic abnormalities. Albuminuria was measured as albumin to creatinine ratio (ACR) in three non consecutive first morning urine samples. Persistent Mi (HtAlb+) was defined as an average ACR between 2.38-19 (males) and 2.96-20 (females). Carotid IMT was assessed by high resolution US scan, cerebral lacunar lesions by magnetic resonance imaging (NMR), left ventricular mass index (LVMI) by M-B mode echocardiography (LV hypertrophy LVH= LVMI ± 125g/m2), and retinal vascular changes by direct ophthalmoscopy. Office as well as 24-h ambulatory pressure monitoring (ABPM, Takeda 2430) were also evaluated. There were no differences between the two groups as for office and ABPM, lipid profile and smoking habits. Ht Alb+ patients showed higher prevalence of cerebral ischemic lacunae (82 vs 27%; P=0.03, OR=12, CI 1.58-91.13) as well as increased carotid IMT (0.9±0.05 vs 0.75±0.06; P=0.03) as compared to Ht Alb- patients. No difference was found in LVMI ( HtAlb+, 145 ±6 vs HtAlb-, 128± 7 g/m2; NS by ANOVA) and prevalence of LVH (HtAlb+, 82 vs HtAlb- 54 %; NS) and retinal vascular changes (HtAlb+, 82 vs HtAlb-73 %; NS). Furthermore patients with ischemic lacunae showed higher prevalence of Mi (75 vs 20%; P=0.03, OR=12, CI 1.58-91.13) and increased UAE (6.9 ±1.8 vs1.3± 0.6 mg/mmol, P=0.01) as compared to patients with normal NMR. In conclusion, Mi is an early marker of preclinical brain damage in EH and therefore can be useful to identify patients at higher risk of cerebral and cardiovascular events for whom preventive therapeutic measures are advisable.
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Maura Ravera (2001) conducted an observational in Essential hypertension (n=22). Microalbuminuria vs. No microalbuminuria was evaluated on Prevalence of cerebral ischemic lacunae (OR 12, 95% CI 1.58-91.13, p=0.03). Essential hypertensive patients with microalbuminuria had a higher prevalence of cerebral ischemic lacunae compared to those without (82% vs 27%; OR 12; 95% CI 1.58-91.13; P=0.03).
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