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Introduction: Cerebral small vessel disease (CSVD) frequently occurs in individuals with vascular risk factors. This condition might go unrecognised or result in only mild functional deficits. Objective: To evaluate the relationship between cardiovascular (CV) risk calculated with the HEARTS app and CSVD burden in a population without cardio-cerebrovascular diseases, and to estimate the prevalence of CSVD in low risk (LR) individuals. Methods: Asymptomatic subjects with vascular risk factors were included from primary health areas in Havana. The WHO's revised CV disease risk prediction chart (HEARTS app) was applied to all individuals, who were classified into two groups: LR and moderate/high risk (M/HR). Brain MRI was performed in all subjects. Results: 170 patients were included: 43 (25.3%) classified as low CV risk and 127 (74.7%) had M/HR CV risk. Half of the neurologically healthy individuals included displayed cerebral small vessel involvement (51.2%). White matter hyperintensities (WMH) and enlarged perivascular spaces were the most frequent lesions observed in both groups. WMH were more severe and more severe global score for CSVD were more frequent in the M/HR group (57.5%). It was noteworthy that 32.6% of LR-patients also exhibited more severe CSVD. The multivariate regression analysis revealed an independent association of arterial hypertension and age with the severity of CSVD. Conclusions: CV risk stratification through the HEARTS app has limited utility for predicting brain health in individuals with low CV risk. Identifying silent CSVD in individuals with apparently low CV risk is important, especially if they suffer from arterial hypertension.
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Background: Cerebral small vessel disease (CSVD) is frequent in patients with cardiovascular risk factors including arterial hypertension, and it is associated with vascular damage in other organs and the risk of stroke, cognitive impairment, and dementia. Early diagnosis of CSVD could prevent deleterious consequences. Objective: To characterize CSVD associated with indicators of subclinical vascular damage in asymptomatic hypertensive patients. Materials and Methods: Participants were hypertensive (HT) and non-hypertensive (non-HT) individuals; without signs of cerebrovascular disease, dementia, and chronic renal failure. For CSVD, white matter hyperintensities (WMH), enlarged Virchow-Robin perivascular spaces (EVRPS), lacunar infarcts, and microbleeds were investigated. Subclinical vascular damage was evaluated (hypertensive retinopathy, microalbuminuria, and extracranial carotid morphology: intima media thickness (IMT) and atheroma plaque). Results: CSVD MRI findings were more frequent in HT; as well as greater intimal thickening. The IMT + plaque was significantly associated with all MRI variables; but retinopathy was correlated with EVRPS and lacunar infarcts. Only microalbuminuria was related to the greater severity of WMH in HT. Multivariate analysis evidenced that CSVD was independently associated with the combination of indicators of vascular damage and systolic blood pressure. Conclusions: Combining indicators of subclinical vascular damage, such as carotid morphological variables, microalbuminuria, and hypertensive retinopathy for early detection of CSVD in asymptomatic hypertensive patients could prove to be useful to take actions for the prevention of irreversible brain damage, which could lead to cognitive impairment, dementia and stroke.
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Dural arteriovenous fistulas (DAVFs) represent 10-15% of intracranial arteriovenous malformations. Of these, only 12-29% cause intracranial hemorrhage. The presentation of DAVF as a subdural hematoma (SDH) and intraparenchymal hemorrhage (IPH) is infrequent; additionally, behavioral changes are not common among these patients. We report, for the first time in our country, the case of a 23-year-old man with no history of head injury, in which a brain computed tomography (CT) scan revealed SDH and IPH with behavioral disturbances. The angiotomography showed ecstatic venous vessels, indicating the presence of a DAVF, which was later confirmed by cerebral angiography. Endovascular therapy, which followed the clinical diagnosis, resulted in satisfactory evolution two years after treatment. A review of the literature concerning cases with DAVF and behavioral disturbances is presented. DAVF may lead to cognitive impairment, behavioral changes, and dementia as a result of diffuse white matter and thalamus modifications related to venous ischemia, and it should be considered as a reversible cause of vascular dementia.
