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Objectives: Endothelial dysfunction (ED) has been linked to the pathogenesis of cerebral small vessel disease (SVD). We aimed to assess ED and cerebrovascular reactivity (CVR) in the patients with a diverse manifestation of SVD, with similar and extensive white matter lesions (WMLs, modified Fazekas scale grade ≥2), compared with a control group (CG) without the MRI markers of SVD, matched for age, gender, hypertension, diabetes, and to evaluate the change of CVR following 24 months.Methods: We repeatedly measured the vasomotor reactivity reserve (VMRr) and breath-holding index (BHI) of the middle cerebral artery (MCA) by the transcranial Doppler ultrasound (TCD) techniques in 60 subjects above 60 years with a history of lacunar stroke (LS), vascular dementia (VaD), or parkinsonism (VaP) (20 in each group), and in 20 individuals from a CG.Results: The mean age, frequency of the main vascular risk factors, and sex distribution were similar in the patients with the SVD groups and a CG. The VMRr and the BHI were more severely impaired at baseline (respectively, 56.7 ± 18% and 0.82 ± 0.39) and at follow-up (respectively, 52.3 ± 16.7% and 0.71 ± 0.38) in the patients with SVD regardless of the clinical manifestations (ANOVA, p > 0.1) than in the CG (respectively, baseline VMRr 77.2 ± 15.6%, BHI 1.15 ± 0.47, p < 0.001; follow-up VMRr 74.3 ± 17.6%, BHI 1.11 ± 0.4, p < 0.001). All the assessed CVR measures (VMRr and BHI) significantly decreased over time in the subjects with SVD (Wilcoxon's signed-rank test p = 0.01), but this was not observed in the CG (p > 0.1) and the decrease of CVR measures was not related to the SVD radiological progression (p > 0.1).Conclusions: This study provided evidence that the change in CVR measures is detectable over a 24-month period in patients with different clinical manifestations of SVD. Compared with the patients in CG with similar atherothrombotic risk factors, all the CVR measures (BMRr and BHI) significantly declined over time in the subjects with SVD. The reduction in CVR was not related to the SVD radiological progression.

Knowledge of risk factors for cerebral small vessel disease (CSVD) may generate hypothesis regarding possible targets for prevention. Our aim was to evaluate if atherothrombotic risk factors differ between patients with CSVD and with subjects without cerebrovascular disease but with high cardiovascular (CVD) risk. A single-center, cohort study was performed in consecutive patients with different CSVD manifestations. The study group consisted of 205 patients: 52 with lacunar stroke (LS), 20 with subcortical hemorrhagic stroke (HS), 50 with vascular dementia (VaD), 28 with vascular parkinsonism (VaP) and 55 controls (CG) with high CVD risk (35 with atherosclerotic CVD, 20 with 10-year risk of CVD with SCORE?5). Logistic regression was used to analyze the influence of clinical and laboratory data on the occurrence of CSVD. Mean age, sex distribution, prevalence of smoking, hyperlipidemia, peripheral artery disease and obesity were similar in CSVD and CG. The factors significantly associated with CSVD compared to controls were diabetes mellitus, polymetabolic syndrome, elevated systolic blood pressure, low levels of eGFR, HDL, albumin and high uric acid, fibrinogen, fasting glucose, HbA1c and intima medic thickness (p

Background and purpose: Natural course of cerebral small vessel disease (CSVD) has not yet been thoroughly studied. The aim of the single center study was to establish risk of vascular events or death in different manifestations of CSVD. Methods: 150 consecutive, functionally independent patients with marked MRI features of CSVD and with recent lacunar stroke (n = 52, LS), deep hemorrhagic stroke (n = 20, HS), vascular parkinsonism (n = 28, VaP), vascular dementia (n = 50, VaD) and 55 controls (CG) with high atherothrombotic risk free of cerebrovascular events were prospectively recruited and followed for 24 months. Results: Mean age and sex distribution were similar in CSVD and CG but patients with CSVD were less likely to have CAD (19% vs 40%, p = 0.02) and tended to have higher prevalence of diabetes (54% vs 37%, p = 0.11). The risk of vascular events or death was increased in any patients with moderate to severe white matter lesions at baseline MRI (HR 2.0; 95% CI 0.85–7.2), in CSVD (4.56; 95% CI 1.3–14.9) vs CG, regardless of its clinical manifestation: LS or HS (HR 4.70; 95% CI 1.3–16.2) and VaD or VaP (HR 4.59; 95% CI 1.3–15.7). Adjustment for confounders did not change the results substantially. Conclusions: Patients with symptomatic CSVD regardless of the clinical (acute or chronic) manifestation had more than fourfold the risk of vascular events or death in 24 months of observation compared with controls with high atherothrombotic risk free of cerebrovascular events.