Neurocognitive functioning and cerebrovascular reactivity after carotid endarterectomy

Lattanzi, Simona; Carbonari, Luciano; Pagliariccio, Gabriele; Bartolini, Marco; Cagnetti, Claudia; Viticchi, Giovanna; Buratti, Laura; Provinciali, Leandro; Silvestrini, Mauro

doi:10.1212/wnl.0000000000004862

Cited by 87 publications

(61 citation statements)

References 37 publications

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“…Previous studies have shown, however, that the studied SERT gene polymorphisms are functional polymorphisms leading to differential transcriptional activity and thereby different levels of serotonin uptake [5]. We did not have information on stroke sub-type or lesion location, which could affect cognitive outcome [28]. This information could reasonably be included in future larger-scale studies.…”

Section: Discussionmentioning

confidence: 99%

Serotonergic Regulation and Cognition after Stroke: The Role of Antidepressant Treatment and Genetic Variation

et al. 2019

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Introduction: Serotonin affects several brain functions including cognition. The serotonin transporter (SERT) regulates brain serotonin levels through reuptake into neurons. The gene encoding this transporter, the SERT gene, has several functional polymorphisms affecting the number of transporters and thereby the serotonin levels. SERT gene expression may be important for cognition and selective serotonin reuptake inhibitors (SSRI) may improve cognition post stroke. We therefore examined the association between SERT genotypes, cognitive function and early treatment with the SSRI citalopram among non-depressed Caucasian stroke patients. Patients and Methods: SERT gene polymorphisms in 270 non-depressed first-ever acute ischemic stroke patients randomized to citalopram, n = 130, or placebo, n = 140, were investigated. Patients were genotyped for a length polymorphism (L = long and S = short allele) and a single nucleotide polymorphism (A/G substitution) dividing the L-allele into L_A and L_G. According to these genotypes, patients were further grouped according to low (S/S, L_G/S and L_G/L_G), medium (S/L_A and L_G/L_A), or high functional gene expression (L_AL_A). Cognition was measured by the Symbol Digit Modalities Test (SDMT) at 1 and 6 months. Mean SDMT scores according to genotype and randomization groups were compared using multiple logistic regression adjusting for age, stroke severity, premorbid functional status, and vascular risk factors including smoking, hypertension, and diabetes. Results: Stratified by genotype groups, there were no statistically significant differences in SDMT scores between randomization groups. Placebo-treated patients with low SERT expression genotypes, however, tended to have lower mean SDMT scores (at 1 month: 30.2, SD 10.8) compared to citalopram-treated patients (33.6, SD 13.7). Within the placebo group, the low genotype expression patients had significantly lower adjusted mean SDMT scores at 1 month compared to the high genotype expression patients (adjusted mean difference of –6 points, CI –12.0 to –0.05). We found similar results at 6 months, although not statistically significant. The genotype expression was not associated with SDMT scores among citalopram-treated patients. Conclusion: There was no difference in cognition between citalopram and placebo-treated patients according to the genotype group. Our results indicate, however, that low expression SERT genotype may contribute to reduced cognitive function post stroke as placebo-treated patients with low SERT expression tended to score lower on the SDMT. The significant difference in SDMT scores between low and high expression patients was present only in the placebo-treated group, thereby warranting further exploration of the potential effect of early citalopram treatment on cognitive functioning. Our results are preliminary and need replication in larger-scale studies.

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Section: Discussionmentioning

confidence: 99%

Serotonergic Regulation and Cognition after Stroke: The Role of Antidepressant Treatment and Genetic Variation

et al. 2019

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“…As hemodynamic variables including BP variability and cerebrovascular reactivity have been shown to be related to target organ damage and clinical outcomes, taking them into consideration could provide a more exhaustive assessment of the detrimental effects of altered BP and allow to explore the potential differences across the clinical phenotypes . Indeed, in this study MHT resembles true hypertension regarding systolic BP variability, whereas true normotension and WCHT not.…”

Section: Discussionmentioning

confidence: 93%

Masked hypertensives: A disguised arterial stiffness population

Antza

Doundoulakis

Stabouli

et al. 2019

J of Clinical Hypertension

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The aim of this study was to determine whether masked hypertension (MHT) and white coat hypertension (WCHT) could be related to increased arterial stiffness and to identify the best office cutoff values of office BP for the diagnosis of MHT and WCHT. A total of 542 consecutive patients (50.2% male, age 42.5 ± 26.2 years) were included in the study. Patients were never treated before for hypertension. Patients were classified as true normotensives (44%), true hypertensives (30%), WC hypertensives (19%), and masked hypertensives (7%). Carotid‐femoral pulse wave velocity (c‐f PWV) was 9.91 ± 0.20 m/s in true normotension, 10.26 ± 0.27 m/s in WCHT, 11.28 ± 0.47 m/s in MHT, and 11.86 ± 0.23 m/s in true hypertension after adjustment for age and sex. Decision limits yielding 65% sensitivity were 130 mm Hg for office systolic BP with 72% specificity for the diagnosis of MHT. The optimal cutoff value of 80 mm Hg for office diastolic BP provides 60% sensitivity and 68% specificity. Decision limits yielding 63% sensitivity were 150 mm Hg for office systolic BP with 72% specificity for the diagnosis of WCHT. The optimal cutoff value of 95 mm Hg for office diastolic BP provides 75% sensitivity and 51% specificity. The presence of MHT should be taken into account when increased c‐f PWV is detected in the absence of office hypertension. The optimal office BP of 130/80 mm Hg provides the best sensitivity and specificity for the diagnosis of MHT. As regards the diagnosis of WCHT, the cutoff value of 150/95 mm Hg seems to provide the best option.

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“…The assessment of office and ambulatory BP may allow the early identification of hypertension phenotypes associated with increased vascular risk and, hence, have prognostic relevance. Further studies are warranted to evaluate whether other hemodynamic variables in addition to arterial stiffening, as total peripheral resistance, carotid intima‐media thickness, amplitudes of the decomposed carotid pressure waves, and cerebrovascular reactivity, may allow a better characterization of the individual cardiovascular risk and whether tailoring treatment according to the hemodynamic profile may actually improve vascular outcome …”

Section: Therapeutic Goals and Perspectivementioning

confidence: 99%