Blood Pressure Variability and Plasma Biomarkers of Neuronal Injury and Alzheimer's Disease: A Clinic-Based Study of Patients with Diseases Along the Heart-Brain Axis.

 Higher blood pressure variability (BPV) predisposes to cognitive decline. To investigate underlying mechanisms, we measured 24-h ambulatory BPV, nocturnal dipping and orthostatic hypotension in 518 participants with vascular cognitive impairment, carotid occlusive disease, heart failure, or reference participants. We determined cross-sectional associations between BPV indices and plasma biomarkers of neuronal injury (neurofilament light chain) and Alzheimer's disease (phosphorylated-tau-181 and Aß42/Aß40). None of the BPV indices were significantly associated with any of the biomarkers. Hence, in patients with diseases along the heart-brain axis, we found no evidence for an association between BPV and selected markers of neuronal injury or Alzheimer's disease.

Cerebral amyloid-ß deposition in patients with heart disease or carotid occlusive disease: A systematic review and meta-analysis.

BACKGROUND: Cardiovascular disease is an important contributor to cognitive impairment. This likely involves prototypical vascular disease mechanisms like ischemia, but cardiovascular disease might also impact the brain by accelerating cerebral amyloid-ß accumulation. We aimed to determine whether there is an association between heart disease or carotid occlusive disease (COD) and cerebral amyloid-ß burden. METHODS: We conducted a systematic review of studies investigating cerebral amyloid-ß burden, measured with positron emission tomography, in adults with and without heart disease or COD. Where possible, we obtained standardized mean differences (SMD) of amyloid-ß standardized uptake volume ratios (SUVr) for meta-analysis. RESULTS: Eight cross-sectional studies were identified (1478 participants, aged 60-81 years, 51% female). Three studies on heart disease (two on atrial fibrillation (AF) only, one on AF, coronary artery disease and heart failure) did not find a difference in amyloid-ß burden between patients and controls. The pooled difference for 746 participants with and without AF did not reach significance (SMD SUVr 0.14, 95%CI -0.06-0.34). Of the five studies on COD (one on differences between participants with and without COD, four on differences between hemispheres in unilateral COD), four did not find a difference in amyloid-ß between participants or hemispheres. The pooled difference in amyloid-ß load between hemispheres in 24 patients with unilateral COD was not significant (SMD SUVr -0.13, 95%CI -0.70-0.43). CONCLUSION: Based on current studies, although limited and heterogeneous, there is insufficient evidence to support the hypothesis that heart disease or COD are associated with increased cerebral amyloid-ß burden.

Effects of carotid endarterectomy or stenting on arterial diameters in the circle of Willis.

BACKGROUND: In patients with internal carotid artery (ICA) stenosis, the circle of Willis (CoW) is the primary collateral pathway. We compared luminal diameters in the CoW before and after carotid revascularization and compared the effects of carotid endarterectomy (CEA) and stenting on these diameters. METHODS: At a single center in the International Carotid Stenting Study, 139 patients with symptomatic ICA stenosis of 50% or more were randomized to stenting (n = 81) or CEA (n = 58). The diameters of all segments of the CoW were assessed on computed tomography angiography (CTA), before and 30 days after revascularization. All evaluations were performed blinded to treatment allocation and order of CTA. RESULTS: A .10-mm increase (95% confidence interval [CI], .02-.17; 7%; P = .01) in diameter after revascularization occurred in the ipsilateral precommunicating anterior cerebral artery (A1), whereas both the ipsilateral and contralateral posterior communicating arteries decreased in diameter by .12 mm (95% CI, .04-.21; 14%; P = .01) and .08 mm (95% CI, .00-.17; 10%; P = .05), respectively. The increase in diameter of the A1 was larger after stenting (.15 mm; 95% CI, .07-.24; P = .001) than after CEA (.02 mm; 95% CI, -.11 to .15; P = .79). Only in patients treated with CEA, the diameters of the contralateral A1 and ipsilateral precommunicating posterior cerebral artery were reduced after revascularization. CONCLUSIONS: Carotid revascularization improves anterior collateralization and reduces reliance on posterior collateral pathways via the CoW. Carotid stenting and endarterectomy appear to have different early effects on collateralization.

Cognitive functioning in patients with a small infarct in the brainstem.

Earlier findings in patients with a small supratentorial white matter infarct demonstrated subtle impairments of cognition. This is in line with reported difficulties in regaining premorbid level of functioning in daily life activities, even though any physical neurological deficits are no longer present. Either a "bystander effect" of adjoining gray matter or a long distance effect through hypometabolism or other neurochemical changes might underlie these impairments. To find the best explanation, a group of 17 patients with a lacunar infarct in the brainstem was neuropsychologically evaluated and compared with a closely matched control group. The patients demonstrated significantly impaired task performance on a constellation of neuropsychological tasks that was very similar to the findings previously found in patients with a supratentorial lacunar infarct (Boston Naming Test, TEA visual elevator, category fluency, Trailmaking Test). We conclude that a small white-matter infarct may affect cognitive functioning in a nonspecific way independently of its location.