Journal of the neurological sciences · 2023
Cerebral amyloid-β deposition in patients with heart disease or carotid occlusive disease: A systematic review and meta-analysis.
МетаанализСистематический обзорСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Starmans Naomi Louisa Paula, Leeuwis Anna Elisabeth, Biessels Geert Jan, Kappelle Laurens Jaap, van der Flier Wiesje Maria, Tolboom Nelleke
Аннотация
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-β accumulation. We aimed to determine whether there is an association between heart disease or carotid occlusive disease (COD) and cerebral amyloid-β burden.
METHODS: We conducted a systematic review of studies investigating cerebral amyloid-β 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-β 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-β 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-β between participants or hemispheres. The pooled difference in amyloid-β 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-β burden.
METHODS: We conducted a systematic review of studies investigating cerebral amyloid-β 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-β 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-β 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-β between participants or hemispheres. The pooled difference in amyloid-β 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-β burden.