TY - JOUR
T1 - Cerebral amyloid-β deposition in patients with heart disease or carotid occlusive disease
T2 - A systematic review and meta-analysis
AU - Starmans, Naomi Louisa Paula
AU - Leeuwis, Anna Elisabeth
AU - Biessels, Geert Jan
AU - Kappelle, Laurens Jaap
AU - van der Flier, Wiesje Maria
AU - Tolboom, Nelleke
N1 - Funding Information: This work is part of the Heart-Brain Connection crossroads (HBCx) consortium of the Dutch CardioVascular Alliance (DCVA). This work was supported by the Dutch Heart Foundation [grant agreements 2018–28 and CVON 2012–06]. Funding Information: This work is part of the Heart-Brain Connection crossroads (HBCx) consortium of the Dutch CardioVascular Alliance (DCVA). This work was supported by the Dutch Heart Foundation [grant agreements 2018–28 and CVON 2012–06]. Publisher Copyright: © 2023 The Authors
PY - 2023/2/15
Y1 - 2023/2/15
N2 - 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.
AB - 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.
KW - Amyloid-β
KW - Cardiovascular disease
KW - Carotid occlusive disease
KW - Dementia
KW - Heart disease
KW - Positron emission tomography
UR - http://www.scopus.com/inward/record.url?scp=85146448099&partnerID=8YFLogxK
U2 - https://doi.org/10.1016/j.jns.2023.120551
DO - https://doi.org/10.1016/j.jns.2023.120551
M3 - Review article
C2 - 36669349
SN - 0022-510X
VL - 445
JO - Journal of the neurological sciences
JF - Journal of the neurological sciences
M1 - 120551
ER -