J Stroke.
2020 May;22(2):206-224. 10.5853/jos.2019.03335.
Left Ventricular Hypertrophy and Cerebral Small Vessel Disease: A Systematic Review and Meta-Analysis
- Affiliations
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- 1Medical School, National and Kapodistrian University of Athens, Athens, Greece
- 2Cardiovascular Prevention and Research Unit, Department of Pathophysiology, National and Kapodistrian University of Athens, Athens, Greece
- 3Cognitive and Movement Disorders Unit and Unit of Neurochemistry and Biological Markers, First Department of Neurology, Eginition University Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece
- 4Second Department of Neurology, Attikon Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece
- 5Department of Neurology, University of Tennessee Health Science Center, Memphis, TN, USA
- 6Institute for Stroke and Dementia Research, LMU University Hospital, Ludwig-Maximilians-University (LMU), Munich, Germany
- KMID: 2503104
- DOI: http://doi.org/10.5853/jos.2019.03335
Abstract
- Background and Purpose
Left ventricular hypertrophy (LVH) is associated with the risk of stroke and dementia independently of other vascular risk factors, but its association with cerebral small vessel disease (CSVD) remains unknown. Here, we employed a systematic review and meta-analysis to address this gap.
Methods
Following the MOOSE guidelines (PROSPERO protocol: CRD42018110305), we systematically searched the literature for studies exploring the association between LVH or left ventricular (LV) mass, with neuroimaging markers of CSVD (lacunes, white matter hyperintensities [WMHs], cerebral microbleeds [CMBs]). We evaluated risk of bias and pooled association estimates with random-effects meta-analyses.
Results
We identified 31 studies (n=25,562) meeting our eligibility criteria. In meta-analysis, LVH was associated with lacunes and extensive WMHs in studies of the general population (odds ratio [OR]lacunes, 1.49; 95% confidence interval [CI], 1.12 to 2.00) (ORWMH, 1.73; 95% CI, 1.38 to 2.17) and studies in highrisk populations (ORlacunes: 2.39; 95% CI, 1.32 to 4.32) (ORWMH, 2.01; 95% CI, 1.45 to 2.80). The results remained stable in general population studies adjusting for hypertension and other vascular risk factors, as well as in sub-analyses by LVH assessment method (echocardiography/electrocardiogram), study design (cross-sectional/cohort), and study quality. Across LV morphology patterns, we found gradually increasing ORs for concentric remodelling, eccentric hypertrophy, and concentric hypertrophy, as compared to normal LV geometry. LVH was further associated with CMBs in high-risk population studies.
Conclusions
LVH is associated with neuroimaging markers of CSVD independently of hypertension and other vascular risk factors. Our findings suggest LVH as a novel risk factor for CSVD and highlight the link between subclinical heart and brain damage.
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