Abstract

BackgroundSystemic cardiac hypoperfusion is a well-acknowledged contributor to ischemic leukoencephalopathy. However, it has remained elusive how atherosclerosis-mediated cardiac remodelling modifies cerebral perfusion homeostasis as well as neuroimaging burden in cerebral small vessel disease (CSVD) development.MethodsThis retrospective study identified 103 arteriosclerotic CSVD (aCSVD) patients (CSVD burdenlow 0 ~ 1, n = 61 and CSVD burdenhigh 2 ~ 4, n = 42) from Sep. 2017 to Dec. 2019 who underwent transthoracic echocardiography(n = 81), structural magnetic resonance imaging and arterial spin labelling (ASL). Total CSVD burden was graded according to the ordinal “small vessel disease” rating score (0–4). We investigated the univariate and multivariate linear regression of mean deep regional cerebral blood flow (CBF) as well as logistic regression analysis of CSVD burdenhigh.ResultsRight atrial diameter (B coefficient, − 0.289; 95% CI, − 0.578 to − 0.001; P = 0.049) and left ventricular ejection fraction (B coefficient, 32.555; 95% CI, 7.399 to 57.711; P = 0.012) were independently associated with deep regional CBF in aCSVD patients. Binary logistic regression analysis demonstrated decreased deep regional CBF (OR 0.894; 95% CI 0.811–0.985; P = 0.024) was independently associated with higher CSVD burden after adjusted for clinical confounders. Multivariate receiver operating characteristics curve integrating clinical risk factors, mean deep CBF and echocardiographic parameters showed predictive significance for CSVD burdenhigh diagnosis (area under curve = 84.25, 95% CI 74.86–93.65%, P < 0.0001).ConclusionThe interrelationship of “cardiac -deep regional CBF-neuroimaging burden” reinforces the importance and prognostic significance of echocardiographic and cerebral hemodynamic assessment in CSVD early-warning.

Highlights

  • Systemic cardiac hypoperfusion is a well-acknowledged contributor to ischemic leukoencephalopathy

  • Though persistent cerebral perfusion has been considered as an attributable mechanism of white matter hyperintensity (WMH), a longitudinal quantitative neuroimaging study reveals that relative cerebral blood flow (CBF) change has no significant correlation with WMH progression [7]

  • Univariate analysis for deep regional CBF associated with cerebral small vessel disease (CSVD) burden In univariate analysis as shown in Table 2, decreased CBF in centrum semiovale and roof of lateral ventricle were significant risk factors of CSVD burdenhigh

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Summary

Introduction

Systemic cardiac hypoperfusion is a well-acknowledged contributor to ischemic leukoencephalopathy. It has remained elusive how atherosclerosis-mediated cardiac remodelling modifies cerebral perfusion homeostasis as well as neuroimaging burden in cerebral small vessel disease (CSVD) development. We investigated the univariate and multivariate linear regression of mean deep regional cerebral blood flow (CBF) as well as logistic regression analysis of CSVD burdenhigh. The pathogenesis of aCSVD remains poorly illustrated and chronic cerebral hypoperfusion secondary to arteriolosclerosis is one of the attributable mechanism [1]. Though persistent cerebral perfusion has been considered as an attributable mechanism of WMH, a longitudinal quantitative neuroimaging study reveals that relative cerebral blood flow (CBF) change has no significant correlation with WMH progression [7]. Aforementioned studies mainly focus on global CBF alteration but not deep regional CBF which represents the circulation perfusion of parenchymal small vessels

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