Visceral adiposity index is associated with silent brain infarct in a healthy population

Visceral adiposity index (VAI) has been associated with various cardio-metabolic diseases; however, there is limited information about its association with cerebrovascular diseases. In this study, we evaluated the relationship between VAI and silent brain infarct (SBI). We evaluated a consecutive series of healthy volunteers over the age of 40 between January 2006 and December 2013. SBI was defined as an asymptomatic, well-defined lesion with a diameter ≥ 3 mm with the same signal characteristics as the cerebrospinal fluid. VAI was calculated using sex-specific equations as described in previous studies. A total of 2596 subjects were evaluated, and SBI was found in 218 (8%) participants. In multivariable analysis, VAI (adjusted odds ratio [aOR] = 1.30; 95% confidence interval [CI] 1.03–1.66; P = 0.030) remained a significant predictor of SBI after adjustment for confounders. The close relationship between VAI and SBI was prominent only in females (aOR = 1.44; 95% CI 1.00–2.07; P = 0.048). In the evaluation between VAI and the burden of SBI, VAI showed a positive dose–response relationship with the number of SBI lesions (P for trend = 0.037). High VAI was associated with a higher prevalence and burden of SBI in a neurologically healthy population.

Visceral Adiposity Index is Associated With Silent Brain Infarct in a Healthy Population

Background Visceral adiposity index (VAI) is a novel indicator of the mass and function of visceral adipose tissue, and it has been associated with metabolic disease, cardiovascular disease, and subclinical atherosclerosis; however, there is limited information about its association with cerebrovascular diseases, especially in subclinical pathology. In this study, we evaluated the relationship between VAI and silent brain infarct (SBI) in a healthy population. Methods We evaluated a consecutive series of healthy volunteers over the age of 40 between January 2006 and December 2013. SBI was defined as an asymptomatic, well-defined lesion with a diameter ≥ 3 mm with the same signal characteristics as the cerebrospinal fluid on T1- or T2 weighted images. VAI was calculated using sex-specific equations as described in previous studies, and was based on a number of parameters including waist circumference, triglycerides, high-density lipoprotein cholesterol, and body mass index. Results A total of 2,596 subjects were evaluated (mean age 56y, male sex: 54%), and SBI was found in 218 (8%) participants. In multivariable analysis, VAI (adjusted odds ratio [aOR] = 1.30; 95% confidence interval [CI] = 1.03–1.66; P = 0.030) remained a significant predictor of SBI after adjustment for confounders. On the other hand, visceral adipose tissue area on computed tomography did not show any statistical significance with SBI. The close relationship between VAI and SBI was prominent only in females (aOR = 1.44; 95% CI = 1.00-2.07; P = 0.048). In the evaluation between VAI and the burden of SBI, VAI showed a positive dose-response relationship with the number of SBI lesions (P for trend = 0.037). Conclusions High VAI was associated with a higher prevalence and burden of SBI in a neurologically healthy population, especially in females. Our findings indicate that VAI could be used as a simple and convenient predictor for SBI.

Abstract TP204: Intima-Media Thickness in the Carotid Bifurcation, But Not Cardio-Ankle Vascular Index or Ankle-Brachial Index, is Related to Silent Brain Infarct on Magnetic Resonance Imaging in Healthy, Middle-Aged Japanese Individuals

Background: Carotid ultrasonography is currently the principal noninvasive tool for evaluating subclinical atherosclerosis and carotid artery disease. Increased carotid intima-media thickness (IMT) may precede the development of atherosclerotic plaques. Several studies have shown that increased IMT is associated with increased incidence of stroke. Silent brain infarct (SBI) has been proposed as a strong subclinical risk marker for future symptomatic stroke onset. However, the relationship between SBI and elevated IMT in healthy, middle-aged Japanese individuals has not been adequately examined. Methods: We examined 280 Japanese adults (92 women; mean age, 52.9 ± 5 years) with no history of cardiocerebrovascular disease. We assessed all participants’ periventricular hyperintensities, deep subcortical white matter hyperintensities, SBI on magnetic resonance imaging, cardio-ankle vascular index (CAVI)/ankle-brachial index (ABI), and various vascular risk factors. In addition, we measured intima-media thickness at the common carotid artery (CCA), carotid bifurcation (CB), and internal carotid artery (ICA). Results: Participants were categorized into two groups according to the presence or absence of SBIs, and we then compared the clinical characteristics of the two groups. Age, hypertension, increased HbA1c level, and decreased estimated glomerular filtration rate were found to be significantly associated with the SBI group. The odds ratio (OR) of the maximum IMT at the CB for the presence of SBI was 4.016 (95% confidence interval [CI], 1.565-10.304), even after adjusting for potential confounding factors. In contrast, the ORs of maximum IMT at the ICA and CCA as well as CAVI and ABI were not significant. Participants with IMTs ≥2 mm at the CB had a higher probability of the presence of SBI (OR, 26.451; 95% CI, 2.404-291.00). Conclusion: The maximum IMT at the CB was significantly correlated with the presence of SBI on MRI, but ABI or CAVI did not show significant correlation. Thus, compared to CAVI or ABI, carotid ultrasonography appears to be a very useful tool for noninvasively detecting SBI. In particular, IMTs ≥2 mm at the CB on carotid ultrasonography may be practical for identifying SBIs among middle-aged Japanese individuals.

Asymptomatic carotid stenosis and concomitant silent brain infarctions

Objectives This review aims to clarify (1) the definition of silent brain infarct (SBI), (2) the diagnostic criteria of SBI using magnetic resonance imaging (MRI), (3) the prevalence of patients with asymptomatic carotid stenosis and SBI based on MRI assessment, (4) the association of SBI and asymptomatic carotid stenosis and the risk of stroke compared to patients without SBI, (5) the association between development of dementia/cognitive impairment in people with asymptomatic carotid stenosis and SBI, and (6) the evidence for treating patients with carotid stenosis and SBI. Methods A systematic search of PubMed and Scopus including all studies published from 2000 to 2018 and written in English. Results No consensus of the definition and diagnostic criteria for SBI was found. The prevalence of SBI in asymptomatic carotid patients is 17–33.3%. SBI is a significant risk factor for future stroke, OR 4.6 (95% CI: 3.0–7.2; p < 0.0001). One substudy showed that immediate CEA is beneficial compared to delayed CEA in these patients, showing a 45% reduction in annual stroke rate from 1.5%/year to 0.7%/year. Conclusion This review emphasizes the need to standardize the definition and diagnostic criteria of SBI on MRI. Current evidence suggests an increased risk and a small potential benefit of offering carotid endarterectomy to patient with silent brain infarct. Prospective studies are warranted to elucidate these issues further.

High Triglyceride/HDL Cholesterol Ratio is Associated with Silent Brain Infarcts in a Healthy Population

Background: Triglycerides (TG)/high-density lipoprotein (HDL) cholesterol ratio is a marker of small/dense low-density lipoprotein particles, which are closely associated with various metabolic and vascular diseases. However, the role of TG/HDL cholesterol ratio in cerebrovascular diseases has not been well studied. In this study, we evaluated the relationship between TG/HDL cholesterol ratio and the presence of silent brain infarct (SBI) in a neurologically healthy population. Methods: We retrospectively evaluated consecutive participants in health check-ups between January 2006 and December 2013. SBI was defined as an asymptomatic, well-defined lesion with a diameter of ≥ 3 mm on T1- or T2-weighted images. TG/HDL cholesterol ratio was calculated after dividing absolute TG levels by absolute HDL cholesterol levels. Results: Of 3,172 healthy participants, 263 (8.3%) had SBI lesions. In multivariate analysis, TG/HDL cholesterol ratio was independently associated with SBI (adjusted odds ratio [aOR] = 1.16, 95% confidence interval [CI] = 1.00 to 1.34, P = 0.047). This association was prominent in males (aOR = 1.23, 95% CI = 1.03 to 1.48, P = 0.021), but not in females. In the analyses of the relationships between lipid parameters and SBI lesion burden, TG/HDL cholesterol ratio was positively correlated, and total cholesterol/TG ratio was negatively correlated with SBI lesion burden, in dose-response manners (P for trend = 0.015 and 0.002, respectively). Conclusions: The TG/HDL cholesterol ratio was positively associated with the prevalence of SBI in a neurologically healthy population.

High Triglyceride/HDL Cholesterol Ratio is Associated with Silent Brain Infarcts in a Healthy Population

Background: Triglycerides (TG)/high-density lipoprotein (HDL) cholesterol ratio is a marker of small/dense low-density lipoprotein particles, which are closely associated with various metabolic and vascular diseases. However, the role of TG/HDL cholesterol ratio in cerebrovascular diseases has not been well studied. In this study, we evaluated the relationship between TG/HDL cholesterol ratio and the presence of silent brain infarct (SBI) in a neurologically healthy population. Methods: We retrospectively evaluated consecutive participants in health check-ups between January 2006 and December 2013. SBI was defined as an asymptomatic, well-defined lesion with a diameter of ≥ 3 mm on T1- or T2-weighted images. TG/HDL cholesterol ratio was calculated after dividing absolute TG levels by absolute HDL cholesterol levels. Results: Of 3,172 healthy participants, 263 (8.3%) had SBI lesions. In multivariate analysis, TG/HDL cholesterol ratio was independently associated with SBI (adjusted odds ratio [aOR] = 1.16, 95% confidence interval [CI] = 1.00 to 1.34, P = 0.047). This association was prominent in males (aOR = 1.23, 95% CI = 1.03 to 1.48, P = 0.021), but not in females. In the analyses of the relationships between lipid parameters and SBI lesion burden, TG/HDL cholesterol ratio was positively correlated, and total cholesterol/TG ratio was negatively correlated with SBI lesion burden, in dose-response manners (P for trend = 0.015 and 0.002, respectively). Conclusions: The TG/HDL cholesterol ratio was positively associated with the prevalence of SBI in a neurologically healthy population.

High Triglyceride/HDL Cholesterol Ratio is Associated with Silent Brain Infarcts in a Healthy Population

Background: Triglycerides (TG)/high-density lipoprotein (HDL) cholesterol ratio is a marker of small/dense low-density lipoprotein particles, which are closely associated with various metabolic and vascular diseases. However, the role of TG/HDL cholesterol ratio in cerebrovascular diseases has not been well studied. In this study, we evaluated the relationship between TG/HDL cholesterol ratio and the presence of silent brain infarct (SBI) in a neurologically healthy population. Methods: We retrospectively evaluated consecutive participants in health check-ups between January 2006 and December 2013. SBI was defined as an asymptomatic, well-defined lesion with a diameter of ≥ 3 mm on T1- or T2-weighted images. TG/HDL cholesterol ratio was calculated after dividing absolute TG levels by absolute HDL cholesterol levels. Results: Of 3,172 healthy participants, 263 (8.3%) had SBI lesions. In multivariate analysis, TG/HDL cholesterol ratio was independently associated with SBI (adjusted odds ratio [aOR] = 1.17, 95% confidence interval [CI] = 1.04 to 1.32, P = 0.012). This association was prominent in males (aOR = 1.20, 95% CI = 1.04 to 1.40, P = 0.015), but not in females. Other lipid parameters, such as HDL cholesterol (aOR = 0.87, 95% CI = 0.75 to 1.00, P = 0.042), TG (aOR = 1.15, 95% CI = 1.02 to 1.31, P = 0.02), and total cholesterol/TG ratio (aOR = 0.86, 95% CI = 0.75 to 1.00, P = 0.043) also showed significant relationships with SBI, when they were respectively adjusted for confounders. In the analyses of the relationships between lipid parameters and SBI lesion burden, TG/HDL cholesterol ratio was positively correlated, and total cholesterol/TG ratio was negatively correlated with SBI lesion burden, in dose-response manners (P for trend = 0.015 and 0.002, respectively). Conclusions: The TG/HDL cholesterol ratio was positively associated with the prevalence of SBI in a neurologically healthy population.