Prevalence Of Silent Brain Infarcts Research Articles

Correlation of Silent Brain Infarction with the Metabolic Abnormality of CKD Stage 3-5 (non-dialytic) Patients

Background: Silent brain infarction (SBI) poses a significant yet often undetected risk in chronic kidney disease (CKD) patients, predisposing them to symptomatic stroke, dementia, and neurological mortality. Despite its implications, the association between SBI and CKD remains elusive, necessitating further exploration to elucidate potential predictive factors. Objective: This cross-sectional study investigated the relationship between SBI and metabolic abnormalities prevalent in CKD stages 3-5 (non-dialytic) patients. Methods: Conducted at the Department of Nephrology, Dhaka Medical College Hospital, Dhaka, from September 2018 to March 2020, the study enrolled 115 participants. Group I comprised 85 CKD stage 3-5 (non-dialytic) patients without neurological symptoms, while Group II comprised 30 healthy controls. Glomerular filtration rate (GFR) was estimated using the Modification of Diet in Renal Diseases equation. Magnetic resonance imaging (MRI) was performed on all subjects. Statistical analysis utilized SPSS-26. Results: The rate of Silent Brain Infarction is 52.9% in CKD patients. SBI was found in 45(52.9%) patients in group I and 4(13.3%) in group II. The differences were statistically significant (p<0.05). Glomerulonephritis (45.9%) was the leading cause of CKD among the study patients. Most of the patients with Hypertensive Nephrosclerosis (76.9%) had SBI, which indirectly showed its strong association. As the CKD stages progressed, the SBI rate also increased (stage-3:8.9%; stage-4:35.6%; stage-5ND:55.6%). In a multivariate logistic regression analysis, CKD had an independent relationship with SBI along with serum phosphate level and serum parathyroid hormone level (CKD had Odds ratio (OR)=1.847 (95.0% CI 0.064 to 53.319), serum PO4 had OR=0.958 (95.0% CI 0.885 to 1.038) and serum PTH had OR=0.996 (95.0% CI 0.993 to 1.000). Spearman rank correlation coefficient test showed a positive correlation between the occurrence of SBI and serum PO4 level (r=0.416; p=0.001) and serum PTH level (r= 0.405; p=0.001) separately. Conclusions: The high prevalence of SBI in CKD stage 3-5 (non-dialytic) patients underscores its clinical significance. Serum phosphate and parathyroid hormone levels positively correlate with SBI occurrence, highlighting their potential as predictive markers. Understanding these associations can inform risk stratification and guide targeted interventions in CKD management.

Covert Cerebrovascular Changes in People With Heart Disease: A Systematic Review and Meta-Analysis.

To determine the prevalence of silent brain infarction (SBI) and cerebral small vessel disease (CSVD) in adults with atrial fibrillation (AF), coronary artery disease, heart failure or cardiomyopathy, heart valve disease, and patent foramen ovale (PFO), with comparisons between those with and without recent stroke and an exploration of associations between heart disease and SBI/CSVD. Medline, Embase, and Cochrane Library were systematically searched for hospital-based or community-based studies reporting SBI/CSVD in people with heart disease. Data were extracted from eligible studies. Outcomes were SBI (primary) and individual CSVD subtypes. Summary prevalence (95% confidence intervals [CIs]) were obtained using random-effects meta-analysis. Pooled prevalence ratios (PRs) (95% CI) were calculated to compare those with heart disease with available control participants without heart disease from studies. A total of 221 observational studies were included. In those with AF, the prevalence was 36% (31%-41%) for SBI (70 studies, N = 13,589), 25% (19%-31%) for lacune (26 studies, N = 7,172), 62% (49%-74%) for white matter hyperintensity/hypoattenuation (WMH) (34 studies, N = 7,229), and 27% (24%-30%) for microbleed (44 studies, N = 13,654). Stratification by studies where participants with recent stroke were recruited identified no differences in the prevalence of SBI across subgroups (phomogeneity = 0.495). Results were comparable across participants with different heart diseases except for those with PFO, in whom there was a lower prevalence of SBI [21% (13%-30%), 11 studies, N = 1,053] and CSVD. Meta-regressions after pooling those with any heart disease identified associations of increased (study level) age and hypertensives with more SBIs and WMH (pregression <0.05). There was no evidence of a difference in the prevalence of microbleed between those with and without heart disease (PR [95% CI] 1.1 [0.7-1.7]), but a difference was seen in the prevalence of SBI and WMH (PR [95% CI] 2.3 [1.6-3.1] and 1.7 [1.1-2.6], respectively). People with heart disease have a high prevalence of SBI (and CSVD), which is similar in those with vs without recent stroke. More research is required to assess causal links and implications for management. PROSPERO CRD42022378272 (crd.york.ac.uk/PROSPERO/).

Analysis of clinical and imaging characteristics of patients with freezing of gait in cerebral small vessel disease (P11-5.004)

<h3>Objective:</h3> This study aims to study the clinical and imaging characteristics of patients with freeing of gait (FOG) in Cerebral small vessel disease (CSVD). <h3>Background:</h3> FOG is prevalent in Parkinson’s disease in those with severe gait disorders. However, little is known about vascular FOG in patients with CSVD. <h3>Design/Methods:</h3> The current study is a case-control study. Symptomatic CSVD patients were recruited. Patients with FOG (CSVD-FOG) and without FOG (CSVD-no-FOG) were categorized into two groups. The differences of clinical and imaging characteristics in these two groups were studied. <h3>Results:</h3> In 444 symptomatic CSVD patients with gait testing records, 24 were CSVD-FOG. 72 CSVD-no-FOG patients were matched according to age and sex. Prevalence of vascular risk factors including hypertension, diabetes mellitus, and hyperlipidemia were not significantly different between two groups. In CSVD-FOG groups, 83.3% were claimed about gait disorder, and had a higher percentage of urinary disorders and impaired cognitive functions compared with CSVD-no-FOG. Patients with apathy were not different between two groups. In assessing quantitative gait parameters, CSVD-FOG patients had slower gait speed, shorter gait stride and gait length, lower gait height and wider gait width. For CSVD imaging burdens, the CSVD-FOG had similar white matter hyperintensity burden with CSVD-no-FOT. However, CSVD-FOG had higher prevalence of silent brain infarction (SBI) and cerebral microbleeds (CMBs) in location of whiter matter and brain stem. <h3>Conclusions:</h3> CSVD-FOG patients had severe clinical symptoms of gait disorder, cognitive impairment and urinary problems, as well as higher imaging burdens of SBI and CMBs in whiter matter and brain stem. <b>Disclosure:</b> Dr. Su has nothing to disclose. Miss Mao has nothing to disclose. Jiangxia Zhang has nothing to disclose. Mr. Zhu has nothing to disclose. Fei Han has nothing to disclose. Ming Yao has nothing to disclose. Lixin Zhou has nothing to disclose. Jun Ni has nothing to disclose. Dr. Fan has nothing to disclose. Feng Tian has nothing to disclose. Yi-Cheng Zhu has nothing to disclose.

Abstract 11401: Silent Brain Infarct on MRI Predicts Clinical Stroke/ Transient Ischemic Attack in Mitral Stenosis

Introduction: Mitral stenosis (MS) is associated with a high risk of cardio-embolic events. However, current recommendations for initiating anti-coagulant therapy in patients with MS is limited to patients with atrial fibrillation (AF),atrial thrombi or those with a prior stroke. In patients with moderate to severe MS who are in sinus rhythm there are no firm recommendations for anti-coagulation despite a known higher risk of thromboembolic events. Moreover there is limited data on the prevalence of silent brain infarcts (SBI) in patients with MS. This study evaluated prevalence and predictors of silent and clinical stroke in MS. Methods: A total of 211 patients with moderate to severe MS (mitral valve area ≤ 1.5 cm2) were recruited in the study and were followed up over a7 year period. Patients with existing left atrial clot(s) or prior valvular intervention were excluded from the study. All patients underwent clinical examination, ECG, echocardiogram, and brain MRI on a 1.5T machine. A 24-hour Holter was performed on patients in sinus rhythm. Results: Among 211 patients, 87(41.2%) were male and 140 (66.3%)were in sinus rhythm. Moderate to severe mitral regurgitation and/or aortic regurgitation was present in 31 (14.7%) and 30 (14.2%)patients respectively. SBI was seen in 44 (20.9 %) patients [26 (18.6%)in sinus rhythm and 18(25.4%) in AF]. Female gender (OR 2.3 95% CI 1.01-5.1, p = 0.043), poorer NYHA functional class (Class II OR 16, 95%CI 4.1-62.8, p=0.001; Class III OR 4.1 95%CI 1.2-13.8, p = 0.024),AF (OR 3.8 95%CI 1.6-8.9 p = 0.002) and aortic regurgitation (OR 3.7 95%CI 1.3-10.4 p = 0.011)were associated with increased risk of SBI. Seventeen patients (8%) were lost to follow up. Among 194patients who completed follow up, clinical stroke/TIA occurred in 15 (7.7%) patients. SBI on MRI was associated with a higher risk of clinical stroke/TIA on follow up on multivariate analysis (OR 3.7 95%CI1.26-10.9, p=0.018). Conclusions: Silent brain infarction is present in a significant minority of patients with MS and is predictive of clinical stroke/TIA on follow up.

Incompleteness of circle of Willis and silent brain infarction in patients with internal carotid artery stenosis

PurposeTo investigate the association between the prevalence of silent brain infarction (SBI) and incompleteness of circle of Willis (CoW) in patients with internal carotid artery stenosis (ICA). MethodsWe included patients with unilateral intra- or extracranial ICA stenosis ≥ 50% or occlusion without previous history of stroke or transient ischemic attack. SBIs were evaluated on magnetic resonance image. We compared SBI prevalence between patients with complete and incomplete CoW, and between ipsilateral and contralateral hemispheres to stenosed ICA. ResultsWe included 257 patients with ICA stenosis, among them 120 patients had complete CoW and 137 patients had incomplete CoW. SBI prevalence was significantly higher in patients with incomplete CoW than those with complete CoW (73.0% vs 43.3%, OR 3.09, 95% CI 1.70–5.63). Further, in patients with incomplete CoW, SBIs prevalence was significantly higher in ipsilateral hemisphere than that in contralateral hemisphere (63.5% vs 46.7%, OR = 2.01, 95% CI 1.21–3.34). While, in patients with complete CoW, SBI prevalence was not significantly different between two hemispheres (31.7% vs 23.3%, OR = 1.51, 95% CI 0.83–2.73). ConclusionIn patients with ICA stenosis, SBI prevalence was associated with incompleteness of CoW.

Prevalence and Risk Factors of Silent Brain Infarction in Patients with Aortic Stenosis

Introduction: Silent brain infarction (SBI) is an independent risk factor for subsequent symptomatic stroke in the general population. Although aortic stenosis (AS) is also known to be associated with an increased risk of future symptomatic stroke, little is known regarding the prevalence and risk factors for SBI in patients with AS. Methods: The study population comprised 83 patients with severe AS with no history of stroke or transient ischemic attack and paralysis or sensory impairment (mean age 75 ± 7 years). All patients underwent brain magnetic resonance imaging to screen for SBI and multidetector-row computed tomography to quantify the aortic valve calcification (AVC) volume. Comprehensive transthoracic and transesophageal echocardiography were performed to evaluate left atrial (LA) abnormalities, such as LA enlargement, spontaneous echo contrast, or abnormal LA appendage emptying velocity (<20 cm/s), and complex plaques in the aortic arch. Results: SBI was detected in 38 patients (46%). Multiple logistic regression analysis indicated that CHA₂DS₂-VASc score and estimated glomerular filtration rate (eGFR) were independently associated with SBI (p < 0.05), whereas LA abnormalities and AVC volume were not. When patients were divided into 4 groups according to CHA₂DS₂-VASc score and eGFR, the group with a higher CHA₂DS₂-VASc score (≥4) and a lower eGFR (<60 mL/min/1.73 m²) had a greater risk of SBI than the other groups (p < 0.05). Conclusion: These findings indicate that AS is associated with a high prevalence of SBI, and that the CHA₂DS₂-VASc score and eGFR are useful for risk stratification.

High triglyceride-glucose index is associated with subclinical cerebral small vessel disease in a healthy population: a cross-sectional study

BackgroundThe triglyceride-glucose (TyG) index is a marker of insulin resistance (IR) and has been associated with various metabolic syndromes, cardiovascular diseases, and cerebrovascular diseases. However, limited information is available regarding its association with subclinical cerebral small vessel disease (cSVD). In this study, we evaluated the relationship between the TyG index and cSVD, including silent brain infarcts (SBIs) and white matter hyperintensity (WMH).MethodsWe assessed health check-up participants aged 40–79 years from 2006 to 2013. The TyG index was calculated using the log scale of fasting triglyceride (mg/dL) × fasting glucose (mg/dL)/2. The Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was also calculated. This was compared with two insulin surrogates and cSVD as another IR indicator and compared the association between two insulin surrogates and cSVD. SBI was measured for both prevalence and burden. The WMH volume was quantitatively rated using a computer-assisted semi-automated technique.ResultsA total of 2615 participants were evaluated (median age: 56 years, male sex: 53%). In the multivariable logistic regression analysis, the TyG index was seen to be associated with SBI prevalence (adjusted odds ratio: 1.39; 95% confidence interval [CI] = 1.06–1.81). Further quantitative analyses showed a positive dose–response relationship between the TyG index and SBI burden (P for trend = 0.006). In multivariable linear regression analysis, the TyG index was also found to be related to the volume of WMH (β = 0.084; 95% CI = 0.013 to 0.154). Additionally, the TyG index showed a similar or slightly stronger association with the prevalence of SBI and the volume of WMH than did HOMA-IR.ConclusionsA high TyG index was associated with a higher prevalence and burden of cSVD in a neurologically healthy population. This marker of IR could be a convenient and useful predictor of cSVD.

Association between KCNQ2, TCF4 and RGS18 polymorphisms and silent brain infarction based on whole‑exome sequencing.

Silent brain infarction (SBI) is a cerebral infarction identified through brain imaging. In particular, studies have shown that the presence of SBI in elderly patients increases their risk of cognitive dysfunction, impairment and dementia. However, little research has been published on the relevance of SBI to these risks for the Korean population. The association between potassium voltage‑gated channel subfamilyQ member2 (KCNQ2), transcription factor4 (TCF4) and regulator of G‑protein signaling18 (RGS18) genotypes and SBI were investigated using whole‑exome sequencing and PCR restriction fragment length polymorphism (RFLP) analysis. The study population included 407patients with SBI (171males) and 401control subjects (172males). Genotyping was performed using PCR RFLP. Interestingly, TCF4 rs9957668T>C polymorphisms were associated with SBI prevalence [TTvs.CC: adjusted odds ratio(AOR), 1.815, 95% confidence intervals (CI), 1.202‑2.740; TT vs. TC+CC: AOR,1.492, 95%CI,1.066‑2.088; TT+TCvs.CC:AOR,1.454, 95%CI,1.045‑2.203]. The combination of KCNQ2 rs73146513A>G and TCF4 rs9957668T>C genotypes was associated with increasing SBI prevalence (AG/CC: AOR,3.719, 95%CI,1.766‑7.833; AA/CC: AOR,3.201, 95%CI,1.387‑7.387). The present study showed that TCF4 rs9957668T>C polymorphisms may be risk factors for SBI. Therefore, the TCF4 rs9957668T>C polymorphism may serve as a biomarker for increased risk of SBI in the Korean population.

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 &lt; 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

BackgroundTriglycerides (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.MethodsWe 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.ResultsOf 3172 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).ConclusionsThe TG/HDL cholesterol ratio was positively associated with the prevalence of SBI in a neurologically healthy population.

Obesity without metabolic disorder and silent brain infarcts in aneurologically healthy population.

Obesity without metabolic disorder [Ob(+)MD(-)] is a unique subcategory of obesity where individuals are protected from the obesity-related complications. Although conflicting clinical outcomes have been reported, there has been no study of the effects of Ob(+)MD(-) on cerebrovascular disease. In this study, we evaluated the association between the Ob(+)MD(-) phenotype and silent brain infarcts (SBI) in a neurologically healthy population. We evaluated a consecutive series of healthy volunteers recruited between January 2006 and December 2013. MD(-) status was assessed using five clinical markers: blood pressure, triglycerides, high-density lipoprotein, fasting plasma glucose, and waist circumference. Obesity was defined when body mass index ≥ 25 kg/m2. SBI was defined as asymptomatic, well-defined lesions with a diameter ≥ 3 mm with the same signal characteristics as the cerebrospinal fluid on T1- or T2-weighted images. A total of 3165 subjects were assessed, and 262 (8%) SBI cases were identified. In multivariate analyses, non-obesity with metabolic disorder [Ob(-)MD(+)] (adjusted odds ratio [aOR] = 1.65, 95% confidence interval [CI] = 1.07-2.56, P = 0.025) and obesity with metabolic disorder [Ob(+)MD(+)] (aOR = 1.75, 95% CI = 1.12-2.75, P = 0.014) were closely associated with SBI after adjustment for confounders. Meanwhile, Ob(+)MD(-) did not show any significant association with SBI (aOR = 0.85, 95% CI = 0.20-3.72, P = 0.832). These findings may indicate that metabolic abnormality, irrespective of obesity status, is a main risk factor of SBI. When we compared SBI burdens between the four metabolic phenotypes, the Ob(+)MD(+) and Ob(-)MD(+) groups had higher rates of multiple lesions than the Ob(+)MD(-) and non-obesity without metabolic disorder groups. The presence of metabolic abnormality, and not obesity per se, is independently associated with the prevalence of SBI in a healthy population.

Parity As a Protective Biomarker Against Silent Brain Infarction in Community-Dwelling Older Adults: The Sefuri Study

Background: Although several studies have reported an association between parity and increased risk of stroke, this relationship remains controversial. Aims: The present study aimed to determine whether parity is associated with silent brain infarction (SBI), independent of other confounders. Methods: We analyzed the brain magnetic resonance imaging findings in 576 of community-dwelling older adults with a mean age of 72.1 years. All female participants were asked to provide information regarding the total number of live births, their age at the last parity, and their age at menopause. Results: The prevalence of SBI and the number of infarcts per participant were higher in men than in women. Although all women who had given birth (0, 1-2, 3-4, or 5+ times) exhibited lower age-adjusted odds ratios (ORs) for SBI than men, a significant difference was observed between women with ≧5 births and men after adjustment for common vascular risk factors (OR: .348, 95% confidence interval [95% CI]: .123-.986). Among women who had given birth, the relationship between fertility and SBI was attenuated, but was enhanced after adjustment for age at the last parity (OR: .300, 95% CI: .102-.886). Conclusions: Our findings indicate that fertile women may be protected against SBI or cerebral small vessel disease via the biological effects associated with reproductive activity, and that high fertility may be a marker of protection against SBI. However, late childbearing may blunt protective effects of fertility against SBI.

Study on the incidence and risk factor of silent cerebrovascular disease in young adults with first-ever stroke.

Silent cerebrovascular diseases, including silent brain infarcts (SBI), white matter hyperintensity (WMH), and cerebral microbleed, are closely correlated with stroke progression. The purpose of this study was to investigate the prevalence and potential risk factors of SBI and WMH in young patients with first-ever stroke.A total of 400 young patients with first-ever stroke were included in this study and received magnetic resonance imaging test. The distributions of stroke subtypes were analyzed based on patients’ age and gender. The prevalence of SBI and WMH was evaluated in different age groups and stroke subtypes. Independent risk factors for SBI and WMH were identified using logistic regression analysis.The distribution of stroke subtypes was not correlated with patients’ age or gender in our study. The incidence of SBI and WMH among all of the young stroke patients was 14.50% and 8.75%, respectively, which showed an upward tendency with age. The percentages of both SBI and WMH were significantly higher in small-vessel disease patients than in cases with other subtype diseases (all P < .05). Hypertension (odds ratio [OR] = 2.645, 95% confidence interval [CI] = 1.429–4.896, P = .002 for SBI; OR = 5.474, 95% CI = 2.319–12.921, P = .000 for WMH; OR = 39.988, 95% CI = 3.988–400.949, P = .002 for SBI and WMH) and homocysteine (OR = 4.033, 95% CI = 2.191–7.425, P = .000 for SBI; OR = 5.989, 95% CI = 2.637–13.602, P = .000 for WMH; OR = 4.068, 95% CI = 1.207–13.715, P = .024 for SBI and WMH) might be potential risk factors for SBI and WMH.The prevalence of silent cerebrovascular disease was elevated with age. Hypertension and elevated homocysteine levels were 2 risk factors for silent cerebrovascular disease in young stroke patients.

Pulmonary Arteriovenous Malformations Are Associated with Silent Brain Infarcts in Hereditary Hemorrhagic Telangiectasia Patients

Background and Purpose: There is a high prevalence of right-to-left shunting pulmonary arteriovenous malformations (PAVMs), which are stroke risk factors, in hereditary hemorrhagic telangiectasia (HHT) patients. While the prevalence of ischemic complications in HHT patients is known, the prevalence of silent brain infarcts (SBI) remains unknown. The purpose of this study was to determine the prevalence and risk factors for SBI in HHT patients. Materials and Methods: Our institutional HHT database was queried to identify HHT patients who received a baseline screening brain MRI from January 2000 to February 2017. This study group was further refined by excluding patients who had a history of clinical ischemic disease as defined by having a stroke or transient ischemic attack (TIA). Brain MRIs were reviewed for SBI. Baseline data on demographics, Curacao criteria, presence of PAVMs, and cardiovascular risk factors were collected. The primary outcome was SBI prevalence. We also examined which baseline patient characteristics were associated with SBI through univariate chi-square and Student t tests and multivariate logistic regression analyses. Results: Three hundred fifty three consecutive HHT patients from January 2000 to February 2017 with a screening brain MRI and no prior history of stroke/TIA were included. SBI prevalence was 9.9% (35/353). SBI patients were more likely to have PAVMs than non-SBI patients (80.6 vs. 53.1%, p = 0.005). The median age was 66 in the SBI group and 52 in the non-SBI group (p = 0.006). SBI patients had higher prevalence of hyperlipidemia (34.3 vs. 9.8%, p < 0.0001), hypertension (48.6 vs. 22.0%, p = 0.005), and tobacco use (25.7 vs. 9.8%, p = 0.005). No patients under 30 had SBI. In the 60-69 age group, the prevalence of SBI was 18.8% with rates of 28.6% in the PAVM group and 10.5% in the non-PAVM group. For patients ≥70 years old, the prevalence of SBI was 21.4% overall and 27.6% in the PAVM group and 10.5% in the non-PAVM group. On multivariate analysis, PAVMs (OR 3.62, 95% CI 1.46-10.40) and increasing age (OR 1.04, 95% CI 1.01-1.07) were independently associated with SBI. Conclusions: Overall, a similar 10% SBI prevalence in the HHT cohort was noted as compared to the general population. However, the prevalence of SBI was higher in HHT patients with PAVMs when compared to that of the general population, particularly among patients than 60 years old. These findings highlight the need to accurately identify, and when appropriate, treat PAVMs in the HHT population especially given the multiple significant, clinical consequences of SBI.

The Association between Carotid Artery Atherosclerosis and Silent Brain Infarction: A Systematic Review and Meta-analysis

Carotid atherosclerosis is responsible for ~20% of ischemic strokes, but it is unclear whether carotid disease is associated with the presence of downstream silent brain infarction (SBI). We performed a systematic review and meta-analysis to study the relationship between SBI and 2 separate manifestations of carotid atherosclerosis, carotid intima-media thickening (IMT) and luminal stenosis. Ovid MEDLINE, Ovid Embase, and the Cochrane Library Database were searched with an additional search of references and citing articles of target studies. Articles were included if they reported an association between carotid IMT or stenosis and magnetic resonance imaging-defined SBI, excluding SBIs found after carotid intervention. We pooled 7 studies of carotid IMT reporting on 1469 subjects with SBI and 5102 subjects without SBI. Subjects with SBI had a larger mean IMT than subjects without SBI (pooled standardized mean difference, .37; 95% confidence interval [CI], .23-.51; P < .0001). We pooled 11 studies of carotid stenosis reporting on 12,347 subjects (2110 subjects with carotid stenosis and 10,237 subjects without carotid stenosis). We found a higher prevalence of SBI among subjects with carotid stenosis (30.4% versus 17.4%). Our pooled random-effects analysis showed a significant positive relationship between carotid stenosis and SBI (odds ratio, 2.78; 95% CI, 2.19-3.52; P < .0001). Two forms of atherosclerotic disease, carotid IMT and stenosis, are both significantly associated with SBI. This review highlights a lack of consistent definitions for carotid disease measures and little evidence evaluating SBI prevalence downstream from carotid stenosis.

Evaluation by Magnetic Resonance Imaging of Silent Brain Infarcts in Preoperative and Postoperative Asymptomatic Carotid Surgery

To report the prevalence of silent brain infarcts (SBI) at magnetic resonance imaging (MRI) before and after surgery for asymptomatic high grade carotid stenosis. This is a single center retrospective observational study. Asymptomatic patients who underwent carotid endarterectomy between October 2012 and October 2014 were included. The preoperative assessment included a Doppler and a computed tomographic (CT) scan dating less than 3months. A neurological examination was performed during the anesthesia consultation and in the 15days before surgery. An MRI angiography was performed the day before and 3 days after surgery and was analyzed by an independent neuroradiologist. Preoperative analysis focused on the presence of ischemic events at MRI. The type of plaque, the supra aortic trunk lesions, and the quality of the circle of Willis were analyzed using Doppler and CT scanning. Postoperatively, we searched for signs of postoperative ischemic events at MRI. Forty-one patients were included (85.4% of men), and the mean age was 72.4±8.3years. We noted 7 (17.1%) contralateral stenoses (>50%) and 2 (4.9%) contralateral thromboses, 6 (14.6%) vertebral stenoses, and 7 (17.1%) abnormalities of the circle of Willis. The morphological analysis described 6 unstable plaques including 4 ulcerated, 1 pseudodissection, and 1 intraplaque hemorrhage. Preoperatively, we noted the presence of 21 (51.2%) ischemic lesions including 9 (21.9%) multiple lacunar ischemic events and 12 (29.3%) silent arterial territory infarcts. Eversion was performed for all patients except for 6 (14.6%), for whom a bypass was necessary. No deaths or major complications were observed in the 30 postoperative days. Postoperatively, MRI showed 3 (7.3%) asymptomatic recent ischemic strokes, 1 ipsilateral middle cerebral artery (MCA) stroke, and 2 contralateral (cerebellar and MCA) strokes. Patients with asymptomatic significant carotid stenosis show many preoperative SBI indicating a significant embolic risk. It is difficult to conclude about intraoperative embolic risk, but we hope that more data could demonstrate the importance of MRI for the preoperative evaluation of carotid plaques and brain parenchyma, to identify high-risk embolic patients.

Silent Brain Infarction in Patients With Asymptomatic Carotid Artery Atherosclerotic Disease

There is a higher prevalence of silent brain infarction (SBI) downstream from internal carotid artery atherosclerotic lesions compared to the contralateral side. This applies only to the cortical infarction and not the lacunar SBI infarcts.

Silent Brain Infarction in Patients With Asymptomatic Carotid Artery Atherosclerotic Disease.

The relationship between carotid atherosclerosis and ipsilateral silent brain infarction (SBI) is unclear. We tested the hypothesis that extracranial internal carotid artery (ICA) stenosis is associated with a greater prevalence of SBI in the cerebral hemisphere ipsilateral to ICA disease compared with the unaffected, contralateral side. We identified patients with unilateral extracranial ICA stenosis ≥50% on angiography by standard imaging criteria. We included patients with recent brain magnetic resonance imaging who had no previous history of stroke or transient ischemic attack. Blinded readers ascertained the presence of anterior circulation SBIs. SBI was defined as either a cavitary lacunar infarction in the white or deep gray matter or cortical infarction defined by T2 hyperintense signal in cortical gray matter. The Wilcoxon signed-rank test was used to compare SBI in the cerebral hemispheres and Cohen κ to assess inter-rater reliability of SBI evaluation. Among 104 patients, we found a higher prevalence of SBIs ipsilateral to ICA disease (33%) compared with the contralateral side (20.8%; P=0.0067). There was no significant difference in the prevalence of lacunar SBIs (including both white and deep gray matter) between hemispheres (P=0.109), but there was a significantly higher prevalence of cortical SBIs occurring downstream from ICA disease (P=0.0045). High inter-rater reliability was observed (κ=0.818). Patients with asymptomatic ICA disease demonstrate a higher prevalence of SBI downstream from their ICA atherosclerotic disease compared with the contralateral side but only of the cortical and not lacunar SBI subtype.

Abstract 14839: Association of Silent Brain Infarction With CHADS2 Score and Left Atrial Abnormalities in Patients With Nonvalvular Atrial Fibrillation

Introduction: The CHADS2 score is widely used for risk stratification of thromboembolism in patients with nonvalvular atrial fibrillation (NVAF). Furthermore, LA abnormalities detected by transesophageal echocardiography (TEE) are also well known risk factors for thromboembolism in NVAF patients. On the other hand, silent brain infarction (SBI) relates to subsequent symptomatic brain infarction; however little is known regarding association among CHADS2 score, TEE parameters and SBI. Methods: The study population consisted of 103 neurologically asymptomatic patients with NVAF (mean age 63 ± 10 years) who underwent TEE. All participating patients underwent brain MRI and were calculated CHADS2 score. SBI was defined as an area of hypointense lesions that measured &gt;3 mm on T1-weighted images and hyperintense lesions on T2-weighted images by brain magnetic resonance imaging (MRI). LA abnormalities were defined as LA thrombus, spontaneous echo contrast, or low LA appendage emptying velocity (&lt;20 cm/s) detected by TEE. Results: Of 103 patients, 31 (30%) showed SBI on brain MRI. Over all mean CHADS2 score was 1.1 ± 0.9, and LA abnormalities were detected in 24 patients by TEE (23%). Mean CHADS2 score in patients with SBI was significantly higher than that in patients without SBI (P&lt;0.05). The prevalence of SBI increased along with increases in CHADS2 score (CHADS2 score of 0, 1, 2 and 3-6 in 13%, 23%, 47% and 80%, respectively, P&lt;0.05). Patients with SBI had a higher prevalence of LA abnormalities than those without SBI (P&lt;0.05). In patients with SBI with CHADS2 score of 0-1, LA abnormalities were detected in 5 of 14 patients (36%). Conclusions: In this study, both CHADS2 score and prevalence of LA abnormalities by TEE were higher in patients with SBI on MRI. LA abnormalities detected by TEE may discriminate risk for SBI even in patients with low CHADS2 score.

Emerging Spectra of Silent Brain Infarction

Silent brain infarction (SBI) is an increasingly recognized, and yet still poorly understood, clinical disorder characterized by the often incidental finding of cerebral infarction on imaging in the absence of clinically apparent neurological deficit. Although first described ≈50 years ago by Fisher1 through autopsy studies, it was not until the development of more sensitive imaging modalities that their characterization has been possible. Of the epidemiological literature available on SBI, the most credible and generalizable data come from representative community samples, from which the general population prevalence of SBI has been estimated as 10% to 20%, with longitudinal studies suggesting a yearly incidence of 3% to 4%.2 However, this climbs as high as 55% in clinical-based studies of otherwise healthy patients3 and is higher than 90% in certain disease-specific populations.4 Despite such a high prevalence, mounting evidence suggests that SBI is not a silent event at all but is associated with subtle neurological deficits, neurocognitive dysfunction, psychiatric disorders, an increased incidence of overt stroke, and early mortality. In light of these associations, it has been proposed that the designation silent be replaced with the term covert.5 The principle objective of this article is to review the current body of published medical research critically to (1) define SBI and highlight problems inherent in that definition; (2) examine the risk factors, incidence and prevalence of SBI; (3) assess theories on the underlying pathogenesis of SBI; and (4) discuss the clinical consequences of these lesions. ### What Constitutes a SBI? There is no universally accepted definition of SBI, which hampers attempts to characterize and investigate these lesions fully. In general, SBI has been described as cerebral infarcts that are observed on either computed tomographic or MRI scans in the absence of any corresponding, clinically apparent cerebrovascular ischemic event.6 ### Problems in the Detection and Diagnosis of SBIs The rigor with which corresponding …