ObjectiveThis study aims to determine whether the risks of cardiocerebrovascular disease are relevant to sensorineural hearing loss (SNHL) based on a national database.MethodsA total of 1,321 participants aged from 18 to 69 with complete data including medical history and audiometry from the NHANES database (2015–2018) were analyzed. All included participants had available hearing data and the average thresholds of the hearing data were measured and calculated as low-frequency pure-tone average (LFPTA; 500, 1,000, and 2,000 Hz) and high-frequency pure-tone average (HFPTA; 3,000, 4,000, 6,000, and 8,000 kHz). SNHL was defined as an average pure tone of more than or equal to 20 dB in at least one better ear. Multivariable models to assess the association between cardiocerebrovascular risks and SNHL were used in this study.ResultsThe prevalence of stroke was 1.6% in individuals with SNHL and 0.4% in individuals without SNHL (p = 0.023). A higher cardiovascular risk score was observed in SNHL patients compared to participants without SNHL (1.58 vs. 0.90, p < 0.001). Stroke was associated with a 3.67-fold increase in the risk of SNHL (95% CI: 1.12–12.00, p = 0.032) in univariable logistic regression, and the association (OR = 4.22, 95%CI = 1.28–13.93, p = 0.020) remained significant after adjusting for several covariates. Multivariable logistic regression models indicated a positive correlation between cardiovascular risk and SNHL (OR = 1.66, 95% CI = 1.40–1.96, p < 0.001), but no significant relationship was shown with all covariates adjusted. However, significant associations were found between SNHL and both age and sex in both univariable and multivariable logistic regression models.ConclusionOur findings suggested that a higher cardiocerebrovascular risk burden was associated with an increased risk of SNHL, and the relationship may be influenced by age and sex. Future longitudinal studies are needed to investigate the mechanistic and pathologic vascular hypothesis of SNHL.

Background:Despite previously reported correlations between intracranial arterial calcification (IAC) and white matter hyperintensities (WMH), little is known about the relationship between IAC pattern and WMH. By differentiating intimal and medical IAC, we aimed to investigate the relationship between IAC pattern and WMH. <break><break>Methods:Consecutive patients with acute ischemic stroke were included. IAC pattern was categorized as intimal or medial on plain brain CT. The number of cerebral arteries involved by IAC for each patient was recorded. IAC severity of each artery was defined as focal or diffuse. On brain MRI, the burden of WMH was graded on a visual rating scale and classified as absent mild, moderate and severe. Multiple logistic regression was performed to examine the relationship between IAC and WMH. <break><break>Results:Among 265 recruited patients, intimal IAC was detected in 54.7% patients, medial IAC in 48.5% patients and coexistent (intimal and medial) IAC in 52.1% patients. Diffuse IAC was in 27.9% patients, all of which were medial IACs. WMH was found in 75.5% patients, including 105 patients (39.6%) with mild WMH, 69 (26.0%) with moderate WMH and 26 (9.8%) with severe WMH. The presence and severity of medial IAC were correlated with WMH occurrence (p<0.001, respectively). Chi-square linear trend suggested the number of arteries involved by medial IAC (p<0.001) and the severity of medial IAC (p<0.001) were correlated with WMH burden. After adjusting age, hypertension, history of stroke and history of ischemic heart disease, multiple ordinal regression demonstrated a positive correlation between the number of arteries involved by medial IAC (p<0.001) and the severity of medial IAC (p<0.001) with the overall burden of WMH. <break><break>Conclusions:Medial IAC was correlated with the burden of WMH. The dose-effect relationship between IAC and WMH suggests the need of further investigations on shared underlying mechanisms of intracranial large artery disease and cerebral small vessel disease.

Objective Intracranial arterial calcification (IAC) is a risk factor of ischemic stroke. However, the relationship between IAC patterns and clinical outcome of ischemic stroke remains controversial. We aimed to investigate the correlation between IAC patterns and the effects of reperfusion therapy among acute stroke patients. Methods Consecutive acute ischemic stroke patients who underwent reperfusion therapy were included. IAC was categorized as intimal or medial. Based on its involvement, IAC was further classified as diffuse or focal. Neurologic dysfunction was assessed by the National Institute of Health stroke scale (NIHSS). Clinical outcome including favorable neurologic outcome (FNO) and early neurologic deterioration (END) were assessed. Results Of 130 patients, 117 had IAC. Intimal IAC was identified in 74.6% of patients and medial IAC was present in 64.6% of patients. Diffuse IAC was present in 31.5% of patients. All diffuse IACs were medial pattern. Diffuse IAC was associated with higher baseline NIHSS (p = 0.011) and less FNO (p = 0.047). Compared with patients with focal or single diffuse IAC, patients with multiple diffuse IAC had higher baseline NIHSS (p = 0.002) and less FNO (p = 0.024). Multivariable linear regression (p < 0.001) and logistic regression (p = 0.027) suggested that multiple diffuse IAC was associated with higher baseline NIHSS and less FNO. No significant association was found between END and different IAC patterns. Interpretation Multiple diffuse medial IAC may predict severer neurologic dysfunction and less favorable neurologic outcome after reperfusion therapy in acute stroke patients.

Background and purpose: Intracranial arterial calcification (IAC) has been found as a risk factor of ischemic stroke. However, the relationship between IAC patterns (intimal or medial) and clinical outcome of ischemic stroke remains controversial. We aimed to investigate the correlation between IAC patterns and the effects of reperfusion therapy among acute stroke patients. Methods: Consecutive acute ischemic stroke patients who underwent reperfusion therapy were included. IAC was categorized as intimal or medial. Based on its involvement in arteries, IAC was further classified as diffuse or focal. Neurologic dysfunction before and after therapy was assessed by the National Institute of Health stroke scale (NIHSS). Clinical outcome including favorable neurologic outcome (FNO) and early neurologic deterioration (END) were assessed within 10 days after reperfusion therapy. Results: Of 130 patients, 117 had IAC. Intimal IAC was identified in 74.6% patients and medial IAC was present in 64.6% patients. Diffuse IAC was present in 31.5% patients. All diffuse IACs were medial pattern. Diffuse IAC was associated with higher baseline NIHSS (p=0.011) and less FNO (p=0.047). Compared with patients with focal or single diffuse IAC, patients with multiple diffuse IAC had higher baseline NIHSS (p=0.002) and less FNO (p=0.024). Multivariable linear regression (p<0.001) and logistic regression (p=0.027) suggested that multiple diffuse IAC was associated with higher baseline NIHSS and less FNO. No significant association was found between END and different IAC patterns. Conclusions: Multiple diffuse medial IAC may predict severer neurologic dysfunction and a less favorable neurologic outcome after reperfusion therapy in acute stroke patients.