Effect of the Blood Pressure and Antihypertensive Drugs on Cerebral Small Vessel Disease: A Mendelian Randomization Study.

BACKGROUND: Previous studies yielded conflicting results about the influence of blood pressure (BP) and antihypertensive treatment on cerebral small vessel disease. Here, we conducted a Mendelian randomization study to investigate the effect of BP and antihypertensive drugs on cerebral small vessel disease. METHODS: We extracted single-nucleotide polymorphisms for systolic BP and diastolic BP from a genome-wide association study (N=757 601) and screened single-nucleotide polymorphisms associated with calcium channel blockers, thiazides, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and ß-blockers from public resources as instrumental variables. Then, we chose the genome-wide association study of white matter hyperintensity (WMH; N=18 381), cerebral microbleed (3556 cases, 22 306 controls), white matter perivascular space (9317 cases, 29 281 controls), basal ganglia perivascular space (BGPVS; 8950 cases, 29 953 controls), hippocampal perivascular space (HIPPVS; 9163 cases, 29 708 controls), and lacunar stroke (6030 cases, 248 929 controls) as outcome data sets. Subsequently, we conducted a 2-sample Mendelian randomization analysis. RESULTS: We found that elevated systolic BP significantly increases the risk of BGPVS (odds ratio [OR], 1.05 [95% CI, 1.04-1.07]; P=1.72×10-12), HIPPVS (OR, 1.04 [95% CI, 1.02-1.05]; P=2.71×10-7), and lacunar stroke (OR, 1.41 [95% CI, 1.30-1.54]; P=4.97×10-15). There was suggestive evidence indicating that elevated systolic BP is associated with higher WMH volume (ß=0.061 [95% CI, 0.018-0.105]; P=5.58×10-3) and leads to an increased risk of cerebral microbleed (OR, 1.16 [95% CI, 1.04-1.29]; P=7.17×10-3). Elevated diastolic BP was significantly associated with higher WMH volume (ß=0.087 [95% CI, 0.049-0.124]; P=5.23×10-6) and significantly increased the risk of BGPVS (OR, 1.05 [95% CI, 1.04-1.06]; P=1.20×10-16), HIPPVS (OR, 1.03 [95% CI, 1.02-1.04]; P=2.96×10-6), and lacunar stroke (OR, 1.31 [95% CI, 1.21-1.41]; P=2.67×10-12). The use of calcium channel blocker to lower BP was significantly associated with lower WMH volume (ß=-0.287 [95% CI, -0.408 to -0.165]; P=4.05×10-6) and significantly reduced the risk of BGPVS (OR, 0.85 [95% CI, 0.81-0.89]; P=8.41×10-19) and HIPPVS (OR, 0.88 [95% CI, 0.85-0.92]; P=6.72×10-9). CONCLUSIONS: Our findings contribute to a better understanding of the pathogenesis of cerebral small vessel disease. Additionally, the utilization of calcium channel blockers to decrease BP can effectively reduce the likelihood of WMH, BGPVS, and HIPPVS. These findings offer valuable insights for the management and prevention of cerebral small vessel disease.

Adiposity and Functional Outcome After Ischemic Stroke: A Mendelian Randomization Study

BACKGROUND AND OBJECTIVES: To investigate the causal relationships of abdominal adiposity (waist-to-hip ratio [WHR]) and overall adiposity (body mass index [BMI]) with functional outcome after ischemic stroke using Mendelian randomization. METHODS: Genetic instruments for WHR and BMI were obtained from the largest available genome-wide association studies meta-analysis of the Genetic Investigation of ANthropometric Traits consortium and the UK Biobank (N max = 806,834). Functional outcome after ischemic stroke was assessed using the modified Rankin Scale (mRS) score at 3-month after stroke onset, with mRS >2 (mRS 3-6) defined as an unfavorable functional outcome. Corresponding genetic estimates for an unfavorable functional outcome were extracted from the Genetics of Ischemic Stroke Functional Outcome network (N = 6,021). We applied a random-effects inverse variance weighted method as our main analysis. RESULTS: Genetically predicted higher WHR (per 0.09 ratio units) was associated with unfavorable functional outcome after ischemic stroke (mRS 3-6, OR = 1.48; 95% CI = 1.03-2.13; p = 0.033). The results remained directionally consistent in sensitivity analyses. Conversely, genetically predicted BMI (per 4.8 kg/m2) was not associated with unfavorable functional outcome after ischemic stroke (OR = 1.01; 95% CI = 0.75-1.36; p = 0.937). DISCUSSION: This study provides genetic evidence supporting the hypothesis that abdominal adiposity has a detrimental effect on functional recovery after ischemic stroke.

Telomere length and multiple sclerosis: a Mendelian randomization study.

PURPOSE OF THE STUDY: Previous studies have established that telomere length is associated with multiple sclerosis (MS). However, confounding factors and reverse causality bias can impair observational research. Here, we conducted a two-sample MR study to see if telomere length is causally linked to MS using publically available GWAS summary statistics. MATERIALS AND METHODS: We screened 13 independent single-nucleotide polymorphisms (SNPs) related to leukocyte telomere length in a recent genome-wide association meta-analysis, which was available for 78,592 samples of European ancestry. The summary statistics for MS were from the latest meta-analyses conducted by the International Multiple Sclerosis Genetics Consortium (IMSGC), which included 115,803 European participants (47,429 MS, 68,374 controls). RESULTS: We found that leukocyte telomere length and MS are correlated (IVW estimate of odds ratio (OR): 2.13 per 1-SD increase in genetically determined telomere length, 95% confidence interval (CI): 1.55-2.92, p = 3.18 × 10-6). CONCLUSION: Our MR study supported that leukocyte telomere length and MS have a positive causal relationship. Further researches are warranted to elucidate the physiological mechanism.

The negative affectivity dimension of Type D personality associated with increased risk for acute ischemic stroke and white matter hyperintensity.

OBJECTIVE: This study was conducted to examine the relationship among type D personality, acute ischemic stroke (AIS), and white matter hyperintensity (WMH). METHODS: In a cross-sectional study conducted between September 2020 and June 2021, 235 patients aged 50-85 years with first-ever ischemic cerebrovascular disease, including 146 males and 89 females, were enrolled. All participants underwent the Type D Scale-14 test containing negative affectivity (NA) and social inhibition (SI) subscales. Clinical and laboratory data were also collected for analysis. The patients were divided into the AIS group (n = 148) and the transient ischemic attack (TIA) group (n = 87) according to whether there was an acute lesion. RESULTS: Patients with type D personality had a higher frequency of AIS and LAA and a higher level of WMH. Multiple logistic regression showed that the NA score was related to a 1.11-fold increase in the odds of AIS (95% CI: 1.03-1.19). Neither NA nor SI showed a clear association with a higher frequency of LAA. Higher scores of NA (OR = 1.07, 95% CI: 1.01-1.15), SI (OR = 1.11, 95% CI: 1.03-1.19), and the interaction between the two dimensions (OR = 1.03, 95% CI: 1.01-1.05) were independently associated with an increased load of WMH. CONCLUSION: Type D personality was related to AIS and WMH. In particular, it was NA, not SI, affected the occurrence of AIS. Our findings may provide new insights regarding behavioral vulnerability for the development of cerebrovascular disorders.

Smoking, alcohol consumption, and age at onset of Huntington's disease: a Mendelian randomization study.

BACKGROUND: Smoking and alcohol consumption have been associated with earlier age at onset (AAO) of Huntington's disease (HD) in observational studies. We conducted this Mendelian randomization (MR) study to evaluate whether these associations are causal. METHODS: We selected genetic instruments for lifetime smoking (n = 462,690) and alcohol consumption (n = 941,280) based on two large genome-wide association studies (GWAS). The summary-level data for residual AAO of HD were derived from a GWAS meta-analysis carried out by the Genetic Modifiers of Huntington's disease Consortium (n = 9,064 HD patients). We conducted univariable and multivariable MR analyses to evaluate the independent impact of smoking and alcohol consumption on AAO of HD. RESULTS: Genetically predicted lifetime smoking was causally related to an earlier AAO of HD in the univariable MR analyses (ß = -2.16 years per standard deviation (SD) increase in lifetime smoking index, 95% confidence interval (CI) = -3.70 to -0.63, P = 0.006). This association persisted significant in the multivariable MR analyses after adjusting for alcohol consumption (ß = -2.04 years per SD increase in lifetime smoking index, 95% CI = -3.85 to -0.22, P = 0.028). However, no significant association was found between alcohol consumption and AAO of HD. CONCLUSIONS: This study suggests that genetically predicted smoking is causally related to an earlier AAO of HD.

Correlation between neutrophil-to-lymphocyte ratio and stability of carotid plaques.

OBJECTIVE: The neutrophil-to-lymphocyte ratio (NLR) has been proved to be a strong predictor of carotid atherosclerotic plaque, but the correlation between NLR and the stability of carotid plaque is not clear. Thus we conducted a study to evaluate the correlation between NLR and the stability of carotid atherosclerotic plaque, and to develop a new evaluation scale for rapid clinical evaluation of carotid plaque stability. METHODS: We recruited 528 patients with acute anterior circulation ischemic stroke who were in accordance with extracranial and intracranial large artery atherosclerosis of Chinese ischemic stroke subtype. Blood routine examination and carotid ultrasound examination were performed on admission. According to the ultrasonic characteristics, the patients were divided into plaque stabilization group and plaque instability group. RESULTS: There was significant difference in NLR between plaque stability and instability groups (P < 0.001). The risk of plaque instability increased with the increase of NLR (odds ratio (OR), 4.737; 95% confidence interval (CI), 3.404-6.592; P < 0.001). Receiver operating characteristic (ROC) curve showed that the critical point of NLR is 2.55 and the area under the curve (AUC) was 0.782 (95%CI, 0.740-0.823; P < 0.001). The best cut-off value of the evaluation scale was ≥ 4 points (sensitivity, 0.77; specificity, 0.75; accuracy, 0.76). CONCLUSION: There is a correlation between NLR and carotid plaque instability. NLR may be useful as a potential inflammation biomarker indicating the risk of unstable carotid plaques. The new scoring scale is a reliable index to predict the stability of carotid plaque.

Genetic predisposition to Parkinson's disease and risk of cardio and cerebrovascular disease: a Mendelian randomization study.

BACKGROUND: Observational studies suggest that Parkinson's disease (PD) is related with the risk of cardio and cerebrovascular disease. However, the causality is not yet fully established. Therefore, we employed Mendelian randomization to assess whether PD is related to risk of ischemic stroke (IS), IS subtypes, coronary artery disease (CAD) and myocardial infarction (MI). METHODS: Eighty-eight and eleven single nucleotide polymorphisms associated with PD at the genome-wide significance level, were used as instrumental variables for PD in European and East Asian population respectively. Using a 2-sample MR, we examined associations with IS, IS related subtypes, CAD and MI in European population. We also assessed the causal association of PD with IS and CAD in East Asian population. The primary MR analyses were performed by using the random-effects inverse variance weighted approach. RESULTS: In European population, genetic predisposition to PD was related to higher risk of IS (odds ratio [OR], 1.03 per doubling in odds of PD; 95% confidence interval [CI], 1.01-1.05; P = 0.002) and cardioembolic stroke (OR, 1.08 per doubling in odds of PD; 95% CI, 1.04-1.12; P = 1.29 × 10-4), but not large artery stroke, small vessel stroke, CAD and MI. In East Asian population, we found no evidence of causal effect of PD on the risk of IS and CAD. CONCLUSIONS: This study found that genetic predisposition to PD is related to higher risk of IS and cardioembolic stroke in European population.

Mendelian randomization study of coffee consumption and age at onset of Huntington's disease.

BACKGROUND & AIM: The association between habitual coffee or caffeine consumption and age at onset (AAO) of Huntington's disease (HD) is unclear. We employed Mendelian randomization to investigate the causal relationship between coffee consumption and AAO of HD. METHODS: The instrumental variable including 14 independent genetic variants associated with coffee consumption was selected from a genome-wide association study (GWAS) meta-analysis of 375,833 individuals of European ancestry. Genetic association estimates for AAO of HD were obtained from the Genetic Modifiers of Huntington's Disease Consortium GWAS meta-analysis including 9064 HD patients of European ancestry. The inverse variance weighted method was used to evaluate the causal estimate and a comprehensive set of analyses tested the robustness of our results. RESULTS: Genetically predicted higher coffee consumption was associated with an earlier AAO of HD (ß = -1.84 years, 95% confidence interval = -3.47 to -0.22, P = 0.026). Results were robust to potential pleiotropy and weak instrument bias. CONCLUSIONS: This genetic study suggests high coffee consumption is associated with an earlier AAO of HD. Coffee is widely consumed and thus our findings, if confirmed, offers a potential way to delay the onset of this debilitating autosomal dominant disease.

Daytime sleepiness and risk of stroke: A Mendelian randomization analysis.

OBJECTIVE: Daytime sleepiness is known to be related to stroke, but whether daytime sleepiness is a risk factor for stroke remains unclear. We conducted a two-sample Mendelian randomization study to assess the relationship between daytime sleepiness and stroke, ischemic stroke (IS) and IS subtypes. METHODS: Thirty-six single-nucleotide polymorphisms (SNPs) associated with daytime sleepiness were selected as instrumental variables, which were identified from a recent genome-wide association study(N = 452,071). Summary statistics of the SNPs on stroke, IS and IS subtypes were derived from the MEGASTROKE consortium with 40,585 stroke cases and 406,111 controls. RESULTS: We found that daytime sleepiness was associated with large artery stroke (OR, 6.75; 95%CI, 1.49-30.57; p = 0.013), but not with all stroke (OR, 1.29; 95%CI, 0.81-2.05; p = 0.282), all ischemic stroke(OR, 1.46; 95%CI, 0.90-2.39; p = 0.136), cardioembolic stroke(OR, 1.0; 95%CI, 0.39-2.64; p = 0.984), or small artery stroke(OR, 1.52; 95%CI, 0.46-5.05; p = 0.485). CONCLUSION: Our findings indicated that daytime sleepiness is causally associated with an increased risk of large artery stroke. Further studies are necessary to verify our results and explain the physiological mechanisms.

Educational attainment protects against epilepsy independent of cognitive function: A Mendelian randomization study.

OBJECTIVE: Observational studies have suggested that increased levels of education and cognition are associated with a reduced risk of epilepsy. However, such associations are easily influenced by confounding or reverse causality. Hence, we conducted a two-sample univariable and multivariable Mendelian randomization (MR) to estimate the total and independent causal effects of educational attainment and cognition on epilepsy risk. METHODS: We performed MR estimates on International League Against Epilepsy (ILAE) Consortium genome-wide association study (GWAS) data (15 212 epilepsy cases and 29 677 controls). We then validated the results in FinnGen (3424 epilepsy cases and 110 963 controls) and applied meta-analysis to all the results. RESULTS: In the meta-analysis of the ILAE and FinnGen results, genetically determined increased educational attainment was associated with a reduced risk of epilepsy (odds ratio [OR] 0.84, 95% confidence interval [CI] 0.80-0.88; P < .001). Similarly, genetically determined increased cognitive function was associated with a reduced risk of epilepsy (OR 0.94, 95% CI 0.88-1.00, P = .043). When educational attainment and cognitive function were included in the same multivariable MR, only educational attainment was still associated with a reduced risk of epilepsy (OR 0.88, 95% CI 0.81-0.95, P = .002). SIGNIFICANCE: This MR study provides evidence to support that increased educational attainment can reduce the risk of developing epilepsy independent of cognitive function.

Serum Creatinine Protects Against Amyotrophic Lateral Sclerosis: a Mendelian Randomization Study.

Association between serum creatinine (sCr) and amyotrophic lateral sclerosis (ALS) has been reported in previous observational studies, but results are at risk of confounding bias and reverse causation. Therefore, whether such association is casual remains unclear. Herein, we performed a two-sample Mendelian randomization study to evaluate the causal relationship between sCr and ALS in both European and East Asian populations. Our analysis was conducted using summary statistics from genome-wide association studies with 358,072 individuals for sCr and 80,610 individuals for ALS in European population, and 142,097 individuals for sCr and 4,084 individuals for ALS in East Asian population. The inverse-variance weighted method was used to estimate the casual-effect of sCr on ALS in both populations, and other MR methods were also performed as sensitivity analyses. We found evidence that genetically predicted sCr was inversely associated with risk of ALS (OR, 0.92; 95% CI, 0.85-0.99; P = 0.028) in European population. However, there was no strong evidence for a causal relationship between sCr and ALS in East Asian population (OR, 0.92; 95% CI, 0.84-1.01; P = 0.084). This study provides evidence that sCr protects against ALS in European population but not in East Asian population.

Usability of Ultrasonic MicroPure Imaging for Evaluating the Vulnerability of Carotid Atherosclerotic Plaques.

OBJECTIVE: MicroPure is an ultrasound imaging technology used for detecting microcalcifications. This study aimed to evaluate the usefulness of the Firefly sign in ultrasonic MicroPure imaging for detecting the vulnerability of carotid plaques. METHODS: Ultrasonic grey-scale imaging was used to detect carotid plaques. Ultrasonic MicroPure imaging was used to detect the Firefly sign and to determine the location and number of Firefly signs. RESULTS: A total of 142 plaques were detected in 72 patients, and 62.0% were Firefly-positive plaques. The length or thickness, the risk of rupture and the percentage of vulnerable plaques were greater in the Firefly-positive plaques than in Firefly-negative plaques. The assessment of plaque vulnerability built on the 4-point Firefly scoring system showed that the area under the ROC curve was 0.750 (P < .001). The sensitivity and specificity of vulnerable plaques with a score of 2 points were 71.9 and 73.6%, respectively. CONCLUSION: The Firefly signs are widely present in carotid atherosclerotic plaques and can be detected with ultrasonic MicroPure imaging. Firefly signs located in fibrous caps may be associated with plaque vulnerability.

The ability of Micropure® ultrasound technique to identify microcalcifications in carotid plaques.

OBJECTIVES: To study the ability of Micropure® ultrasound technique to identify microcalcifications in carotid plaques. METHODS: Forty-four carotids in 22 patients were enrolled in this study and were detected by routine ultrasound examination and Micropure® examination at the same time to identify microcalcifications in plaques. The results were compared with the tissue-background ratio (TBR) in 18F-NaF PET-CT imaging, which was performed one or two days after the ultrasound examination. RESULTS: In the 44 carotids, plaques were detected in 37 carotids. Microcalcifications were detected by the Micropure® technique in 32 carotids, which were located surrounded by macrocalcifications in 23 carotids, in the fibre cap in 12 carotids, and in the base of the plaque in 6 carotids. Microcalcifications were not detected in 12 carotids. In 18F-NaF PET-CT examination, TBR > 1.61 (range 1.62-3.99, mean 2.25 ± 0.58) was detected in 37 carotids, and TBR < 1.61 was detected in 7 carotids. There were no significant differences between the two methods in detecting microcalcifications (p = 0.180). The sensitivity of the Micropure® technique in detecting microcalcifications was 81.08 %, and the specificity was 71.43 %. CONCLUSIONS: Microcalcifications in the carotid artery detected by the Micropure® technique were well in accordance with 18F-NaF PET-CT scanning, with better sensitivity and specificity.

Higher tea consumption is associated with decreased risk of small vessel stroke.

BACKGROUND & AIM: Observational studies have reported that tea consumption is associated with risk of stroke. However, this observed association is inconsistent, and whether this observed association is due to confounding factors or reverse causation remains unclear. Thus, we applied a two-sample mendelian randomization (MR) approach to determine whether genetically predicted tea consumption is causally associated with risk of stroke, ischemic stroke (IS), and IS subtypes. METHODS: UK Biobank available data (349,376 samples of European ancestry) was used to identify single nucleotide polymorphisms associated with tea consumption (cups/day). The summary statistics for stroke, IS, and IS subtypes were obtained from the MEGASTROKE consortium with 40,585 stroke cases and 406,111 controls. RESULTS: We found that genetically predicted an extra daily cup of tea consumption was casually associated with a reduced risk of small vessel stroke (odds ratio (OR), 0.79; 95% confidence interval (CI), 0.69-0.91; P = 0.001), but not with cardioembolic stroke (OR, 0.97; 95% CI, 0.86-1.09; P = 0.582), large artery stroke (OR, 0.95; 95% CI, 0.82-1.10; P = 0.506), stroke (OR, 1.00; 95% CI, 0.95-1.06; P = 0.889) or IS (OR, 0.95; 95% CI, 0.89-1.01; P = 0.083). CONCLUSIONS: Our study provided evidence that genetically predicted an extra daily cup of tea consumption is causally associated with a reduced risk of small vessel stroke.

The effect of an overall healthy lifestyle on early-onset stroke: a cross-sectional study.

BACKGROUND: The impact of an overall healthy lifestyle on early-onset stroke is still unclear. Our study thus aimed to investigate the association of overall healthy lifestyle on early-onset stroke in Chinese hospitalized stroke patients. METHODS: This retrospective study included 821 hospitalized stroke patients from the First People's Hospital of Changzhou. An overall healthy lifestyle was defined as the presence of more than 2 of the following items: healthy diet, no smoking, normal body mass index (BMI <24 kg/m2 ), engaging in moderate to high physical activity (≥3 times/week, and ≥30 minutes each time). Early-onset stroke was defined as a stroke first occurring at 50 years old or younger. RESULTS: Among all participants, there were 98 early-onset stroke patients and 723 late-onset stroke patients. Early-onset patients had a lower prevalence of overall healthy lifestyles than that of late-onset patients (P<0.001). Multivariate logistic regression revealed that an overall healthy lifestyle significantly reduced the risk of early-onset stroke. In reference to those without an overall healthy lifestyle, the multivariate-adjusted odds ratios (ORs) for early-onset stroke among participants with an overall healthy lifestyle was 0.27 [95% confidence interval (CI): 0.07-0.98]. CONCLUSIONS: In Chinese stroke patients, a healthy lifestyle was significantly associated with early-onset stroke. Individuals who were adhering to an overall healthy lifestyle had a lower risk of early-onset stroke compared to those who were not.

TNFRSF11B polymorphisms predict poor outcome after large artery atherosclerosis stroke.

Osteoprotegerin is involved in the progression of atherosclerosis. This study aimed to determine whether TNFRSF11B polymorphisms are associated with prognosis of large artery atherosclerosis (LAA) stroke. Three TNFRSF11B polymorphisms (rs2073617, rs2073618 and rs3134069) were genotyped in 1010 patients with LAA stroke. Short-term outcome was evaluated using the modified Rankin Scale score at 3-month after stroke onset. Long-term outcome was assessed using the stroke recurrence. We found that rs2073617G was associated with an increased risk of poor outcome of LAA stroke (additive model: odds ratio (OR) = 1.35, 95% confidence interval (CI) = 1.06-1.73). This association was also observed in rs3134069C (additive model: OR = 1.53, 95% CI = 1.10-2.12). Furthermore, when we combined these two polymorphisms according to the numbers of risk alleles (rs2073617G and rs3134069C), we found that the patients with 3-4 risk alleles were statistically significantly associated with an increased risk of poor outcome of LAA stroke (OR = 1.90, 95% CI = 1.10-3.28) compared with 0-2 risk alleles, and this increased risk was more evident among those with hypertension (OR = 2.02, 95% CI = 1.04-3.91), those without diabetes (OR = 2.02, 95% CI = 1.02-4.01) and those with smoking (OR = 2.43, 95% CI = 1.09-5.42). In silico analysis showed that rs2073617 and rs3134069 are located in various histone modification marked regions, DNase I hypersensitive sites and can change the binding of regulatory motifs. Moreover, rs2073617 is also located in the binding site of transcription factors. Our findings suggested that TNFRSF11B polymorphisms may be associated with an increased risk of short-term poor outcome of LAA stroke.

Serum Cystatin C and Arterial Stiffness in Middle-Aged and Elderly Adults without Chronic Kidney Disease: A Population-Based Study.

BACKGROUND Cystatin C is a protease inhibitor that is increased in the serum of patients with chronic kidney disease (CKD) and is associated with an increased risk of developing cardiovascular disease (CVD). This study aimed to evaluate the association between serum levels of cystatin C and arterial stiffness, associated with dyslipidemia, obesity, and increased pulse pressure, in middle-aged and elderly individuals without CKD in a population in China. MATERIAL AND METHODS A cross-sectional population-based study included 1,138 patients aged ≥40 years without CKD, defined as an estimated glomerular filtration rate measured by serum creatinine (eGFRSCr) ≥60 ml/min/1.73 m². Study participants provided clinical details, including height and weight, and blood samples for serum measurements of cystatin C and lipid profiles and completed a clinical questionnaire. Pulse pressure was calculated as the mean systolic pressure (SBP) minus the diastolic pressure (DBP). Data underwent multivariate logistic regression analysis. RESULTS An increase in serum levels of cystatin C was associated with an increased risk of arterial stiffness. Each standard deviation in the increase of cystatin C resulted in a 22% increased risk of dyslipidemia, a 27% increased risk of obesity, and a 24% increased risk of increased pulse pressure, after adjusting for confounders. These associations were further confirmed in a sensitivity analysis by excluding participants with hypertension, diabetes, and patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). CONCLUSIONS In middle-aged and elderly individuals without CKD, arterial stiffness determined by obesity, dyslipidemia and increased pulse pressure, was significantly associated with increased serum levels of cystatin C.

Complications and predictors associated with persistent hemodynamic depression after carotid artery stenting.

We aimed to investigate the complications and predictors associated with persistent hemodynamic depression (PHD) after carotid artery stenting (CAS). A total of 204 patients undergoing CAS in two centers between January 2011 and November 2013 were enrolled for study into two cohorts: PHD (systolic blood pressure <90 mm Hg and heart beat rate <60/min, which lasted more than 1h) and non-PHD according to their periprocedure detections. The complications were recorded and compared between the two groups. The predictors of PHD were analyzed by univariate analysis and logistic regression model. 43 patients developed PHD, which lasted for 17.22 h on average. The complications occurred in 9 patients of PHD group (angina pectoris 2, myocardial infarction 1, cerebral infarction 3, transient ischemic attack 2 and intestinal obstruction 1), which was significantly more than non- PHD group (angina pectoris 1, cerebral infarction 1, transient ischemic attack 5, p=0.001). Regression analysis revealed that diabetes, severe calcified plaque and a balloon dilation pressure of more than 8 atmospheres (atm) were the independent predictors for PHD after CAS. We concluded that PHD may be related to increased complications of CAS. Patients with diabetes, more severe calcified plaque and more balloon dilation pressure are more prone to develop PHD after CAS.