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Objective:To investigate the correlation between paroxysmal slow-wave events (PSWEs) and cerebral small vessel disease (CSVD) and CSVD-related cognitive impairment.Methods:Patients with CSVD visited Weihai Municipal Hospital from March 2021 to April 2022 were included, and sex- and age-matched healthy controls were recruited for cross-sectional analysis. The patients with CSVD were further divided into cognitive impairment group and non-cognitive impairment group. The self-developed Python script was used to detect the PSWE parameters in electroencephalogram records. Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE) were used to evaluate cognitive function. Multivariate logistic regression analysis was used to determine whether PWSE parameters were the independent related factors of CSVD and CSVD-related cognitive impairment. Multiple linear regression analysis was used to determine the correlation between the PSWE parameters and overall cognitive function (MoCA total score) in patients with CSVD. Results:A total of 76 patients with CSVD (including 41 patients with cognitive impairment and 35 patients without cognitive impairment) and 45 healthy controls were included. Compared with the healthy control group, PWSEs in the F3 (left frontal area) and O1 (left occipital area) regions of the CSVD group occurred more frequently and lasted longer (all P<0.05). Multivariate logistic regression analysis showed that the frequency (odds ratio [ OR] 1.080, 95% confidence interval [ CI] 1.023-1.140; P=0.005) and duration ( OR 1.006, 95% CI 1.001-1.011; P=0.023) of PWSEs in the left frontal area, as well as the frequency ( OR 1.052, 95% CI 1.010-1.095; P=0.014) and duration ( OR 1.003, 95% CI 1.000-1.006; P=0.028) of PWSEs in the left occipital region were the independent related factors for CSVD. The frequency ( OR 1.106, 95% CI 1.033-1.183; P=0.004) and duration ( OR1.010, 95% CI 1.003-1.017; P=0.004) of PWSEs in the left frontal area were the independent risk factors for cognitive impairment in patients with CSVD. Multiple linear regression analysis showed that the frequency ( β= –0.242, P=0.045) and duration ( β= –0.235, P=0.046) of PWSEs in the left frontal region were negatively correlated with the overall cognitive function score in patients with CSVD. Conclusions:The frequency and duration of PSWEs in some brain regions of patients with CSVD increase, and there is an independent correlation between PSWEs and cognitive impairment, suggesting that the damage of blood-brain barrier may participate in the pathogenesis of cognitive impairment in patients with CSVD.
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Objective:To investigate the effect of the possibility of sleep-disordered breathing (SDB) as assessed by the four-variable score on the platelet function and the risk of stroke recurrence in patients with acute ischemic stroke.Methods:Patients with acute ischemic stroke admitted to the Department of Neurology, Weihai Municipal Hospital from January 2020 to January 2021 were enrolled prospectively. Main inclusion criteria: admission within 24 h of onset; National Institutes of Health Stroke Scale score ≤3; Receiving aspirin + clopidogrel dual antiplatelet therapy. All patients were divided into a high possibility group and a low possibility group of SDB according to the four-variable score. 7±2 d after dual antiplatelet therapy, PL-12 multi-parameter platelet function analyzer was used to detect the maximum aggregation rate (MAR). The patients were followed up for 6 months after discharge and the recurrence of ischemic stroke was observed. The mediating effect model was established with the high possibility of SDB as the independent variable, MAR as the intermediary variable and stroke recurrence as the dependent variable. Firstly, MAR as the dependent variable and high probability of SDB as the independent variable were analyzed by linear regression; then, a binary logistic regression analysis was performed with ischemic stroke recurrence as the dependent variable and the high probability of SDB and MAR as independent variables. Results:A total of 213 patients were enrolled in the study. The average age of the patients was 62.70 ± 10.04 years old. There were 146 male (68.5%) and 121 patients (56.8%) were in the high possibility group (56.8%). During the follow-up period, 24 patients (11.3%) had stroke recurrence. Univariate analysis showed that arachidonic acid (AA) induced MAR (MAR-AA) and adenosine diphosphate (ADP) induced the MAR (MAR-ADP) in the high possibility group of SDB were significantly higher than those in the low possibility group (all P<0.05); MAR-AA and MAR-ADP in the recurrent group were significantly higher than those in the non-recurrent group (all P<0.05), and the proportion of high possibility of SDB in the recurrent group was significantly higher ( P=0.008). Binary logistic regression analysis showed that homocysteine (odds ratio 1.132, 95% confidence interval 1.048-1.223; P=0.002) and having high possibility of SDB (odds ratio 6.351, 95% confidence interval 1.134-35.566; P=0.035) were the independent risk factors for stroke recurrence in patients treated with dual antiplatelet therapy. Intermediary effect analysis showed that MAR had a significant intermediary effect on the risk of stroke recurrence in patients with high probability of SDB. Conclusion:The MAR and stroke recurrence rates in the high possibility group of SDB were significantly higher than those in the low possibility group, and its stroke risk was probably mediated by platelet hyperreactivity.
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Objective:To investigate the correlation between heart rate variability (HRV) and early neurological deterioration (END) and poor outcomes in patients with branch atheromatous disease (BAD).Methods:Patients with BAD admitted to the Department of Neurology, Weihai Municipal Hospital from September 2020 to September 2022 were enrolled prospectively. END was defined as an increase of ≥2 points in the total score of the National Institutes of Health Stroke scale (NIHSS) or an increase of ≥1 in motor item score within 72 h of admission compared with the baseline. Poor outcome was defined as the score of the modified Rankin Scale >2 at 6 months after the onset. Multivariate logistic regression analysis was used to determine whether HRV parameters were the independent influencing factors of END and poor outcomes in patients with BAD. Results:A total of 117 patients with BAD were enrolled, including 76 males (65.0%), aged 64.27±6.95 years. Thirty-eight patients (32.4%) had END, and 21 (17.9%) had poor outcomes. Percentage of the number of pairs of adjacent R-R intervals differentiating by more than 50 ms (pNN50), number of adjacent R-R intervals differentiating by more than 50 ms (NN50), power in low frequency range (LF) and power in high frequency range (HF) in the END group were significantly lower than those in the non-END group, and the LF/HF ratio was significantly higher than the non-END group (all P<0.05). The standard deviation of the R-R interval (SDNN), standard deviation of the average of R-R intervals in all 5-min segments (SDANN), and HF in the poor outcome group were significantly lower than those in the good outcome group. Multivariate logistic regression analysis showed that HF (odds ratio [ OR] 0.994, 95% confidence interval [ CI] 0.991-0.998; P<0.001) was an independent protective factor of END in patients with BAD, and LF/HF ratio ( OR 1.455, 95% CI 1.056-2.005; P=0.022) was an independent risk factor for END in patients with BAD; SDANN ( OR 0.997, 95% CI 0.993-0.999; P=0.023) was an independent protective factor of good outcomes in patients with BAD. Conclusion:HF and LF/HF ratios are the independent influencing factors of END in patients with BAD, and SDANN is an independent influencing factor of the poor outcomes in patients with BAD, suggesting that autonomic dysfunction is involved in the pathophysiological mechanism of END and poor outcomes in patients with BAD.
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Objective:To investigate the correlation between heart rate variability (HRV) and cognitive impairment in patients with obstructive sleep apnea (OSA).Methods:Patients received polysomnography in Weihai Municipal Hospital from June 2019 to November 2020 were enrolled as the subjects of cross-sectional analysis. According to the Montreal Cognitive Assessment score, the patients with OSA were divided into a cognitive impairment group and a non-cognitive impairment group. Multivariate logistic regression analysis was used to determine whether HRV parameters were the independent influencing factors of cognitive impairment in patients with OSA. Multiple linear regression analysis was used to determine the independent correlation between HRV parameters and overall cognition as well as each cognitive domain in patients with OSA. Results:A total of 115 patients with OSA were included, including 80 males (69.6%), aged 58.25±9.88 years. Among them, there were 61 in the cognitive impairment group (53.0%) and 54 in the non-cognitive impairment group (47.0%). The standard deviation of the R-R interval in normal sinus beats (SDNN), the square root of the mean of the sum of the squares of the difference between adjacent NN intervals (RMSSD), the percentage of the number of pairs of adjacent R-R intervals differing by more than 50 ms (pNN50) and the power in high-frequency range (HF; 0.15-0.40 Hz) in the cognitive impairment group were significantly lower than those in non-cognitive impairment group (all P<0.05). Multivariate logistic regression analysis showed that SDNN (odds ratio [ OR] 0.551, 95% confidence interval [ CI] 0.380-0.798; P=0.002), RMSSD ( OR 0.516, 95% CI 0.342-0.779; P=0.002), pNN50 ( OR 0.900, 95% CI 0.834-0.971; P=0.006), LF ( OR 0.821, 95% CI 0.687-0.982; P=0.030) and HF ( OR 0.687, 95% CI 0.525-0.899; P=0.006) were the independent protective factors of cognitive impairment in patients with OSA. Multiple linear regression analysis showed that SDNN ( β=0.208, P=0.023), RMSSD ( β=0.228, P=0.011), pNN50 ( β=0.186, P=0.040), HF ( β=0.235, P=0.010) is independently correlated with overall cognitive function in patients with OSA. Conclusion:The decline of HRV parameters SDNN, RMSSD, pNN50 and HF is independently correlated with cognitive impairment in patients with OSA, suggesting that the decline of vagus nerve function may be involved in the mechanism of cognitive impairment in patients with OSA.
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Objective:To investigate the correlation between heart rate variability (HRV) and cerebral small vessel disease (CSVD) in patients with obstructive sleep apnea (OSA).Methods:Patients with OSA received polysomnography and brain MRI examination in Weihai Municipal Hospital from July 2019 to July 2020 were consecutively collected for cross-sectional analysis. The 5 min HRV before sleep (awake state) was analyzed. The patients were divided into CSVD group and non-CSVD group according to the overall burden of CSVD. The demographic data, clinical data, polysomnography parameters and HRV time domain and frequency domain parameters were compared between the two groups. Multivariate logistic regression analysis was used to determine the correlation between the HRV parameters and CSVD in patients with OSA. Results:A total of 100 patients with OSA were enrolled, including 79 males (79.0%), aged 52.36±8.66 years, apnea hypopnea index (AHI) 38.70±24.65/h. There were 46 patients (46.0%) in the CSVD group and 54 (54.0%) in the non-CSVD group. Univariate analysis showed that there were significant differences in age, AHI, oxygen desaturation index (ODI), percentage of blood oxygen saturation <90% in total sleep time (T90), square root of the mean of the sum of the squares of the difference between adjacent RR intervals (RMSSD), power in high frequency range (HF), power in low frequency range (LF) to HF ratio (LF/HF) between the CSVD group and the non-CSVD group (all P<0.05). Multivariate logistic regression analysis showed that after adjusting for age, body mass index, systolic blood pressure, AHI, ODI, and T90, RMSSD (odds ratio 0.625, 95% confidence interval 0.389-0.981; P=0.041) and LF/HF ratio (odds ratio 1.429, 95% confidence interval 1.011-2.020; P=0.043) were the independent influencing factors of CSVD in patients with OSA. Conclusion:Increased LF/HF and decreased RMSSD in OSA patients with CSVD suggest that the increased sympathetic excitability and decreased vagus function, which may be one of the pathophysiological mechanisms of occurring CSVD in patients with OSA.
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Objective@#To investigate the impact of obstructive sleep apnea hypopnea syndrome (OSAHS) on platelet function in patients with ischemic stroke.@*Methods@#Patients with ischemic stroke treated in the Department of Neurology, Weihai Municipal Hospital from January 2017 to November 2017 were collected prospectively. The presence or absence of OSAHS was determined by polysomnography. After oral administration of aspirin enteric coated tablets for 7±1 d, the maximum aggregation ratio (MAR) induced by arachidonic acid (AA) was determined by PL-12 Platelet Function Analyzer. MAR-AA ≥50% was defined as platelet hyperresponsiveness. Multivariate logistic regression analysis was used to evaluate the risk factors for platelet hyperresponsiveness in patients with ischemic stroke, and multiple linear regression analysis was used to determine the correlation between sleep parameters reflecting the severity of sleep apnea and MAR-AA.@*Results@#Among the 124 patients with ischemic stroke, 58 (46.77%) complicated with OSAHS, 66 (53.23%) without complicated with OSAHS; 84 (67.74%) had platelet hyperresponsiveness, and 40 (32.26%) had not platelet hyperresponsiveness. MAR-AA in the complicated OSAHS group was significantly higher than that in the non-complicated OSAHS group (48.98%±20.61% vs. 26.45%±15.15%; t=-6.858, P<0.001). Multivariate logistic regression analysis showed that OSAHS was an independent risk factor for platelet hyperresponsiveness in patients with ischemic stroke (odds ratio 9.551, 95% confidence interval 3.051-29.905; P<0.001). Multiple linear regression analysis showed that there was a significant linear relationship between apnea hypopnea index and MAR-AA (β=0.499, P<0.001).@*Conclusions@#OSAHS is an independent risk factor for platelet hyperresponsiveness in patients with ischemic stroke. Apnea hypopnea index is significantly correlated with MAR-AA.
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Objective To investigate the changes of platelet reactivity and its influencing factors after aspirin treatment in patients with ischemic stroke complicated with diabetes. Methods From September 2016to December 2017, patients with acute ischemic stroke admitted to the Department of Neurology, Weihai Municipal Hospital within 24 h of onset were enrolled. All patients took aspirin (100 mg/d) within 24 h ofadmission, and after taking the drug (7 ±2 d), the PL-11 platelet function analyzer was used to determine the maximum platelet aggregation ratio (MAR) induced by arachidonic acid (AA). The baseline data of the patients were documented. The factors affecting high platelet reactivity (HPR) were analyzed. Results A total of 398 patients with ischemic stroke were enrolled, including 137 in the diabetes group and 261 in the non-diabetes group. MARAA (43. 45％ ± 14. 11％ vs. 31. 55％ ± 19. 39％; t = 6. 996, P < 0. 001) and the incidence of HPR (34. 3％ vs. 19. 9％; χ2 = 9. 946, P = 0. 002) in the diabetes group were significantly higher than in those in the non-diabetes group. Of the 137 patients with ischemic stroke complicated with diabetes, 47 had HPR. The proportions of patients with hyperlipidemia, previous history of stroke or transient ischemic attack and baseline NIHSS score, HOMA-IR (homeostatis model assessment-insulin resistance),high-sensitivity C-reactive protein, fasting blood glucose, and glycosylated hemoglobin in the HPR group were significantly higher than those in the non-HPR group (all P < 0. 05). Multivariate logistic regression analysis showed that HOMA-IR (odds ratio [OR] 1. 153, 95％ confidence interval [CI] 1. 027-1. 295; P =0. 016), high-sensitivity C-reactive protein (OR 9. 416, 95％ CI 2. 271-39. 049; P = 0. 002), fasting blood glucose (OR 1. 125, 95％ CI 1. 025-1. 235; P = 0. 013), and glycosylated hemoglobin (OR 1. 458, 95％ CI 1. 170-1. 816; P = 0. 001) were the independent risk factors for HPR. Conclusion The platelet reactivity during aspirin therapy in patients with ischemic stroke complicated with diabetes mellitus was high, and platelet activity was associated with multiple mechanisms, such as inflammation, insulin resistance, and hyperglycemia.
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Objective To observe the changes of spleen volume in patients with acute cerebral infarction, and to explore the relationship between the spleen volume and platelet reactivity , inflammatory factors'lymphocyte subsets.Methods This is a case control study.Thirty patients with acute cerebral infarction from January 2017 to June 2017 in Department of Neurology , Weihai Municipal Hospital were included.The spleen volume, arachidonic acid-induced maximum platelet aggregation ratio ( AA-MAR), interferon gamma (IFN-γ) and lymphocyte subsets of patients were monitored in 24 hours of stroke, at 48 hours of stroke, at four days of stroke and at seven days of stroke.Twenty patients without acute cerebral infarction with the same baseline data were selected as the control group , to determine the baseline of spleen volume, AA-MAR, IFN-γand lymphocyte subsets.A t test was used to describe the changes of spleen volume, AA-MAR, IFN-γand lymphocyte subsets at different time points , and Pearson's correlation analysis was used to estimate the relationship between the spleen volume and these variables .Results Compared with the control group ((120.12 ±10.28) cm3), the patients with acute cerebral infarction in 24 hours of stroke ((117.48 ±7.93) cm3) and at 48 hours of stroke ((111.61 ±9.21) cm3) had smaller spleen volume (t＝-2.142, P＜0.05; t＝-2.790, P＜0.01), whereas at four days ((121.31 ±8.16) cm3) and seven days of stroke ((126.11 ±10.31) cm3) had bigger spleen volume (t＝2.242, P＜0.05;t＝2.762, P＜0.01), with the spleen volume decreased first and increased later.Compared with the control group, the patients with acute cerebral infarction had more AA-MAR (control group:20.97%±8.21%;24 h:31.86%±9.54%,t＝3.165,P＜0.01;48 h:41.38%±8.55%,t＝3.254,P＜0.01;4 d:35.34%± 8.15%, t＝3.203,P＜0.01;7 d:29.38% ±10.46%,t＝2.494,P＜0.05) and IFN-γ(pg/L, control group:15.21 ±5.21;24 h:29.75 ±4.57,t＝3.262,P＜0.01;48 h:43.37 ±12.15,t＝3.304,P＜0.01;4 d:40.44 ±9.86, t＝3.291,P＜0.01;7 d:20.93 ±5.51, t＝2.417,P＜0.05) at different time points, with the most AA-MAR at 48 hours of onset, and the most IFN-γat four days of stroke.Compared with the control group, the patients with acute cerebral infarction had more T 4, B lymphocytes and natural killer lymphocytes at the four time points , while the level of T8lymphocytes did not show statistically significant difference even though also increased at the four time points.The correlation analysis results showed that in patients with acute cerebral infarction , the level of AA-MAR (r＝-0.397, P＜0.05; r＝-0.515, P＜0.01; r＝-0.382, P＜0.05) and IFN-γ(r＝-0.408, P＜0.05; r＝-0.479, P＜0.01; r＝-0.378, P＜0.05) was negatively corelated with the spleen volume in 24 hours of onset, at 48 hours of stroke and at four days of stroke; the level of T4, B and natural killer lymphocytes were negatively corelated with the spleen volume in 24 hours of stroke and at 48 hours of stroke.Conclusion After the acute cerebral infarction onset, the spleen volume tends to reduce and then increases , the levels of platelet reactivity , inflammatory factors and lymphocyte subsets are correlated with the spleen volume , and the spleen may aggravate the brain injury by releasing platelets inflammatory factors and lymphocyte subsets.
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Minocycline is the second generation semisynthetic tetracycline antibiotics.A variety of animal models and clinical trials have shown that it has neuroprotective effect.Its mechanism is associated with inhibiting apoptosis, alleviating inflammatory reaction, reducing infarct volume, and alleviating vascular injury.This article reviews the neuroprotective effect of minocycline in preclinical phase and early clinical trials of acute ischemic stroke.
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<p><b>OBJECTIVE</b>To observe the clinical effects of acupuncture combined with auricular point sticking based on the western medication for post stroke depression (PSD).</p><p><b>METHODS</b>Sixty patients with PSD were randomly assigned into an acupuncture plus auricular application group (a combination group) and a medication group, 30 cases in each one. 20 mg paroxetine hydrochloride was prescribed orally in the medication group, once a day for continuous 8 weeks. Based on the above treatment, 30-minute acupuncture was used in the combination group for 8 weeks at Baihui (GV 20), Sishencong (EX-HN 1), Shenting (GV 24), Yintang (GV 29), Shenmen (HT 7), Neiguan (PC 6), Taichong (LR 3), Hegu (LI 4), Zusanli (ST 36), Sanyinjiao (SP 6) and Fenglong (ST 40), once the other day and three times a week. Auricular point sticking therapy for 8 weeks was applied at shenmen (TF), pizhixia (AT), xin (CO), and gan (CO), with pressing 3 times a day and once 3-5 days. The total score and each factor scores of Hamilton's depression scale (HAMD) were observed in the two groups before and after treatment, and Asberg's antidepressant side-effect rating scale (SERS) and clinical effect were evaluated.</p><p><b>RESULTS</b>After treatment, the total HAMD scores of the two groups decreased compared with those before treatment (both<0.05), with better effect in the combination group (<0.05). The scores of the combination group after treatment were lower than those in the medication group, including the anxiety/somatization factor, sleep disturbance factor, hopelessness factor (all<0.05). The total effective rate of the combination group was 86.7% (26/30), which was better than 66.7% (20/30) of the medication group (<0.05). The SERS score of the combination group was lower than that of the medication group (<0.05).</p><p><b>CONCLUSIONS</b>Acupuncture combined with auricular point sticking can improve the clinical symptoms and are effective and safe for PSD.</p>
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Secondary immune response is an important endogenous mechanism of neurological injury after ischemic stroke.Spleen and interferon-γγplay an important role in it.Monitoring the spleen size and the level of interferon-γγhave an important reference significance for the severity of stroke and outcome assessment.
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Prediabetes is a glucose metabolism status between normal glucose metabolism and diabetes.It can not only increase the risks of occurrence and recurrence of stroke, but also affect stroke outcomes.Prediabetes causes ischemic stroke mainly through the insulin resistance and blood-brain barrier damage.Non-drug or drug intervention in patients with prediabetes can delay progression from prediabetes to diabetes and reduce the risks of occurrence and recurrence of stroke.
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Diabetes mellitus is an independent predictor of high platelet reactivity after antiplatelet therapy in patients with ischemic stroke,and the latter is closely related to the increased risk of recurrence of stroke.The mechanisms of high platelet reactivity in patients with diabetes or insulin resistance are associated with a variety of factors.Some circulating molecules can be used as markers for predicting the reactivity of platelets.Monitoring of platelet reactivity after treatment with new antiplatelet agents may provide basis for individualized antithrombotic therapy in ischemic stroke patients with diabetes or insulin resistance.
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Sleep disorder is a common complication after is chemicstroke.If it is nottimely diagnosed and treated, it may affect the rehabilitation of stroke and recurrence. The manifestations of sleep disorders have various forms according to the different locations of infarction. For the treatment of sleep disorder after stroke, the method of the combination of drugs and physical therapy is used in clinical practice at present. In recent years, w ith the w idely use of the polysomnography, poststroke sleep disorders can be diagnosed clearly and carefuly. The treatment for sleep disorders after stroke may significantly improve the prognosis of patients.
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Objective To investigate the correlation between serum cystatin C (CysC) levels and cerebral microbleeds (CMBs) in patients with acute ischemic stroke.Methods The patients with acute ischemic stroke were enrolled.Susceptibility weighted imaging was used to identify the presence of CMBs.Particle-enhanced turbidimetric immunoassay was used to detect the levels of serum CysC.Results A total of 485 patients with acute ischemic stroke were enrolled,including 151 (31.1％) with CMBs.The level of serum CysC of the CMB group was significantly higher than that of the non-CMB group (1.24± 0.13 mg/L vs.1.02± 0.11 rmg/L; t=4.261,P＜ 0.001).Multivariate logistic regression analysis showed that the increased serum CysC level was an independent risk factor for the presence of CMBs in patients with acute ischemic stroke (each increase in one standard deviation,odds ratio 4.063,95％ confidence interval 2.142-8.127; P ＜0.001).Multiple linear regression analysis showed that the number of CMBs in patients with acute ischemic stroke increased with the increasing serum CysC level after adjusting for other confounders (r2 =0.361,P =0.017).Conclusions In patients with acute ischemic stroke,the serum CysC levels are independently associated with the CMBs,and the number of CMBs increases with the serum CysC level.
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Clopidogrel can inhibit platelet aggregation and reduce the risk of recurrent stroke.However,it is a great difference in antiplatelet inhibition in different populations.This article reviews the mechanism of clopidogel resistance and its countermeasures in the prevention of ischemic stroke.
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Objective To investigate whether Bushen-Huoxue compound adjuvant therapy can be effective on mild cognitive impairment in Parkinson's disease and the influence on plasma phospholipids(PLs) levels. Methods 87 PD patients were recruited and collected for the general information. The patients were evaluated by Unified Parkinson's Disease Rating Scale(UPDRS) Ⅲ and Montreal Cognitive Assessment(MoCA). According to MoCA scores, patients with PD-MCI were divided into a Bushen-Huoxue compound treatment group and a control group(basic L-dopa or dopamine agonist). Reevaluating cognitive function by MoCA and plasma phopholipids levels at posttreatment 12 month and 18 month. Plasma PLs was assayed by measuring its inorganic phosphorus after separation by chromatograph.Results 39 cases in 87 PD patients(44.8%)were with PD-MCI.After 12 months or 18 months treatment period, MoCA scores was significantly higher in Bushen-Huoxue compound treatment group than in controls(P<0.05 or 0.01 respectively). Plasma PLs levels were significantly decreased in Bushen-Huoxue compound treatment group than in controls(P<0.01 or 0.01 respectively). Conclusions Bushen-Huoxue compound could be effective in the adjuvant treatment of PD-MCI, and could delay cognitive rate of decline in patients with PD. Meanwhile, Bushen-Huoxue compound could significantly decrease plasma PLs levels in PD-MCI. The evidence from present study suggested that Bushen-Huoxue compound have neuroprotective effects on patients with PD-MCI.
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Objective To study the clinical type and features of cerebral watershed infarction (CWI)in eldedy patients and its relationship with plasma lysophosphatidic acid(LPA).Method Analyzed the clinical data of 106 cases of CWI patients(CWI group)confirmed by cranial MRI,and compared plasma LPA levels in patients with different types of CWI,non-CWI patients(non-CWI group,36 cases)and healthy controls(control group,32 cases).Results In CWI group,anterior-cortex type 22 cases,LPA(4.93±0.72)μmol/L,posterior-cortex type 17 cases,LPA(4.75±0.81)μmoi/L,subcortical type 47 cases,LPA (5.46±1.03)μmol/L,mixed type 20 cages,LPA(6.02±1.12)μmol/L.In non-CWIgroup,LPA(5.37±1.24)μmol/L.In control group,LPA(2.92 ±0.36)μmol/L.The levels of LPA significandy increased in various types of CWI(P<0.05 or<0.01).of which mixed type and subcortical type were the highest,and the level of LPA in mixed type WaS higher than that in anterior-cortex type and posterior-cortex type(P<0.05).The level of LPA in non-CWI group was higher than that in control group,but there wss no significant difference compared with various types of CWI.Conclusions Subcortical type is the primal type in elderly CWI patients,the main cause of which is the atherosclerotic plaque formation and lumen stenosis.Platelet activation and its microemboli play an important role in the pathophysiology.LPA levels are significantly higher in various types of CWI,of which mixed type is the highest.LPA can be used as an important molecular marker to guide the sub-type treatment of CWI in elderly patients.
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Objective To observe the changing characteristics of plasma lysophosphatidic acid (LPA) or acidia phospholipid (AP) levels in patients with obstructive sleep apnea syndrome-associated(OSAS)acute cerebral infarction and to explore the pathophysiological mechanisms of OSAS-related stroke so as to provide basis for clinical antithrombotic therapy. Methods Thirty-six patients of OSAS, 32 patients of OSAS-related acute stoke and 36 patients of acute stoke without OSAS diagnosed by clinical and accessory examinations were enrolled in the current study. Thirty-eight age-matched healthy subjects were recruited as controls. The changes of the plasma LPA and AP levels were measured. Results Within 24 hours after symptom onset, the plasma LPA and AP levels in the OSAS-related acute cerebral infarction group (LPA(3. 78 ±0. 56) μmol/L; AP(7. 63 ± 1. 38) μmol/L) were significantly higher than those in the OSAS group(LPA(3. 17 ±0. 65) μmol/L; AP(6. 60 ± 1. 20) μmol/L) ,the not OSAS-related acute cerebral infarction group (LPA (3. 40 ± 0. 59)μmol/L; AP (6. 41 ± 1. 37)μmol/L) and the control group (LPA(2.76±0.45)μmol/L;AP(4.52±0. 83) μmol/L (P < 0. 01)) . The levels of LPA and AP in the OSAS group and the not OSAS-related acute cerebral infarction group were significantly higher than those in the control group(P<0. 01). Seven days after symptom onset, the plasma LPA and AP levels in the OSAS-associated acute cerebral infarction group (LPA(3.08 ± 0. 58) μmol/L; AP(6. 15 ±1. 14)μmol/L) were still higher(P < 0. 01) . The plasma LPA levels were not significantly different among the OSAS-related acute cerebral infarction group, the not OSAS-related acute cerebral infarction group and the control group 21 days after symptom onset, whereas the plasma AP levels in the OSAS-related acute cerebral infarction group (5. 04 ± 0. 83) μmol/L were still significantly higher than those in the not OSAS-related acute cerebral infarction group (4. 57 ± 0. 94) μmol/L and the control group (P < 0.05). Conclusions The significantly elevated plasma LPA and AP levels in patients with OSAS suggested that platelets in vivo are in an activated state and in cerebral ischemia and hypoxia state, especially for the OSAS-related acute cerebral infarction patients. The activated state of platelet may persist for a long time, thus the time window for antithrombotic therapy may be longer.
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Objective To observe the effects of different antithrombotic interventions on the changes of plasma lysophosphatidic acid (LPA) level in patients with nonvalvular atrial fibrillation (NVAF) and to provide the basis for clinical antithrombotic therapy. Methods A total of 235 patients with NVAF who did not receive antithrombotic therapy diagnosed by clinical and auxiliary examinations were randomly allocated to receive aspirin (100 mg/d) plus dipyridamole (100 mg/d) (n =76), aspirin (100 mg/d) plus fixed-dose warfarin (1.25 mg/d) (n =79), and dose-adjusted warfarin (international normalized ratio (INR) range of 1.5 to 2. 1) (n =80). They gore redivided into <60, 60-75, and ≥76 year-old groups according to their age. The plasma LPA levels were measured and compared before treatment and 2 and 6 weeks after treatment. Results 1he plasma LPA levels were decreased more significantly in the aspirin plus fixed-dose group than those in the aspirin plus dipyridamole and dose-adjusted warfarin groups (all P < 0.01). Two and 6 weeks after treatment with aspirin plus dipyridamole in the < 60 year-old group, the plasma LPA levels were significantly lower than those before treatment (all P<0. 01). Two and6 weeks after treatment with aspirin plus fixed-dose warfarin in the < 60 year-old group, the plasma LPA levels were significantly lower than those before treatment (all P <0. 01). Two and 6 weeks after treatment with aspirin plus fixed-dose warfarin in the 60-75 year-old group, the plasma LPA levels were significantly lover than those before treatment (all P <0.01). Two and 6 weeks after the treatment with dose-adjusted warfarin (INR 1.5-2. 1) in patients in each age group, the plasma LPA levels were significantly lower than those before treatment. Conclusions 1he different antithromhotic therapeutic modalities have different effects on platelet activation in patients with NVAF in different age groups. The patients in the < 60 year-old group can receive aspirin plus dipyridamole, the patients in the < 75 year-old group can receive aspirin plus fix-dose warfarin, and the patients > 75 year-old, dose-adjusted warfarin (INR 1. 5-2. 1) should he recommend.