Background: and Purpose This study aimed to investigate the association between residual inflammatory risk (RIR) and vulnerable plaques using high-resolution magnetic resonance imaging (HRMRI) in symptomatic intracranial atherosclerotic stenosis (ICAS). Methods: This retrospective study included 70%–99% symptomatic ICAS patients hospitalized from January 2016 to December 2022. Patients were classified into four groups based on high-sensitivity C-reactive protein (hs-CRP) and low-density lipoprotein cholesterol (LDL-C): residual cholesterol inflammatory risk (RCIR, hs-CRP ≥3 mg/L and LDL-C ≥2.6 mmol/L), RIR (hs-CRP ≥3 mg/L and LDL-C <2.6 mmol/L), residual cholesterol risk (RCR, hs-CRP <3 mg/L and LDL-C ≥2.6 mmol/L), and no residual risk (NRR, hs-CRP <3 mg/L and LDL-C <2.6 mmol/L). Vulnerable plaque features on HRMRI included positive remodeling, diffuse distribution, intraplaque hemorrhage, and strong enhancement. Results: Among 336 included patients, 21, 60, 58, and 197 were assigned to the RCIR, RIR, RCR, and NRR groups, respectively. Patients with RCIR (adjusted odds ratio [aOR], 3.606; 95% confidence interval [CI], 1.346–9.662; P=0.011) and RIR (aOR, 3.361; 95% CI, 1.774–6.368, P<0.001) had higher risks of strong enhancement than those with NRR. Additionally, patients with RCIR (aOR, 2.965; 95% CI, 1.060–8.297; P=0.038) were more likely to have intraplaque hemorrhage compared with those with NRR. In the sensitivity analysis, RCR (aOR, 2.595; 95% CI, 1.201–5.608; P=0.015) exhibited an additional correlation with an increased risk of intraplaque hemorrhage. Conclusion In patients with symptomatic ICAS, RIR is associated with a higher risk of intraplaque hemorrhage and strong enhancement, indicating an increased vulnerability to atherosclerotic plaques.

Background: and Purpose This study aimed to investigate the association between residual inflammatory risk (RIR) and vulnerable plaques using high-resolution magnetic resonance imaging (HRMRI) in symptomatic intracranial atherosclerotic stenosis (ICAS). Methods: This retrospective study included 70%–99% symptomatic ICAS patients hospitalized from January 2016 to December 2022. Patients were classified into four groups based on high-sensitivity C-reactive protein (hs-CRP) and low-density lipoprotein cholesterol (LDL-C): residual cholesterol inflammatory risk (RCIR, hs-CRP ≥3 mg/L and LDL-C ≥2.6 mmol/L), RIR (hs-CRP ≥3 mg/L and LDL-C <2.6 mmol/L), residual cholesterol risk (RCR, hs-CRP <3 mg/L and LDL-C ≥2.6 mmol/L), and no residual risk (NRR, hs-CRP <3 mg/L and LDL-C <2.6 mmol/L). Vulnerable plaque features on HRMRI included positive remodeling, diffuse distribution, intraplaque hemorrhage, and strong enhancement. Results: Among 336 included patients, 21, 60, 58, and 197 were assigned to the RCIR, RIR, RCR, and NRR groups, respectively. Patients with RCIR (adjusted odds ratio [aOR], 3.606; 95% confidence interval [CI], 1.346–9.662; P=0.011) and RIR (aOR, 3.361; 95% CI, 1.774–6.368, P<0.001) had higher risks of strong enhancement than those with NRR. Additionally, patients with RCIR (aOR, 2.965; 95% CI, 1.060–8.297; P=0.038) were more likely to have intraplaque hemorrhage compared with those with NRR. In the sensitivity analysis, RCR (aOR, 2.595; 95% CI, 1.201–5.608; P=0.015) exhibited an additional correlation with an increased risk of intraplaque hemorrhage. Conclusion In patients with symptomatic ICAS, RIR is associated with a higher risk of intraplaque hemorrhage and strong enhancement, indicating an increased vulnerability to atherosclerotic plaques.

Background: and Purpose This study aimed to investigate the association between residual inflammatory risk (RIR) and vulnerable plaques using high-resolution magnetic resonance imaging (HRMRI) in symptomatic intracranial atherosclerotic stenosis (ICAS). Methods: This retrospective study included 70%–99% symptomatic ICAS patients hospitalized from January 2016 to December 2022. Patients were classified into four groups based on high-sensitivity C-reactive protein (hs-CRP) and low-density lipoprotein cholesterol (LDL-C): residual cholesterol inflammatory risk (RCIR, hs-CRP ≥3 mg/L and LDL-C ≥2.6 mmol/L), RIR (hs-CRP ≥3 mg/L and LDL-C <2.6 mmol/L), residual cholesterol risk (RCR, hs-CRP <3 mg/L and LDL-C ≥2.6 mmol/L), and no residual risk (NRR, hs-CRP <3 mg/L and LDL-C <2.6 mmol/L). Vulnerable plaque features on HRMRI included positive remodeling, diffuse distribution, intraplaque hemorrhage, and strong enhancement. Results: Among 336 included patients, 21, 60, 58, and 197 were assigned to the RCIR, RIR, RCR, and NRR groups, respectively. Patients with RCIR (adjusted odds ratio [aOR], 3.606; 95% confidence interval [CI], 1.346–9.662; P=0.011) and RIR (aOR, 3.361; 95% CI, 1.774–6.368, P<0.001) had higher risks of strong enhancement than those with NRR. Additionally, patients with RCIR (aOR, 2.965; 95% CI, 1.060–8.297; P=0.038) were more likely to have intraplaque hemorrhage compared with those with NRR. In the sensitivity analysis, RCR (aOR, 2.595; 95% CI, 1.201–5.608; P=0.015) exhibited an additional correlation with an increased risk of intraplaque hemorrhage. Conclusion In patients with symptomatic ICAS, RIR is associated with a higher risk of intraplaque hemorrhage and strong enhancement, indicating an increased vulnerability to atherosclerotic plaques.

BACKGROUND:Rotator cuff muscle degeneration(muscle atrophy,fibrosis and fatty infiltration)is a common condition after rotator cuff tears,which seriously affects shoulder function and surgical outcomes.Ginsenoside Rg1 has biological effects such as anti-oxidation,anti-apoptosis and lipid-lowering.However,the effect of ginsenoside Rg1 on muscle degeneration after rotator cuff tear has not been reported. OBJECTIVE:To investigate the effect of ginsenoside Rg1 on muscle degeneration after massive rotator cuff tear in mice. METHODS:Sixty C57BL/6J mice were randomly divided into sham group,model group,ginsenoside Rg1 low dose group and ginsenoside Rg1 high dose group,with 15 mice in each group.The skin of the right shoulder of mice in the sham group was cut and sutured.Massive rotator cuff tear mouse models of the right shoulder were established in the other three groups.Supraspinatus tendon and suprascapular nerve compression were administrated.Mice in the sham and model groups were intraperitoneally injected with 0.5 mL of saline after operation,while those in the ginsenoside Rg1 low and high dose groups were intraperitoneally injected with ginsenoside Rg1 30 and 60 mg/kg respectively,once a day,for 6 weeks.Mice were assessed for limb function by gait analysis the day after the last injection.After euthanasia,the supraspinatus muscle on the operated side was taken to measure the muscle atrophy rate and muscle contractility.Muscle tissue was stained with oil red O and Masson.RT-PCR was used to detect the expression of atrophy,fibrosis,and fatty infiltration related genes. RESULTS AND CONCLUSION:Compared with the model group,low-and high-dose ginsenoside Rg1 significantly increased paw print area and step length(P<0.05).Compared with the model group,low-and high-dose ginsenoside Rg1 significantly increased myofiber cross-sectional area and supraspinatus contractility(P<0.05),and significantly decreased wet muscle mass reduction ratio,fatty infiltration area ratio,and collagen fiber area ratio(P<0.05).Compared with the model group,low-and high-dose ginsenoside Rg1 significantly decreased the expression of atrophy,fibrosis,and fatty infiltration related genes(P<0.05).There was no significant difference in paw print area,supraspinatus muscle contractility,and myofiber cross-sectional area between ginsenoside Rg1 low and high dose groups(P>0.05),and all other indexes were better in the ginsenoside Rg1 high dose group than in the ginsenoside Rg1 low dose group(P<0.05).To conclude,ginsenoside Rg1 could significantly reduce muscle atrophy,fibrosis and fatty infiltration following massive rotator cuff tear in mice,which is beneficial to improve muscle strength and limb function.

Objective To investigate the effect of left bundle branch area pacing(LBBaP)on new-onset atrial fibrillation(NOAF)and atrial high rate episodes(AHREs)in patients with atrioventricular block(AVB).Methods Eighty-four patients with Ⅲ°AVB for pacemaker implantaion were divided into the LBBaP group(n=42)and the RVSP group(n=42)based on the site of the ventricular leads.The two groupswere compared in terms of the pre-and post-operative QRSd,ventricular pacing parameters,complications,incidence of stroke,NOAF and AHREs.Results(1)The incidence of postoperative NOAF and AHREs in the LBBaP group was significantly lower compared with RVSP group(P<0.05).(2)The p-QRSd in the LBBaP group was significantly shorter compared with RVSP group(P<0.05).(3)The two groups showed no significant differences in ventricular pacing parameters,incidence of complications and stroke events(P>0.05).Conclusion LBBaP is superior to right ventricular pacing in reducing the incidence of postoperative AHREs and NOAF in patients after implantation and improving the prognosis of patients.

Mendelian Randomization Analysis ; Bone Density ; Genome-Wide Association Study ; Minerals ; Life Expectancy ; Polymorphism, Single Nucleotide

A 66-year-old female patient with infiltrating adenocarcinoma in left lung received anlotinib 12 mg orally once daily (2-week medication followed by 1-week discontinuation, 3 weeks was a cycle). After 14 months of regular medication, the patient developed palpitation and chest tightness. Laboratory tests showed that the N-Terminal pro-brain natriuretic peptid (NT-proBNP) was 1 698 ng/L; echocardiography showed decreased apical wall motion and left ventricular diastolic dysfunction. Heart failure was condsidered, which was suspected to be related to anlotinib. Anlotinib was stopped and symptomatic treatments were given. Eight days later, her symptoms above-mentioned were alleviated and NT-proBNP was 485 ng/L. Because of the illness condition, the patient took anlotinib again at original dose according to the doctor′s instructions. Three months later, the above symptoms recurred and ventricular fibrillation occurred suddenly. Considering that the heart failure in the patient might be caused by anlotinib. Anlotinib was stopped again. After 11 days of treatments with diuretics, cardiac function improvement, myocardial nutrition, and potassium supplement, the patient′s condition was improved obviously. After that, the patient did not take anlotinib again.

A 66-year-old female patient with infiltrating adenocarcinoma in left lung received anlotinib 12 mg orally once daily (2-week medication followed by 1-week discontinuation, 3 weeks was a cycle). After 14 months of regular medication, the patient developed palpitation and chest tightness. Laboratory tests showed that the N-Terminal pro-brain natriuretic peptid (NT-proBNP) was 1 698 ng/L; echocardiography showed decreased apical wall motion and left ventricular diastolic dysfunction. Heart failure was condsidered, which was suspected to be related to anlotinib. Anlotinib was stopped and symptomatic treatments were given. Eight days later, her symptoms above-mentioned were alleviated and NT-proBNP was 485 ng/L. Because of the illness condition, the patient took anlotinib again at original dose according to the doctor′s instructions. Three months later, the above symptoms recurred and ventricular fibrillation occurred suddenly. Considering that the heart failure in the patient might be caused by anlotinib. Anlotinib was stopped again. After 11 days of treatments with diuretics, cardiac function improvement, myocardial nutrition, and potassium supplement, the patient′s condition was improved obviously. After that, the patient did not take anlotinib again.

Background: and Purpose Despite administration of evidence-based therapies, residual risk of stroke recurrence persists. This study aimed to evaluate the residual risk of recurrent stroke in acute ischemic stroke or transient ischemic attack (TIA) with adherence to guideline-based secondary stroke prevention and identify the risk factors of the residual risk. Methods: Patients with acute ischemic stroke or TIA within 7 hours were enrolled from 169 hospitals in Third China National Stroke Registry (CNSR-III) in China. Adherence to guideline-based secondary stroke prevention was defined as persistently receiving all of the five secondary prevention medications (antithrombotic, antidiabetic and antihypertensive agents, statin and anticoagulants) during hospitalization, at discharge, at 3, 6, and 12 months if eligible. The primary outcome was a new stroke at 12 months. Results: Among 9,022 included patients (median age 63.0 years and 31.7% female), 3,146 (34.9%) were identified as adherence to guideline-based secondary prevention. Of all, 864 (9.6%) patients had recurrent stroke at 12 months, and the residual risk in patients with adherence to guidelinebased secondary prevention was 8.3%. Compared with those without adherence, patients with adherence to guideline-based secondary prevention had lower rate of recurrent stroke (hazard ratio, 0.85; 95% confidence interval, 0.74 to 0.99; P=0.04) at 12 months. Female, history of stroke, interleukin-6 ≥5.63 ng/L, and relevant intracranial artery stenosis were independent risk factors of the residual risk. Conclusions There was still a substantial residual risk of 12-month recurrent stroke even in patients with persistent adherence to guideline-based secondary stroke prevention. Future research should focus on efforts to reduce the residual risk.