2.The relationship between LDL-C and ischemic stroke in 2 470 patients with nonvalvular atrial fibrillation in Xinjiang region
Min WU ; Xianhui ZHOU ; Baolatejiang RUOZHA ; Shifei SONG ; Yaodong LI ; Jianghua ZHANG ; Qiang XING ; Yanmei LU ; Baopeng TANG
Chinese Journal of Internal Medicine 2017;56(4):258-262
Objective To evaluate the association between LDL-C and ischemic stroke in patients with nonvalvular atrial fibrillation (AF).Method A total of 2 470 patients with nonvalvular AF were included in the present study.The clinical data and laboratory examination results of the patients in the hospital were collected.The subjects were either divided into the ischemic stroke history (n =560),and non-ischemic stroke history groups (n =1 910),or divided into the low-middle risk (n =566) and high risk groups (n =1 904) based on CHA2 DS2-VASc score.Results There were significant differences in the proportion of Han,the ratio of gender,age,hemoglobin,hematocrit,ALT,serum uric acid,HDL-C and LDL-C between the patients with ischemic stroke history and without (all P < 0.05).Similarly,there were significant differences in the proportion of Han,the ratio of gender,age,white blood cell count,hemoglobin,hematocrit,platelet count,ALT,albumin,TG and LDL-C between subjects in the low-middle risk group and those in the high risk group (all P < 0.05).A logistical regression analysis showed that LDL-C was an independent risk factor for both the ischemic stroke history (OR 2.089,95% CI 1.860-2.347,P <0.05),and future ischemic stroke risk (OR 1.270,95% CI 1.079-1.494,P < 0.05) in patients with nonvalvular AF.Conclusion LDL-C is associated with ischemic stroke in patients with nonvalvular AF,and it is also an independent risk factor for future ischemic stroke in these patients.
3.Pioglitazone's Therapeutic Effect and Electrophysiological Mechanism on Rat Ventricular Arrhythmias Induced by β1-adrenergic Receptor Autoantibodies
Linqiang XI ; Huaxin SUN ; Luxiang SHANG ; Qianhui WANG ; Jie SONG ; Na YANG ; Xing ZHANG ; Taiwaikuli DILARE ; Rejiepu MANZEREMU ; Ling ZHANG ; Baopeng TANG ; Xianhui ZHOU
Chinese Circulation Journal 2024;39(7):716-724
Objectives:This study aims to explore the effects of pioglitazone on the attenuation of ventricular arrhythmias(VAs)induced by β1-adrenergic receptor autoantibodies(β1AAb)and its potential mechanisms. Methods:48 SD rats were uniformly randomly divided into four groups using number table:control group received vehicle injection,β1AAb group received back multi-point injection of β1AR-ECLⅡ antigen peptide with adjuvant,2 mg/(kg·time),pioglitazone group received pioglitazone gavage for 2 weeks after 8 weeks of immunization,4 mg/(kg·d),and GW9662 group received pioglitazone+GW9662 intraperitoneal injection for 2 weeks after 8 weeks of immunization,1 mg/(kg·d).Powerlab recorded electrocardiograms and blood collection every 2 weeks.Baseline and week 10 echocardiography were recorded,followed by electrophysiology,histopathology,immunohistochemical staining,and electron microscopy examination after 10 weeks. Results:Compared to control group,β1AAb group showed a higher incidence of ventricular arrhythmias,shorter ventricular effective refractory period(VERP),longer action-recovery interval(ARI),lower left ventricular ejection fraction(LVEF)and left ventricular fractional shortening(LVFS),lower positive staining area ratio of glucose transporter 1(GLUT1)and carnitine palmitoyltransferase 1a(CPT1a),all P<0.05.Mitochondrial morphology abnormalities and network damage were also significantly observed(P<0.05).In contrast to β1AAb group,pioglitazone group showed a reduced incidence of ventricular arrhythmias,prolonged VERP,shortened ARI,recovered LVEF and LVFS,increased the positive staining area ratio of GLUT1 and CPT1a,all P<0.05.Improvement was observed in mitochondrial morphology abnormalities and network damage(P<0.05).Compared to pioglitazone group,GW9662 group exhibited a higher incidence of ventricular arrhythmias,shorter VERP,and longer ARI,lower LVEF and LVFS,lower positive staining area ratio of GLUT1 and CPT1a,all P<0.05.Mitochondrial morphology abnormalities and network damage did not recover(P<0.05). Conclusions:Pioglitazone can reduce VAs induced by β1AAb,improve ventricular electrical conduction and activation recovery time heterogeneity,and mitigate ventricular remodeling caused by β1AAb at the tissue pathology level,accompanied by upregulation of ventricular cardiomyocyte glucose and lipid transport channel proteins and repair of damaged mitochondrial networks.