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BackgroundThe high prevalence of patent foramen ovale (PFO) in cryptogenic stroke suggested a stroke-causing role for PFO. As risk factors for recurrence of such stroke are not recognized, clinicians cannot sufficiently identify, treat, and follow-up high-risk patients. Therefore, this study aimed to establish a prediction model for PFO-related stroke recurrence.MethodsThis study included 392 patients with PFO-related stroke in a training set and 164 patients with PFO-related stroke in an independent validation set. In the training set, independent risk factors for recurrence identified using forward stepwise Cox regression were included in nomogram 1, and those identified using least absolute shrinkage and selection operator(LASSO)regression were included in nomogram 2. Nomogram performance and discrimination were assessed using the concordance index (C-index), area under the curve (AUC), calibration curve, and decision curve analyses (DCA). The results were also validated in the validation set.ResultsNomogram 1 was based on homocysteine (Hcy), high-sensitivity C-reactive protein (hsCRP), and albumin (ALB), and nomogram 2 was based on age, diabetes, hypertension, right-to-left shunt, ALB, prealbumin, hsCRP, and Hcy. The C-index of nomogram 1 was 0.861, which was not significantly different from that of nomogram 2 (0.893). The 2- and 5-year AUCs of nomogram 1 were 0.863 and 0.777, respectively. In the validation set, nomogram 1 still had good discrimination (C-index, 0.862; 2-year AUC, 0.839; 5-year AUC, 0.990). The calibration curve showed good homogeneity between the prediction by nomogram 1 and the actual observation. DCA demonstrated that nomogram 1 was clinically useful. Moreover, patients were successfully divided into two distinct risk groups (low and high risk) for recurrence rate by nomogram 1.ConclusionsNomogram 1, based on Hcy, hsCRP, and ALB levels, provided a more clinically realistic prognostic prediction for patients with PFO-related stroke. This model could help patients with PFO-related stroke to facilitate personalized prognostic evaluations.

To analyze the management of ventricular electrical storm with amiodarone and esmolol. We conducted a retrospective analysis during last 5 years in our hospital. To review and assess the causes, differential diagnosis and treatment with ventricular electrical storm (VES). VES was defined by 2 or

Objectives To provide evidence that rosuvastatin could improve insulin-resistance and inhibit atherogenesis by modulating insulin signalling, and whether this effect beyond its plasma cholesterol-lowering effect. Methods Thirty-two 6-week-old low-density lipoprotein receptor deficient (LDLR- /-) mice were randomised into four groups (n = 8 in each group): Normal control group (NC); High fat and high fructose diet group (HFF); HFF plus rosuvastatin group (HFFR); HFFR plus mevalonic acid group (HFFRMA). After 12 weeks, we measured the fasting blood sugar (FBS), fasting insulin (FINS) and total cholesterol (TC); the morphological concentrations of the aorta artery and aorta sinus; the expression of insulin receptor substrate 2 (IRS-2), phosphorylated insulin receptor substrate 2 (P-IRS-2), protein kinase B (AKT, also known as PKB) and phosphorylated protein kinase B (P-AKT) in liver. Results Compared with other groups, FBS and FINS increased significantly in HFF group. Furthermore, HFF group had an increase in the morphological concentrations of the aorta artery and aorta sinus, but there was a significant decrease in HFFRMA group and HFFR group. Moreover, there was a high expression of IRS-2, P- IRS-2, AKT and P-AKT in HFFRMA group and HFFR group, but a low expression in HFF group. And there is no significant difference regarding to each afore-mentioned index in HFFR group and HFFRMA group. Conclusions Our data show that rosuvastatin could improve insulin-resistance and inhibit atherogenesis in HFF-fed mice by partially reversing the decrease in the insulin stimulated IRS-2/PI3-K/AKT pathway in liver, and this effect is independent of its cholesterol-lowering effect.

Objectives Acording an investigaion of 417 Grade A hospitals in China of recent 10 years, pacemaker implantation has been raising at an average of 11% per year. Overwhelming majority were received right-side DDD pacemaker. Among those patients there area great part need cardiac resynchronisation therapy (CRT), especially when they had got cardiomyopathy and/or heart failure. No definite guidelines were for how to update the resynchronisation system in these patients. Methods Two CRT upgrading cases were done from right-side DDDpacemakers. In case one, the patient’s left subclavian vein was chosen for the convenience of inserting the left ventricular lead. The CRT pacemaker was still put at the primary bag. The left lead was connected to the pacemaker through a small subcutanous tunnel. In case two, the left ventricular lead was inserted through the right subclavian vein. His DDD pacemaker was upgraded in the primary bag. Results Two procedures were done successfully, differently and individually for the maximising benefit. Post-operation follow-up showed the obvious parameters improvement, including ECG/LVEDD/EF and symptoms. Conclusions CRT upgrading is a new path for those who had got heart failure with DDD pacemakers. It really do improve heart function through increasing the synchrony of ventricular contraction. More clinical cases and practice need for confirming this benefit.

Objectives To explore clinical characteristics and emergency treatment of patients with arrhythmias caused by acute aconitine poisoning. Methods We conducted a retrospective analysis during the period of 2010 to 2012, Clinical data of patients with arrhythmias caused by acute aconitine poisoning was analyzed. Results A total of 19 patients (male: 79%; mean age 49 years) with acute aconitine poisoning were included. All 19 cases showed arrhythmias under their ECGs including: sinus bradycardia (HR Conclusions The key point of emergency treatment with arrhythmias caused by acute aconitine poisoning is its diagnosis in early stage, early use of antiarrhythmic drugs is necessary. If ventricular fibrillation occurred, electrical defibrillation emergently and combining use of lidocaine and amiodarone can increase success rate.

Objectives Recent studies have demonstrated an important role of chronic high glucose concentration for collagen deposition in fibroblasts. However, little is known about the action of angiotensin II type 1 receptor blocker and inflammatory cytokines on ACE inhibitor on matrix metalloproteinase (MMP) regulation and collagen synthesis in human cardiac fibroblasts. In this article, we determined the influence of chronic high glucose concentration on human cardiac fibroblasts functions and the effects of 606A and imidaprilat in these responses. Methods Human cardiac fibroblasts were long-time exposure in normal or high glucose media in the absence or presence of 606A or imidaprilat. We have determined their MMP-2 activities by using in-gel zymography. In addition, the collagen IV synthesis was evaluated by the means of ELISA. Results show that chronic high glucose concentration inhibits the activity of MMP-2 and accelerates collagen IV synthesis. When Equimolar mannitol was used as an osmotic control, the activity inhibition of MMP-2 were also observed, however, it is not as strong as that by using high glucose. Inhibition of MMP-2 activity and enhancement of collagen IV synthesis were reserved incompletely by 606A. But complete reservation of MMP-2 activity and collagen IV synthesis was observed by using imidaprilat in cultured media in the experiments. Results show that chronic high glucose concentration inhibits the activity of MMP-2 and accelerates collagen IV synthesis. When Equimolar mannitol was used as an osmotic control, the activity inhibition of MMP-2 were also observed, however, it is not as strong as that by using high glucose. Inhibition of MMP-2 activity and enhancement of collagen IV synthesis were reserved incompletely by 606A. But complete reservation of MMP-2 activity and collagen IV synthesis was observed by using imidaprilat in cultured media in the experiments. Conclusions Chronic high glucose inhibits the activity of MMP-2 and increases collagen IV synthesis by means of regulating MMP-2 mRNA expression in human cardiac fibroblasts through osmotic and non-osmotic pathways. Inhibition of MMP-2 activity and enhancement of collagen IV synthesis were reserved incompletely by 606A. But complete reservation of MMP-2 activity and collagen IV synthesis was observed by using imidaprilat in cultured media in the experiments.

Objectives To provide evidence that rosuvastatin could improve insulin-resistance and inhibit atherosclerosis by modulating insulin signalling, and whether this effect beyond its plasma cholesterol–lowering effect. Methods Thirty-two 6-week-old low-density lipoprotein receptor deficient (LDLR- /-) mice were randomised into four groups (n=8 in each group): Normal control group (NC); High fat and high fructose diet group (HFF); HFF plus rosuvastatin group (HFFR); HFFR plus mevalonic acid group (HFFRMA). After 12 weeks, we measured the fasting blood sugar (FBS), fasting insulin (FINS) and total cholesterol (TC); the morphological concentrations of the aorta artery and aorta sinus; the expression of insulin receptor substrate 2(IRS-2), phosphorylated insulin receptor substrate 2 (P-IRS-2), protein kinase B (AKT, also known as PKB) and phosphorylated protein kinase B (P-AKT) in liver. Results The HFF diet alone resulted in a plasma FBS concentration of 28.15±1.53 mmol/l and FINS concentration of 1.62±0.07 ng/ml, and administration of rosuvastatin lowered plasma FBS and FINS to 19.99±1.40 mmol/l and 0.79±0.12 ng/ml, while the plasma FBS and FINS levels in HFFR group were partially improved compared to NC group. And administration of rosuvastatin showed a good lipid-lowering effect in HFFR group (33.21±1.12), while this cholesterol-lowering effect of rosuvastatin was significantly reversed by the mevalonic acid in HFFRMA group (39.31±1.57). Furthermore, HFF group had an increase in the morphological concentrations of the aorta artery and aorta sinus, but there was a significant decrease in HFFRMA group and HFFR group. Moreover, there was a high expression of IRS-2, P- IRS-2, AKT and P-AKT in HFFRMA group and HFFR group, but a low expression in HFF group. And there is no significant difference regarding to each afore-mentioned index in HFFR group and HFFRMA group. Conclusions Our data show that rosuvastatin could improve insulin-resistance and inhibit atherosclerosis in HFF-fed mice by partially reversing the decrease in the insulin stimulated IRS-2/PI3-K/AKT pathway in liver, and this effect is independent of its cholesterol-lowering effect.