Values of Radial Artery Provocation Tests at Different Doses of Ergonovine in the Diagnosis of Coronary Artery Spasm.

The intracoronary drug provocation test has been the gold standard for diagnosis of coronary artery spasm (CAS); however, it has been identified with severe complications. In this study, we investigated the sensitivity, specificity, and safety of radial artery provocation test at different doses of ergonovine in the diagnosis of CAS. This study enrolled 57 patients, which were then divided into CAS group (n = 24) and control group (n = 33) after intracoronary ergonovine provocation test. All patients underwent radial artery provocation test at different doses of ergonovine. The predictive values of radial artery provocation test for the diagnosis of CAS were analyzed using receiver operator characteristic curve. In the radial artery provocation test at different doses of ergonovine, radial artery stenosis degree was all found to be significantly higher in the CAS group than in the control group (all P < 0.001). In the control group, significant differences were noted in the radial artery stenosis degree between different doses of ergonovine (all P < 0.05). In the CAS group, the radial artery stenosis degree was significantly higher in 160 µg and 100 µg of ergonovine than in 60 µg of ergonovine (all P < 0.001). The radial artery provocation test at 60 µg and 100 µg of ergonovine did not cause CAS, chest pain, and ECG ischemic changes. In the radial artery provocation test at 160 µg of ergonovine, some patients had CAS, chest pain, and ECG ischemic changes. The specificity and sensitivity of radial artery provocation test were 90.91% and 50.00% at 60 µg of ergonovine, 96.97% and 66.67% at 100 µg of ergonovine, and 90.91% and 95.83% at 160 µg of ergonovine for the diagnosis of CAS. As per our findings, we can conclude that the basic tension of radial artery increases in the CAS group. With the increase of ergonovine doses, its sensitivity and specificity improve, but its safety decreases. We will explore the most optimal dose of ergonovine in future studies.

Ciliary Neurotrophic Factor (CNTF) Protects Myocardial Cells from Oxygen Glucose Deprivation (OGD)/Re-Oxygenation via Activation of Akt-Nrf2 Signaling.

BACKGROUND/AIMS: Oxygen glucose deprivation (OGD)/re-oxygenation (OGDR) exposure to myocardial cells mimics ischemia-reperfusion injuries. We studied the potential activity of ciliary neurotrophic factor (CNTF) on OGDR-treated myocardial cells. METHODS: CNTF and CNTFR expression were tested by RT-PCR assay and Western blotting assay. Cell viability and death were tested by MTT assay and LDH release assay, respectively. Akt-Nrf2 signalings were tested by Western blotting assay and qPCR assay. RESULTS: CNTF and its receptor CNTFR were functionally expressed in established H9c2 myocardial cells and primary murine myocardiocytes. Pretreatment of CNTF significantly attenuated OGDR-induced viability reduction and death in myocardial cells. Further studies show that in the myocardial cells CNTF activated NF-E2-related factor 2 (Nrf2) signaling to inhibit OGDR-induced reactive oxygen species (ROS) production and programmed necrosis, preventing adenine nucleotide translocator 1 (ANT-1)-p53-cyclophilin D (Cyp-D) mitochondrial association and mitochondrial depolarization. Nrf2 silencing or knockout almost abolished CNTF-induced H9c2 cytoprotection against OGDR. CNTF activated Akt in H9c2 cells and primary murine myocardiocytes. Conversely, Akt blockage by the pharmacological inhibitors not only blocked CNTF-induced Nrf2 Ser-40 phosphorylation and activation, but also nullified anti-OGDR actions by CNTF in myocardial cells. CONCLUSION: CNTF activates Akt-Nrf2 signaling to protect myocardial cells from OGDR.

Sulforaphane, a Natural Isothiocyanate Compound, Improves Cardiac Function and Remodeling by Inhibiting Oxidative Stress and Inflammation in a Rabbit Model of Chronic Heart Failure.

BACKGROUND The aim of this study was to investigate the effects of sulforaphane (SFN), a natural isothiocyanate compound, in a rabbit ascending aortic cerclage model of chronic heart failure (CHF). MATERIAL AND METHODS Thirty New Zealand White rabbits were divided into the sham operation group (n=10), the CHF group (n=10), and the CHF + SFN group (n=10) treated with subcutaneous SFN (0.5 mg/kg) for five days per week for 12 weeks. After 12 weeks, echocardiography and biometric analysis were performed, followed by the examination of the rabbit hearts. Enzyme-linked immunosorbent assay (ELISA) and Western blot were used to detect levels of inflammatory cytokines, superoxide dismutase (SOD), and malondialdehyde (MDA). RESULTS In the CHF group, compared with the sham operation group, there was an increase in the heart weight to body weight ratio (HW/BW), the left ventricular weight to body weight ratio (LVW/BW), the left ventricular end diastolic diameter (LVEDD), the left ventricular end systolic diameter (LVESD), plasma brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) levels, the cardiac collagen volume fraction (CVF), apoptotic index, expression levels of collagen I, collagen III, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and malondialdehyde (MDA) in the myocardial tissue, and a decrease in the left ventricular shortening fraction (LVFS) and left ventricular ejection fraction (LVEF), and cardiac superoxide dismutase (SOD) activity. These changes were corrected in the SFN-treated group. CONCLUSIONS In a rabbit model of CHF, treatment with SFN improved cardiac function and remodeling by inhibiting oxidative stress and inflammation.

Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on cardiovascular events in patients with heart failure: a meta-analysis of randomized controlled trials.

BACKGROUND: Heart failure (HF) remains a significant cause of morbidity and mortality. Multiple trials over the past several years have examined the effects of both angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) in the treatment of left ventricular dysfunction, both acutely after myocardial infarction and in chronic heart failure. Yet, there is still confusion regarding the relative efficacy of rennin-angiotensin-aldosterone system (RAAS) inhibition. Our study was conducted to assess efficacy of ACEIs and ARBs in reducing all-cause and cardiovascular mortality in heart failure patients. METHODS: We included randomized clinical trials compared ACEIs and ARBs treatment (any dose or type) with placebo treatment, no treatment, or other anti-HF drugs treatment, reporting cardiovascular or total mortality with an observation period of at least 12 months. Data sources included Pubmed, EMBASE, the Cochrane Central Register of Controlled Trials. Dichotomous outcome data from individual trials were analyzed using the risk ratio measure and its 95%CI with random-effects/ fixed-effects models. We performed meta-regression analyses to identify sources of heterogeneity. All-cause mortality and CV mortality were thought to be the main outcomes. RESULTS: A total of 47,662 subjects were included with a mean/median follow-up ranged from 12 weeks to 4.5 years. Of all 38 studies, 32 compared ACEIs with control therapy (included 13 arms that compared ACEIs with placebo, 10 arms in which the comparator was active treatment and 9 arms that compared ACEIs with ARBs), and six studies compared ARBs with placebo. ACEIs treatment in patients with HF reduced all-cause mortality to 11% (risk ratio (RR): 0.89, 95% confidence interval (CI): 0.83-0.96, p = 0.001) and the corresponding value for cardiovascular mortality was 14% (RR: 0.86, 95% CI: 0.78-0.94, p = 0.001). However, ARBs had no beneficial effect on reducing all-cause and cardiovascular mortality. In head-to-head analysis, ACEIs was not superior to ARBs for all-cause mortality and cardiovascular deaths. CONCLUSIONS: In HF patients, ACEIs, but not ARBs reduced all-cause mortality and cardiovascular deaths. Thus, ACEIs should be considered as first-line therapy to limit excess mortality and morbidity in this population.

Low-concentration of perifosine surprisingly protects cardiomyocytes from oxygen glucose deprivation.

Here we found that low-concentration of perifosine, an Akt inhibitor, surprisingly protected cardiomyocytes from oxygen glucose deprivation (OGD)/re-oxygenation. In H9c2 cardiomyocytes, non-cytotoxic perifosine (0.1-0.5 µM) suppressed OGD/re-oxygenation-induced reactive oxygen species (ROS) production, p53 mitochondrial translocation and cyclophilin D complexation, as well as mitochondrial membrane potential (MMP) reduction. Molecularly, perifosine activated AMP-activated kinase (AMPK) signaling to increase intracellular NADPH (nicotinamide adenine dinucleotide phosphate) content in H9c2 cells. On the other hand, AMPK inhibition by AMPKα1 shRNA-knockdown in H9c2 cells significantly reduced perifosine-induced NADPH production, and alleviated perifosine-mediated anti-oxidant and cytoprotective activities against OGD/re-oxygenation. In primary murine cardiomyocytes, perifosine similarly activated AMPK signaling, and offered significant protection against OGD/re-oxygenation, which was largely attenuated with siRNA knockdown of AMPKα1. We demonstrate an unexpected function of perifosine (low-concentration) in protecting cardiomyocytes from OGD/re-oxygenation.

Outcomes of catheter ablation of atrial fibrillation in patients with hypertrophic cardiomyopathy: a systematic review and meta-analysis.

AIMS: Over the past decade, catheter ablation (CA) has become an established therapy for symptomatic atrial fibrillation (AF). Atrial fibrillation is common in hypertrophic cardiomyopathy (HCM) patients, and restoring sinus rhythm is of great clinical benefit to them. Therefore, we conducted a systematic review and meta-analysis of the available data to evaluate the effectiveness and safety of CA for AF in patients with HCM. METHODS AND RESULTS: Six databases were searched to identify studies describing outcomes of CA of AF in HCM patients with a mean follow-up of ≥12 months after the index procedure. The following data were extracted: (i) single-procedure success, (ii) multiple-procedure success, and (iii) drug-free success. Fifteen studies involving 531 patients were included. Single-procedure freedom from atrial arrhythmia at the latest follow-up was 45.5% [95% confidence interval (CI): 34.8-56.2%]. With multiple procedures, the final success rate was 66.1% (95% CI: 55.3-76.9%) overall, 71.8% (95% CI: 61.6-82.0%) in paroxysmal AF, and 47.5% (95% CI: 36.0-59.0%) in non-paroxysmal AF. Without anti-arrhythmic drugs (AADs), single-procedure success rate at latest follow-up was 32.9% (95% CI: 21.7-41.1%); after multiple procedures, this raised to 50.4% (95% CI: 39.2-61.6%). The incidence of serious periprocedural complications was acceptable [5.1% (95% CI: 2.8-9.6%)]. Substantial heterogeneity (I(2)> 50%) was noted in the above groups. CONCLUSIONS: Catheter ablation of AF in patients with HCM is feasible, although more repeat procedures and AAD are needed to prevent AF recurrence.

Salidroside inhibits oxygen glucose deprivation (OGD)/re-oxygenation-induced H9c2 cell necrosis through activating of Akt-Nrf2 signaling.

Oxygen glucose deprivation (OGD)/re-oxygenation has been applied to cultured cardiomyocytes to create a cellular model of ischemic heart damage. In the current study, we explored the potential role of salidroside against OGD/re-oxygenation-induced damage in H9c2 cardiomyocytes, and studied the underlying mechanisms. We found that OGD/re-oxygenation primarily induced necrosis in H9c2 cells, which was inhibited by salidroside. Salidroside suppressed OGD/re-oxygenation-induced reactive oxygen species (ROS) production, p53 mitochondrial translocation and cyclophilin D (Cyp-D) association as well as mitochondrial membrane potential (MMP) decrease in H9c2 cells. Meanwhile, salidroside activated Akt and promoted transcription of NF-E2-related factor 2 (Nrf2)-regulated genes (heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1)). Significantly, Nrf2 shRNA knockdown or Akt inhibitors (LY 294002 and wortmannin) not only prevented salidroside-induced HO-1/NQO-1 transcription, but also alleviated salidroside-mediated cytoprotective effect against OGD/re-oxygenation in H9c2 cells. These observations suggest that salidroside activates Nrf2-regulated anti-oxidant signaling, and protects against OGD/re-oxygenation-induced H9c2 cell necrosis via activation of Akt signaling.

Ganoderic acid A inhibits ox-LDL-induced THP-1-derived macrophage inflammation and lipid deposition via Notch1/PPARγ/CD36 signaling.

BACKGROUND: Atherosclerosis (AS), a chronic inflammatory disease, is a major contributor to deaths worldwide. Ganoderic acid A (GAA) has been widely applied for various diseases due to its excellent anti-inflammatory properties. OBJECTIVES: To investigate the underlying mechanism of GAA inhibition of inflammation and lipid deposition in human monocyte (THP-1) cells. MATERIAL AND METHODS: The Cell Counting Kit-8 (CCK-8) assay was used to assess the potential effect of GAA on the viability of THP-1 cells. The release of inflammatory cytokines and oxidative stress was measured using enzyme-linked immunosorbent assay (ELISA) and the corresponding kit, respectively. The levels of lipid deposition and total cholesterol (TC) were also evaluated. Next, the scavenger receptors and proteins in Notch1/PPARa/CD36 signaling were measured with western blot. As Notch1 was overexpressed in the THP-1 cells induced by oxidized low-density lipoprotein (ox-LDL), the above assays were performed again to confirm the underlying mechanism. RESULTS: Ganoderic acid A suppressed ox-LDL-induced inflammation and oxidative stress in THP-1 cells. At the same time, it inhibited the TC level and lipid deposition. The effects of GAA on alleviating inflammation, oxidative stress and lipid accumulation were relieved after the overexpression of Notch1 in the treated cells, and the effects of GAA on alleviating inflammation, oxidative stress and lipid accumulation were diminished. The PPARa activator also weakened the effects of GAA on relieving inflammation, oxidative stress and lipid accumulation in ox-LDL-induced THP-1 cells. CONCLUSIONS: Ganoderic acid A inhibits ox-LDL-induced macrophage inflammation and lipid deposition in THP-1 cells through Notch1/PPARa/CD36 signaling, which may provide theoretical guidance for the clinical applications of GAA in AS treatment.

A Four-MicroRNA Panel in Peripheral Blood Identified as an Early Biomarker to Diagnose Acute Myocardial Infarction.

Objective: This study aimed to evaluate suitable circulating microRNAs (miRNAs) as diagnostic biomarkers of acute myocardial infarction (AMI). Methods: Patients with AMI were enrolled as study participants. All patients with AMI coming from the Second Affiliated Hospital of Nantong University between October 1, 2017 and May 31, 2019 were screened. At the same time, 80 patients with coronary angiographic stenosis <50% during the same period were selected as the control group. Peripheral blood samples were collected at different time points (0, 6, 12, and 24 h after disease onset) to detect the expression of a previously identified promising four-microRNA panel. The expression levels of miRNAs were tested by real-time polymerase chain reaction (RT-PCR), and the receiver operating characteristic curve (ROC) was used to analyze the diagnostic value of circulating miRNAs. Results: Based on the inclusion and exclusion criteria, 80 patients with AMI and 80 controls were enrolled in this study. The expression of circulating miR-1291, miR-217, miR-455-3p, and miR-566 was significantly downregulated in patients with AMI compared with controls. The area under the ROC curve (AUC) of circulating miR-1291, miR-217, miR-455-3p, and miR-566 were 0.82, 0.79, 0.82, and 0.83, respectively. The AUC of these four miRNAs was 0.87 with 83% sensitivity and 87% specificity. The expression peaks of these four miRNAs occurred earlier than those of cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB). Furthermore, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that the targets of these four miRNAs were significantly enriched in several signaling pathways associated with AMI progression. Conclusion: Circulating miR-1291, miR-217, miR-455-3p, and miR-566 expression levels were significantly lower in patients with AMI; and combined, this panel of four miRNAs acted as a novel and potential early diagnostic biomarker of AMI.

Diagnosis of coronary artery spasm by ergonovine provocation test of radial artery.

We investigated the sensitivity, specificity and safety of ergonovine provocation test of radial artery in the diagnosis of coronary artery spasm (CAS). The patients who came to our hospital for chest pain from January to June 2020 as well as had coronary stenosis < 50% and no radial artery stenosis, were enrolled in this study. These patients were divided into CAS group and control group after intracoronary ergonovine provocation test. All patients underwent ergonovine provocation test of radial artery, the inner diameter (D0 and D1) and the peak systolic velocities (PSV0 and PSV1) of the radial artery were measured by ultrasound before and after ergonovine provocation. The predictive value of ergonovine provocation test of radial artery for the diagnosis of CAS was analyzed using receiver operator characteristic (ROC) curve. There were 19 patients in the CAS group and 28 patients in the control group. Low density lipoprotein cholesterol and smoking rate were significantly higher in the CAS group than in the control group (all P < 0.05), but there were no significant differences in other items (P > 0.05) between the two groups. In the ergonovine provocation test of radial artery, degree of radial artery stenosis was significantly higher in the CAS group [41.50% (35.60%, 50.00%)] than in the control group [11.25% (5.15%, 23.00%)] (P = 0.000), but there were no siginificant differences in D0, PSV0 and PSV1 between the two groups (P > 0.05). The area under ROC curve of ergonovine (120 µg) provocation test of radial artery for the diagnosis of CAS was 0.912 with 95%CI: 0.792-0.975, P = 0.001, cut-off of 31%, specificity of 92.86% and sensitivity of 84.21%. The ergonovine (120 µg) provocation test of radial artery did not cause any adverse reactions. We concluded that the ergonovine provocation test of radial artery has high sensitivity, specificity and safety in the diagnosis of CAS.

Correlation of the ORBIT Score With 30-Day Mortality in Patients With ST-Segment Elevation Myocardial Infarction.

A new scoring system Outcomes Registry for Better Informed Treatment (ORBIT) score is used to assess the bleeding risk in anticoagulated patients with atrial fibrillation (AF). Our aim is to investigate the possible correlations of the ORBIT score with 30-day mortality in patients with ST-segment elevation myocardial infarction (STEMI). A total of 639 patients with STEMI were enrolled in this study. The ORBIT, HAS-BLED, and TIMI scores were recorded during admission. After 30 days' follow-up, 639 patients were divided into 2 groups: the survival group and the nonsurvival group. Different clinical parameters were compared. The predictive values of the ORBIT, HAS-BLED, and TIMI scores for 30-day mortality were assessed from receiver operating characteristic (ROC) analyses. The univariate and multivariate Cox proportional hazards analyses were applied to evaluate the relationships between variables and 30-day mortality. Sixty-seven deaths occurred after a 30-day follow-up. The ORBIT, HAS-BLED, and TIMI scores in the death group were higher than those in the survival group (P < .05). The areas under the ROC curve for the ORBIT, HAS-BLED, and TIMI scores to predict the occurrence of 30-day mortality were 0.811 (95% CI: 0.779-0.841, P < .0001), 0.717 (95% CI: 0.680-0.752, P < .0001), and 0.844 (95% CI: 0.813-0.871, P < .0001), respectively. In multivariate Cox proportional hazards modeling, the high ORBIT score was positively associated with 30-day mortality (hazard ratio: 1.309, 95% CI: 1.101-1.556, P = .013) after adjustment. A graded relation is found in the elevated ORBIT score and 30-day mortality in patients with STEMI. Thus, the ORBIT score can be an independent predictor of 30-day mortality in patients with STEMI.

Relationship of the ORBIT and HAS-BLED scores with Killip class 3-4 in patients with ST-segment elevation myocardial infarction.

Heart failure (HF) complicating ST-segment elevation myocardial infarction (STEMI) is recognized as an ominous complication. The HAS-BLED and Outcomes Registry for Better Informed Treatment (ORBIT) scores are used to assess the bleeding risk in patients with anticoagulated atrial fibrillation. This study aimed to investigate the relationship of the ORBIT and HAS-BLED scores with Killip class 3-4 in patients with STEMI.639 patients with STEMI were enrolled in this study. The ORBIT and HAS-BLED scores were recorded after admission, and all patients were divided into 2 groups: the Killip class 1-2 and Killip class 3-4 groups. Different clinical parameters were compared. The predictive values of the ORBIT and HAS-BLED scores for Killip classes 3 to 4 were assessed using receiver-operating characteristic (ROC) analyses. Univariate and multivariate logistic analyses were used to evaluate the relationships between variables and Killip class 3-4.The ORBIT and HAS-BLED scores were higher in the Killip class 3-4 group than in the Killip class 1-2 group (P < .05). The areas under the ROC curve of the ORBIT and HAS-BLED scores for predicting the higher Killip classification were 0.818 (95% CI: 0.786-0.847, P < .0001) and 0.674 (95% CI: 0.636-0.710, P < .0001), respectively. In multivariate logistic analysis, the high ORBIT score was positively associated with Killip classes 3 to 4 after adjustment (odds ratio: 2.306, 95% CI: 1.084-4.911, P = .012).A graded relationship was found in the elevated ORBIT and HAS-BLED scores and Killip classes 3 to 4 in patients with STEMI. The ORBIT score is independently associated with the Killip 3-4 in patients with STEMI.

Correlations of soluble osteoclast-associated receptor (sOSCAR) with acute coronary syndrome.

BACKGROUND: An osteoclast-associated receptor (OSCAR) is an immunoglobulin receptor expressed in an osteoclast, and takes part in the formation of an osteoclast. While the soluble OSCAR (sOSCAR) component is reported to be involved in the pathogenesis of arteriosclerosis, the aim of this present study is to investigate the relationship between sOSCAR and acute coronary syndrome (ACS). METHODS: This study enrolled 41 patients with ACS and 33 patients without ACS as a control, from March 2017 to June 2017. The baseline clinical parameters and serum levels of sOSCAR were collected in the participants. The univariate and multivariate logistic regressions were applied to explore the independent association of sOSCAR with ACS. A receiver operating characteristic (ROC) curve was applied to explore the ability of sOSCAR to indicate ACS. RESULTS: The results showed that the levels of sOSCAR in the patients with ACS was lower than the patients without ACS (P=0.005). The multivariate logistic regression tests demonstrated that a decreased sOSCAR level was independently associated with the presence of ACS (OR: 0.174, 95% CI: 0.047-0.638, P=0.008). ROC analysis showed that the optimal sOSCAR cut-off value for the indication of ACS was <110.87 pg/mL, the corresponding sensitivity was 65.85%, and the specificity was 69.70%. CONCLUSIONS: The decreased levels of sOSCAR are independently associated with the presence of ACS. sOSCAR could then be considered as a potential biomarker for the prediction of ACS.

[Study of carvedilol on plaque stability in carotid atherosclerotic rabbits transfected by p53 gene].

OBJECTIVE: To investigate the effects of carvedilol on stabilizing atherosclerosis plaque. METHODS: Forty five male Japanese white rabbits were divided randomly into 5 groups with 9 for each. One group was fed up with normal diet as blank control. In other four groups, the common carotid artery of rabbits fed up with high cholesterol diet were injured by balloon. Three groups of them were transfected by wild-type p53 gene 8 weeks later, and then two groups of them were treated with carvedilol (3 mgxkg(-1)xd(-1)) and metoprolol (6 mgxkg(-1)xd(-1)) respectively, high cholesterol diet should be continued for other 4 weeks. Serum lipid, hypersensitive C-reaction protein (hsCRP), oxidized low density lipoprotein (oxLDL), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-PX) were measured in 0, 8, 12 weeks after experiment. The apoptosis rate of smooth muscle cell (SMC) in endomembrane and the local expression of p53, bcl-2, bax, alpha-actin were examined after experiment, and the carotid arteries were examined by light microscopy and transmission electron microscopy. RESULTS: The typical carotid atherosclerotic plaques were observed in balloon-injured groups. The local expression rates of p53 in groups transfected by wild type p53 gene were higher obviously than them in other two groups (P < 0.01). Compared with the rabbits received simple transfection, the thickness of the fibrous cap in rabbits received carvedilol and metoprolol were all increased, but the change could be observed significantly in carvedilol group (P < 0.05). Compared with metoprolol, carvedilol could reduce the level of serum hsCRP, oxLDL, MDA, and increase the concentration of SOD and GSH-PX significantly (P < 0.05 or 0.01), but two medicines had no obvious influence to serum lipid. The apoptosis rate of SMC in endomembrane, the local expression of bax gene and bax/bcl-2 ratio were decreased, the positive expression rates of alpha-actin and bcl-2 were enhanced in carvedilol group (P < 0.01). CONCLUSIONS: Both carvedilol and metoprolol can improve the stability of the plaque, but carvedilol is superior. Its mechanisms may lie in that carvedilol still has function of anti-inflammation, anti-oxidation, decreasing the apoptosis rate of SMC in addition to its function of blocking beta-receptor.

Activation of Akt by SC79 protects myocardiocytes from oxygen and glucose deprivation (OGD)/re-oxygenation.

SC79 is a novel Akt activator. The current study tested its potential effect against oxygen and glucose deprivation (OGD)/re-oxygenation-induced myocardial cell death. We showed that SC79 activated Akt and protected H9c2 myocardial cells and primary murine myocardiocytes from OGD/re-oxygenation. Reversely, Akt inhibitor MK-2206 or Akt1 shRNA knockdown almost completely abolished SC79-mediated myocardial cytoprotection. SC79 treatment in H9c2 cells inhibited OGD/re-oxygenation-induced programmed necrosis pathway, evidenced by mitochondrial depolarization and cyclophilin D-p53-ANT-1 (adenine nucleotide translocator 1) association. Further, SC79 activated Akt downstream NF-E2-related factor 2 (NRF2) signaling to suppress OGD/re-oxygenation-induced reactive oxygen species (ROS) production. Reversely, NRF2 shRNA knockdown in H9c2 cells largely attenuated SC79-induced ROS scavenging ability and cytoprotection against OGD/re-oxygenation. Together, we conclude that activation of Akt by SC79 protects myocardial cells from OGD/re-oxygenation.

Sick sinus syndrome associated with hypopituitarism: a case report and literature review.

Though an association between autoimmune diseases and sick sinus syndrome has been reported, there has been no report on the association of hypopituitarism and sick sinus syndrome. Herein, we provide the first case report of hypopituitarism accompanying sick sinus syndrome in a 51-year-old woman presented to our hospital with syncope due to cardiac arrest. The patient was successfully managed by pacemaker installation and hormone replacement therapy.

Assessment of short-term prognosis by sinus heart rate turbulence in patients with unstable angina.

The aim of this study was to explore the correlation between sinus heart rate turbulence (HRT) and short-term prognosis in patients with unstable angina (UA). Seventy-five patients with UA received Holter monitoring for 24 h, within 48 h of hospitalization to obtain parameters of HRT, including turbulence onset (TO) and turbulence slope (TS), as well as parameters of heart rate variability (HRV), including standard deviation of all NN intervals (SDNN) and average R-R interval. The left ventricular ejection fraction (LVEF) was measured with an ultrasound cardiogram. Patients were divided into a stable group and a refractory group based on the prognosis during a 7- to 21-day hospital stay. The correlation between the prognosis and each risk factor was analyzed. Of the 75 patients with UA, the pathogenetic condition was stable in 50 patients (stable group) and cardiac events occurred in 25 patients (refractory group). Univariate analysis indicated that the risk factors of short-term poor prognosis of UA include TS ≤2.5 msec/R-R, age ≥70 years, LVEF <40% and SDNN <70 msec. Logistic multivariate regression analysis revealed that only TS ≤2.5 msec/R-R and LVEF <40% were independent risk factors of short-term poor prognosis. Our study revealed that weakening or disappearance of HRT is an independent predictor of short-term poor prognosis in patients with UA.

Meta-analysis of the therapeutic effects of various methods for the treatment of chronic atrial fibrillation.

The aim of this study was to analyze the therapeutic effects of various methods for the treatment of chronic atrial fibrillation (AF). Randomized controlled trials (RCT) concerning drug therapy and catheter ablation for the treatment of chronic AF were retrieved. The RevMan 5.1 software package was used for the meta-analysis. A total of 20 papers were assessed in this study. The results of the analysis indicated that the success rate was lower [odds ratio (OR), 8.94; 95% confidence interval (CI), 4.70-17.02; P<0.0001] and the relapse rate was higher (OR, 0.07, 95% CI, 0.05-0.10; P<0.0001) for drug therapy compared with that for catheter ablation. With regard to different catheter ablation procedures, the success rate for pulmonary vein antrum isolation (PVAI) was lower compared with that for PVAI plus complex fractionated atrial electrogram (CFAE; OR, 0.53; 95% CI, 0.37-0.78; P=0.0001). Pulmonary vein isolation (PVI) plus left atrial ablation (LAA) had a higher success rate compared with PVI alone (OR, 2.79; 95% CI, 1.59-4.88, P=0.0003). There was not identified to be a significant difference in the success rates between PVAI and CFAE (OR, 2.05; 95% CI, 0.06-205.74; P=0.76) or between PVI and circumferential pulmonary vein isolation (CPVI; OR, 0.94; 95% CI, 0.29-3.00; P=0.91). All the funnel plots of publication bias were essentially symmetrical. In conclusion, the success rate was higher and the relapse rate was lower for catheter ablation compared with drug therapy. Among the different procedures of catheter ablation, there were no significant differences in success rate between two single procedures; however, the success rates were higher for the combined methods compared with those for the single methods.