A rare focal atrial tachycardia arising from the proximal middle cardiac vein: a case report.

BACKGROUND: Focal atrial tachycardia (FAT) always originates from atrium specific sites and can be successfully cured by radiofrequency (RF) ablation. However, the middle cardiac vein (MCV) is a rare site of focal atrial tachycardia. Herein, we present a case of a 20-year-old young woman with FAT. Electrophysiological examination showed FAT arising from the proximal middle cardiac vein (pMCV), and successful RF ablation was applied with a low power and short-ablation. CASE PRESENTATION: A 20-year-old woman with no structural heart disease suffered recurrent supraventricular tachycardia for 1 year. Physical examination, laboratory studies and the echocardiography results of this patient were normal. A 12-lead electrocardiogram (ECG) showed a narrow QRS and long RP tachycardia which was always triggered by a sinus rhythm. The patient underwent an electrophysiological study and found the earliest activation was in the proximal MCV (pMCV). After a low power and short-ablation, AT was terminated and noninducible by programmed pacing with or without isoproterenol infusion. CONCLUSION: This case presented a rare case of FAT arising from the pMCV. We demonstrate that low power and short-ablation are effective in AT arising from specific areas such as the coronary sinus ostium and pMCV.

MicroRNA-30c-5p protects against myocardial ischemia/reperfusion injury via regulation of Bach1/Nrf2.

MicroRNAs (miRNAs) are critical regulatory factors in myocardial ischemia/reperfusion (I/R) injury. The miRNA miR-30c-5p has been reported as a key mediator in several myocardial abnormalities. However, the precise roles and mechanisms of miR-30c-5p in myocardial I/R injury remain not well-studied. This project aimed to explore the potential function of this miRNA in mediating myocardial I/R injury. Significant induction of miR-30c-5p was observed in myocardial tissue of rats with myocardial I/R injury in vivo and cardiomyocytes with hypoxia/re­oxygenation (H/R) injury in vitro. Functional studies elucidated that forced expression of miR-30c-5p in rats effectively reduced infarct area, cardiac apoptosis, oxidative stress and inflammation induced by myocardial I/R injury. Moreover, in vitro cardiomyocytes with forced expression of miR-30c-5p were also protected from H/R-induced apoptosis, oxidative stress and inflammation. Importantly, BTB domain and CNC homology 1 (Bach1) was identified as a new target of miR-30c-5p. miR-30c-5p was shown to promote the activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) via the inhibition of Bach1. The re-expression of Bach1 reversed miR-30c-5p-mediated-cardioprotective effects against myocardial I/R injury in vivo or H/R injury in vitro. Overall, our results demonstrate that forced expression of miR-30c-5p exhibited beneficial effects against myocardial I/R injury through enhancement of Nrf2 activation via inhibition of Bach1. This work reveals a novel molecular mechanism for myocardial I/R injury at the miRNA level and suggests a therapeutic value of miR-30c-5p in treatment of myocardial I/R injury.

ITRAQ-based proteomics reveals the potential mechanism of fluoride-induced myocardial contraction function damage.

Fluorosis is a worldwide public health problem, and its adverse effects on the heart have been confirmed by many studies. Abnormal myocardial contractions are often associated with impairment of cardiac function as a cause or consequence. We designed two-part experiments to search for biomarkers and clarify the underlying molecular mechanism of fluoride on myocardial contraction. First, we used Pressure-volume Loop analysis to evaluate changes in myocardial function indexes with multiple fluoride exposure levels in mice (0, 30, 70, and 150 mg/L) exposed for 4 weeks. The results showed that fluoride exposure affects the heart pump function and reduces cardiac contractility. Then, we established a rat model of fluoride exposure (0, 30, 60, and 90 mg/L) for 6 months to carry out proteomic analysis of fluoride-induced myocardial contractile injury. Hematoxylin-eosin (H&E) staining was used to determine the severity of myocardial injury, and myocardial tissue samples were submitted for isobaric tags for relative and absolute quantitation (ITRAQ) analysis. A total of 1607 proteins were successfully identified with 294 differentially expressed proteins (DEPs) in fluoride treated groups. According to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, 12 DEPs were confirmed to be involved in pathways related to myocardial contraction. Furthermore, we constructed a protein-protein interaction (PPI) network for these 12 core DEPs to illustrate the role and location of each DEP in the myocardial contraction pathway. The results of this study are helpful for identify a potential mechanism and biomarkers of fluoride-induced myocardial contraction function damage, moreover, which can provide a new insight into the heart toxicity of fluoride in animals at the proteomics level.

[Effect of ginsenoside on fine particulate matter induced oxidative injury in human endothelial cells].

OBJECTIVE: To explore the mechanism of fine particulate matter (PM(2.5)) induced endothelial injury and the efficacy and mechanism of ginsenoside Rg1 on the inhibition of endothelium injuries in human endothelial cells exposure to PM(2.5). METHODS: Human umbilical vein endothelial cells (HUVECs) were stimulated with various concentrations PM(2.5) (0.1, 0.2, 0.4, 0.8 mg/ml) and PM(2.5) at concentration 0.8 mg/ml induced significant endothelial injury and was chosen for the main study in the presence or absence of Rg1 (0.04 mg/ml). After 24 h treatment, cell growth A value was detected through MTT, intracellular reactive oxygen species (ROS) level through fluorescence labeling probe method and HO-1, Nrf2 mRNA expression was detected by RT-PCR. RESULTS: The cell A value was significantly lower while the ROS fluorescence gray value and the average optical density ratio of HO-1 were significantly higher in PM(2.5) group than in the control group (all P < 0.05). The average optical density ratio of Nrf2 was similar between PM(2.5) group and control group (P > 0.05). The A value and the average optical density ratio of HO-1 were significantly higher while the ROS fluorescence gray value was significantly lower in co-treated PM(2.5) (0.8 mg/ml) + Rg1 (0.04 mg/ml) group than in the PM(2.5) (0.8 mg/ml) group (all P < 0.05). CONCLUSION: PM(2.5) could induce human endothelial cells injury by increasing oxidative stress which could be attenuated by ginsenoside Rg1.

Coronary hypercontractility to acidosis owes to the greater activity of TMEM16A/ANO1 in the arterial smooth muscle cells.

BACKGROUND: Severe acidosis deteriorates cardiac injury. Rat coronary arteries (RCAs) are unusually hypercontractive to extracellular (o) acidosis (EA). TMEM16A-encoded anoctamin 1 (ANO1), a Ca2+-activated chloride channel (CaCC), plays an important role in regulating coronary arterial tension. PURPOSE: We tested the possibility that the activation of CaCCs in the arterial smooth muscle cell (ASMC) contributes to EA-induced RCA constriction. METHODS: ANO1 expression was detected with immunofluorescence staining and Western blot. TMEM16A mRNA was assessed with quantitative Real-Time PCR. Cl- currents and membrane potentials were quantified with a patch clamp. The vascular tension was recorded with a myograph. Intracellular (i) level of Cl- and Ca2+ was measured with fluorescent molecular probes. RESULTS: ANO1 was expressed in all tested arterial myocytes, but was much more abundant in RCA ASMCs as compared with ASMCs isolated from rat cerebral basilar, intrarenal and mesenteric arteries. EA reduced [Cl-]i levels, augmented CaCC currents exclusively in RCA ASMCs and depolarized RCA ASMCs to a greater extent. Cl- deprivation, which depleted [Cl-]i by incubating the arteries or their ASMCs in Cl--free bath solution, decreased EA-induced [Cl-]i reduction, diminished EA-induced CaCC augmentation and time-dependently depressed EA-induced RCA constriction. Inhibitor studies showed that these EA-induced effects including RCA constriction, CaCC current augmentation, [Cl-]i reduction and/or [Ca2+]i elevation were depressed by various Cl- channel blockers, [Ca2+]i release inhibitors and L-type voltage-gated Ca2+ channel inhibitor nifedipine. ANO1 antibody attenuated all observed changes induced by EA in RCA ASMCs. CONCLUSION: The greater activity of RCA ASMC CaCCs complicated with an enhanced Ca2+ mobilization from both [Ca2+]i release and [Ca2+]o influx plays a pivotal role in the distinctive hypercontractility of RCAs to acidosis. Translation of these findings to human beings may lead to a new conception in our understanding and treating cardiac complications in severe acidosis.

The clinical effects of a new management mode for hypertensive patients: a randomized controlled trial.

BACKGROUND: The Internet, smartphones, and the application of health technology have great potential for hypertension management. We aim to evaluate a new mode of mobile health management with a social network application to guide blood pressure management in patients with hypertension. METHODS: Using a randomized controlled trial design, 120 hypertensive patients in the First Hospital of Shanxi Medical University who volunteered to participate in the study were randomly divided into an experimental group and a control group. The experimental group was divided into low, middle, or high-risk groups according to the cardiovascular risk stratification. The blood pressures of both the experimental group (the WeChat-guided new mode group) and the control group (the conventional mode group) were administered for three months. RESULTS: With intervention, both systolic blood pressure (SBP) and diastolic blood pressure (DBP) in the experimental group were significantly lower than those in the control group (P=0.016). The SBP and DBP of the experimental group after intervention were lower than those before intervention (P<0.001), which was not observed in the control group (P=0.056). There was no difference in the SBP drops in the low-risk, middle-risk, and high-risk groups (P=0.402). Similarly, no difference in DBP drop was observed (P=0.628). There were no differences in Colorado Pretrial Assessment Tool (CPAT) scores between the experimental group and the control group before intervention (P=0.509). After intervention, CPAT scores in the experimental group were higher than those in the control group (P<0.001). Before intervention, there was no significant difference in the Hypertension Patients Self-Management Behavior Rating Scale (HPSMBRS) scores, blood lipid, body mass index (BMI), and urinary microalbumin between the experimental group and the control group (P>0.05). After intervention, the HPSMBRS score in the experimental group was significantly higher than that in the control group (P<0.05). The HPSMBRS score of the experimental group after intervention was higher than before intervention, and BMI, urinary microalbumin, TC, LDL-C were lower than before intervention (P<0.05). CONCLUSIONS: This new mode of mobile health management has a good effect on blood pressure control in patients with hypertension. It provides evidence for the application of mobile information technology for hypertension patients in clinical practice.

TMEM16A-encoded anoctamin 1 inhibition contributes to chrysin-induced coronary relaxation.

BACKGROUND: Chrysin, a natural flavonoid available in honey, propolis and medicinal plants, has been shown to be vasorelaxant in some vascular beds. Proper intake of an alimental vasodilator as a food additive may be a promising strategy for prevention and treatment of coronary spasmodic disorders. PURPOSE: TMEM16A-encoded anoctamin 1 (ANO1), a Ca2+ activated Cl- channel (CaCC), plays an important role in the modulation of vascular tone. We tested the possibility that inhibition of CaCCs contributes to chrysin-induced coronary arterial relaxation. METHODS: The vascular tone of the rat coronary artery (RCA) was recorded with a wire myograph. CaCC currents were assessed using whole-cell patch clamp in arterial smooth muscle cell (ASMC) freshly isolated from RCAs. An inhibitor study was performed to explore the mechanisms underlying the vasomotor and electrophysiological effects of chrysin. RESULTS: Pre-incubation with chrysin depressed the contractions elicited by thromboxane A2 analog U46619, vasopressin (VP), depolarization and extracellular Ca2+ elevation/depolarization without significant preference among these vasoconstrictors. Besides, chrysin inhibited both intracellular Ca2+ release-dependent and extracellular Ca2+ influx-dependent components of contractions induced by U46619 or VP. In RCAs pre-contracted with U46619, VP or KCl, chrysin elicited concentration-dependent relaxations, which were weakened by Cl- -deprivation. The electrophysiological study showed that chrysin reduced ANO1-antibody-sensitive CaCC currents and depressed CaCC increments induced by U46619. Inhibitor study showed that both the vasorelaxation and the CaCC current reduction induced by chrysin were attenuated by blocking CaCCs and inhibiting cAMP/PKA and NO/PKG pathways. CONCLUSION: The present findings indicate that inhibition of RCA ASMC CaCC currents, which may be consequential following intracellular Ca2+ availability reduction and activation of cAMP/PKA and NO/cGMP signaling pathways, contributes to chrysin-induced RCA relaxation.