Relationship between abnormal vagus nerve tension and basal ganglia cerebral infarction induced paroxysmal atrial fibrillation

OBJECTIVE@#To investigate the relationship between basal ganglia cerebral infarction and paroxysmal atrial fibrillation (PAF) caused by abnormal vagus nerve tension.@*METHODS@#A total of 1483 cases of elder patients with cerebral infarction who received head CT or MRI examination during the period were enrolled, including 830 male and 613 female, with the average age as 78 years. These cases were divided into basal infarction ganglia group (n = 1045) and non-basal ganglia infarction group (n = 438) according to the anatomic site of cerebral infarction. The differences of the incidence of PAF, left atrial diameter and heart rate variability were compared between the two groups.@*RESULTS@#In basal ganglia infarction group, the incidence rate of PAF was significantly higher than that of non-basal ganglia infarction group (P 79 years basal ganglia cerebral infarction group, the incidence of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). There was no significant difference in the left atrial diameter between the basal ganglia infarction group and non-basal ganglia infarction group. Basal ganglia cerebral infarction patients with high PAF had higher heart rate variability than non-basal ganglia infarction group.@*CONCLUSION@#Elderly patients with basal ganglia infarction have high incidence of PAF. Sympathetic nerve damage in cerebral basal ganglia, increased vagal tension and cardiac vagal tension are the direct causes of PAF. The results indicates that the increased central vagal nerve tension mediated PAF probably is an indication of supplying sympathetic neurotransmitter or cardiac vagal denervation treatment.

Relationship between abnormal vagus nerve tension and basal ganglia cerebral infarction induced paroxysmal atrial fibrillation

Objective To investigate the relationship between basal ganglia cerebral infarction and paroxysmal atrial fibrillation (PAF) caused by abnormal vagus nerve tension. Methods A total of 1 483 cases of elder patients with cerebral infarction who received head CT or MRI examination during the period were enrolled, including 830 male and 613 female, with the average age as 78 years. These cases were divided into basal infarction ganglia group (n = 1 045) and non-basal ganglia infarction group (n = 438) according to the anatomic site of cerebral infarction. The differences of the incidence of PAF, left atrial diameter and heart rate variability were compared between the two groups. Results In basal ganglia infarction group, the incidence rate of PAF was significantly higher than that of non-basal ganglia infarction group (P 79 years basal ganglia cerebral infarction group, the incidence of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). There was no significant difference in the left atrial diameter between the basal ganglia infarction group and non-basal ganglia infarction group. Basal ganglia cerebral infarction patients with high PAF had higher heart rate variability than non-basal ganglia infarction group. Conclusion Elderly patients with basal ganglia infarction have high incidence of PAF. Sympathetic nerve damage in cerebral basal ganglia, increased vagal tension and cardiac vagal tension are the direct causes of PAF. The results indicates that the increased central vagal nerve tension mediated PAF probably is an indication of supplying sympathetic neurotransmitter or cardiac vagal denervation treatment.

Glucagon-like peptide-1 protects against cardiac microvascular endothelial cells injured by high glucose

OBJECTIVE@#To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose.@*METHODS@#CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis.@*RESULTS@#High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (P<0.05).@*CONCLUSIONS@#GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.

Glucagon-like peptide-1 protects against cardiac microvascular endothelial cells injured by high glucose

Objective: To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose. Methods: CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis. Results: High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (. P<0.05). Conclusions: GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.

The changes of cardioelectrical activity of rat with myocardial infarction receiving sarcoplasmic reticulum Ca(2+)-ATPase gene modified bone marrow stem cell transplantation by microelectrode array technology / 中华心血管病杂志

<p><b>OBJECTIVE</b>Therapy effects and cardiac electrical activity comparison of bone marrow stem cells (BMSCs) transplantation and sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) gene modified BMSCs transplantation after acute myocardial infarction (AMI) in rats.</p><p><b>METHODS</b>Rats with AMI were divided into 4 groups (n = 30) randomly: normal group (n = 6), saline group (control group, n = 8), BMSCs transplantation group (BMSCs group, n = 8) and SERCA2a gene modified BMSCs transplantation group (BMSCs + rAd.SERCA2a group, n = 8). After 14 days, cardiac function was evaluated by echocardiography and heart electrical activity was evaluated by electrocardiogram and microelectrode array (MEA) technology.</p><p><b>RESULTS</b>(1) The transduction ratio of rAd.SERCA2a to BMSCs were 80% to 90%. (2) Left ventricular ejection fraction on 14 days after therapy was significantly higher in BMSCs group and BMSCs + rAd.SERCA2a group than in control group (all P < 0.05). (3) QT duration was significantly shorter [(80.30 ± 6.53) ms vs. (105.31 ± 21.89) ms, P < 0.05] and ventricular premature beats less frequent in BMSCs + rAd. SERCA2a group than in the control group. (4) MEA results suggested that isolated heart beat was significantly slowed down and frequent ventricular arrhythmias and atrioventricular block were recorded in control group. The maximum field potential and field potential duration on infarcted myocardium area in BMSCs group and BMSCs + rAd.SERCA2a group were significantly longer than those in control group[the maximum field potential: (0.51 ± 0.15), (0.55 ± 0.16), (0.23 ± 0.10) mV; field potential duration: (104.5 ± 25.43), (107.67 ± 24.01), (63.00 ± 20.34) ms; all P < 0.05]. (5) The conduction time was the shortest and the cardiac electrical conduction consistency in myocardial infarction tissue was significantly improved in BMSCs + rAd.SERCA2a group.</p><p><b>CONCLUSIONS</b>BMSCs and SERCA2a gene modified BMSCs transplantation could significantly improve cardiac function and BMSCs + rAd.SERCA2a could also effectively improve electrical conduction of infarcted myocardium and attenuate the incidence of arrhythmia after myocardial infarction in rats.</p>

Impact of magnetic field exposure on cardiac autonomic tone and inducibility of atrial fibrillation in dogs / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the maximal heart rate changes, atrioventricular (A-V) conduction block and atrial fibrillation (AF) inducibility in dogs with vagosympathetic trunk exposed to electromagnetic fields (EMFs).</p><p><b>METHODS</b>The vagosympathetic trunk of adult dogs was separated and exposed to EMFs 0.043 kHz (2.87 microG, n = 5) and to EMFs 2 kHz (0.34 microG, n = 6) for two to three hours. Simultaneously, the vagosympathetic trunk was stimulated with 20 Hz frequency and 1 - 8 V intensity for 0.1 ms. Heart rate, presence of A-V conduction block and AF inducibility were determined.</p><p><b>RESULTS</b>After 5-minutes exposure to EMFs 0.043 kHz (2.87 microG), the maximal heart rate decreased 29%, the voltage applied to vagosympathetic trunk required to induce A-V conduction block decreased by 60% in experimental group versus 5% increase in control group. This effect lasted 2 to 3 hours. While vagosympathetic trunk exposure to EMFs 2 kHz (0.34 microG) was associated with significant increase in the incidence of atrial premature beats, atrial tachycardia and AF, these effects could be blocked by propranolol and atropine.</p><p><b>CONCLUSIONS</b>Our results showed that 0.043 kHz (2.87 microG) EMFs exposure might reduce while 2 kHz (0.34 microG) EMFs exposure might increase AF inducibility. Our study thus suggested autonomic nervous system of dogs could be affected by EMFs exposure and 0.043 kHz (2.87 microG) EMFs exposure might be a novel option for AF prevention.</p>

Efficacy of sequential ablation of sinus atrial node fat pad and atrial ventricular node fat pad on inducibility of atrial fibrillation evoked by vagus trunk stimulation / 中华心血管病杂志

<p><b>OBJECTIVE</b>To explore the efficacy of sequential ablation of epicardial fat pad on inducibility of atrial fibrillation (AF) evoked by stimulating vagus trunk.</p><p><b>METHODS</b>Eighteen adult mongrel dogs were randomly divided into 2 groups (n = 9 each): Group A underwent pre-ablation of sinus-atrial node fad pad (SANFP) and subsequent ablation of atria-ventricular node fad pad (AVNFP). Group B underwent pre-ablation of AVNFP and subsequent ablation of SANFP. AF was induced by high-frequency electrical stimulation of bilateral vagus trunks. The AF inducibility and effective refractory period (ERP) changes during vagus trunk stimulation were examined before and after ablation in atria and pulmonary veins.</p><p><b>RESULTS</b>(1) AF could be induced by vagus trunk stimulation and the incidence was higher during right vagus trunk (RVG) stimulation than left vagus trunk (LVG) stimulation [(60.0 ± 0.0)% vs (18.4 ± 22.1)%]. (2) SANFP ablation significantly attenuated AF inducibility with LVG stimulation and RVG stimulation at 2 V (decreased 67.0% and 72.0%, respectively). Subsequent AVNFP ablation after SANFP ablation further reduced AF inducibility with LVG and RVG stimulation at 2 V (decreased 100.0% and 95.5%, respectively). (3) AVNFP ablation (decreased 95.7% and 96.3%, respectively) and subsequent SANFP ablation after AVNFP ablation (decreased 98.0% and 100.0%, respectively) significantly attenuated AF inducibility with LVG stimulation and RVG stimulation at 2V. (4) Vagal stimulation induced ERP shortening was significantly attenuated by isolated SANFP ablation or AVNFP. Subsequent AVNFP ablation after SANFP induced significant ERP shortening in right atrial site compared with isolated SANFP ablation. However, changes of ERP shortening were similar between AVNFP ablation and subsequent SANFP ablation after AVNFP ablation.</p><p><b>CONCLUSIONS</b>Epicardial fat pad ablation reduced the AF inducibility and prolonged ERP of atria and pulmonary veins during vagus trunk stimulation. AVNFP, as the "integration centers" modulating the vagal innervation to the atria, may be the more effective target of ablation for treating AF.</p>

Metal stress-induced arrhythmia and thoracic spinal cord 1-5 nerve remodeling and myocardial electrophysiological remodeling in rats / 中华心血管病杂志

<p><b>OBJECTIVE</b>The study aimed to investigate the relationship between arrhythmia occurrence and nerve remodeling of thoracic spinal cord 1-5 nerves as well as myocardial electrophysiological remodeling in a metal stress rat model.</p><p><b>METHODS</b>Thirty SD rats (weight 180-250 g) were randomly divided into control group (n = 10), stress group (n = 10) and fluoxetine group (n = 10, 10 mg/kg i.p. for 3 weeks). Stress model (given by unpredicted chronic mild stress) was established according to Cronli's protocol. Following parameters were observed:(1) ECG waveform change and arrhythmias;(2) tissue field action potential duration (FAPD) of thoracic spinal cord 1-5 and cardiac tissue mapped by microelectrode arrays (MEA) technique;(3) myocardial growth-associated protein (GAP-43), tyrosine hydroxylase (TH), choline acetyltransferase (CHAT) distribution observed by immunofluorescence and confocal laser scanning microscope (LSCM).</p><p><b>RESULTS</b>Three weeks later: (1) The body weight, food intake, consumption of sugar water, the horizontal and vertical movement score, cleaning action of rats were significantly decreased, and fecal grains significantly increased, P-wave, P-R interval, QRS-wave and Q-T interval were significantly prolonged and heart rate was significantly reduced in stress group compared with control group (all P < 0.05). Incidence of ventricular premature beat was 80% in stress group and 0% in control group (P < 0.05). The FAPD of thoracic spinal cord 1-5 nerves [(144.25 ± 12.63)ms vs (79.56 ± 8.01)ms] and of cardiac tissue [LA(122.43 ± 19.34)ms vs (92.59 ± 7.61)ms, RA(149.89 ± 14.68)ms vs (105.18 ± 15.94)ms, LV(162.62 ± 7.04)ms vs (110.45 ± 6.92)ms, RV(152.21 ± 30.49)ms vs (131.06 ± 12.04)ms] were significantly prolonged, FAPD dispersion (FAPDd) significantly increased [thoracic spinal cord 1-5(13.3 ± 9.11)ms vs (9.36 ± 7.01)ms] in stress group compared with the control group. Disarrangement of myocardial cells, proliferation of collagen fiber, infiltration of neutrophil and lymphocytes in the cardiac tissue were also observed and distribution of GAP-43, TH and CHAT was significantly increased in stress group. (2) All these changes could be partly reversed by the treatment with fluoxetine.</p><p><b>CONCLUSION</b>Metal stress induced cardiac autonomic nerve and myocardial electrophysiological remodeling and ventricular arrhythmia in rats which could be significantly attenuated by fluoxetine in this model.</p>

Value of aVR lead four steps algorithm on differential diagnosis of wide QRS complex tachycardia / 中华心血管病杂志

<p><b>OBJECTIVE</b>The aVR lead four steps is a new algorithm for differential diagnosis of wide QRS complex tachycardia (WCT). The study explores the clinical value of this new algorithm on differential diagnosis of WCT.</p><p><b>METHODS</b>Application of aVR lead four steps to analysis the electrocardiogram of patients with WCT proved by electrophysiological study. Every step's accuracy rate, sensitivity and specificity to differential diagnosis of ventricular tachycardia (VT) were calculated. The first step diagnosed VT according to presence of an initial R wave in the aVR lead. The second step diagnosed VT according to width of an initial r or q wave > 40 ms in the aVR lead. The third step diagnosed VT according to notching on the initial downstroke of a predominantly negative QRS complex in the aVR lead. The fourth step diagnosis VT according to ventricular activation-velocity ratio (Vi/Vt) in the aVR lead, Vi/Vt ≤ 1 suggested VT. Results derived from aVR lead four steps algorithm were compared with results derived from Brugada and Vereckei four steps algorithm.</p><p><b>RESULTS</b>A total of 113 patients with WCT were analyzed (31 supraventricular tachycardia, SVT and 82 ventricular tachycardia, VT). The accuracy rate of differential diagnosis VT is 91.2%, sensitivity is 90.2% and specificity is 77.4%. The accuracy and sensitivity of the aVR lead four steps algorithm for differential diagnosis of WCT were superior to the Brugada Vereckei four steps algorithm (P < 0.05). The specificity of the Vereckei four steps algorithm was superior to aVR lead and Brugada four steps algorithm (P < 0.05), while the specificity of the aVR lead four steps algorithm was similar as Brugada four steps algorithm (P > 0.05).</p><p><b>CONCLUSIONS</b>The aVR lead four steps algorithm is associated with excellent accuracy rate, sensitivity for differential diagnosis of WCT. This algorithm is simple and could be easily learned and applied by physician.</p>

Nerve remodeling in a canine model of atrial fibrillation induced by 48 hours right atrial pacing / 中华心血管病杂志

<p><b>OBJECTIVE</b>To evaluate the nerve remodeling induced by 48 hours right atrial pacing in a canine model.</p><p><b>METHODS</b>Rapid right atrial pacing (600 beats/min) was performed in 6 mongrel dogs of either sex for 48 hours to induce sustained atrial fibrillation (AF). Six dogs without pacing served as controls. Cardiac nerves were immunocytochemically stained using anti-growth-associated protein 43 (GAP43) and anti-choline acetyltransferase (CHAT) antibodies to compare nerve sprouting and pneumogastric nerve remodeling between the 2 groups.</p><p><b>RESULTS</b>In dogs with AF, the GAP43-positive and CHAT-positive nerve densities in the left atrium, left auricular appendage, right atrium and right auricular appendage were significantly higher than in control animals (all P < 0.05). Moreover, nerve density was significantly higher in the right atrium than in the left atrium in dogs with AF. Microscopic examinations revealed an inhomogeneous distribution of cardiac nerves.</p><p><b>CONCLUSION</b>Significant nerve sprouting and pneumogastric nerve remodeling were evidenced in the right and left atrium in a canine model of sustained AF induced by 48 hours right atrial pacing.</p>

Microelectrode arrays mapped tissue field action potential duration changes of thoracic spinal cord 1 - 5 nerves and heart in chronic stress rat model / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate chronic stress induced tissue action potential and pathological changes of thoracic spinal cord 1 - 5 nerves and heart in SD rats.</p><p><b>METHODS</b>SD rats (weighing 180 - 250 g) were randomly divided into depressive group and control group (n = 10 each). Depressive model (unpredicted chronic mild stress) was established according to Gronli's protocol. The heart rhythm, tissue field action potential duration (FAPD) of thoracic spinal cord 1 - 5 nerves, atrium and ventricle were mapped by microelectrode arrays (MEA) technique. Heart was sectioned and stained with Massion and HE for pathological analysis.</p><p><b>RESULTS</b>After 3 weeks chronic stress, P wave [(35.09 +/- 7.92) ms vs. (25.43 +/- 3.38) ms, P<0.05] and Q-T interval [(114.64 +/- 35.08) ms vs. (81.93 +/- 16.35) ms, P<0.01] were significantly increased, FAPD of thoracic spinal cord 1 - 5 nerves and heart was significantly prolonged, atrial field action potential duration dispersion (FAPDd) was significantly increased, atrial premature beats (n = 2) and ventricular premature beats ( n = 3) were also recorded in rats from depressive group. Moreover, increased collagen deposition was evidenced in Massion stained myocardium and increased inflammatory cell infiltration in the heart was found by both HE stain and electron microscope from depressive rats.</p><p><b>CONCLUSION</b>Chronic mild stress could activate sympathetic nerves system, promote inflammatory cell myocardial infiltration and myocardial fibrosis, induce arrhythmias by prolonging FAPD and increasing FADPd in thoracic spinal cord 1 - 5 nerves and/or heart tissue.</p>

Cardiac field potentials and activation sequence in Langendorff perfused heart, cardiac tissue slices and cultured ventricular myocytes recorded by microelectrode arrays system / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe field potentials (FPs) and activation sequence at Langendorff perfused guinea pigs heart, SD rat cardiac tissue strips perfused by Tyrode's solution and cultured ventricular cardiomyocytes of suckling mice by microeletrode arrays (MEA) technique.</p><p><b>METHOD</b>FPs and activation sequence were recorded from perfused heart, cardiac tissue strips (5 mm x 5 mm) and cultured ventricular cardiomyocytes by MEA.</p><p><b>RESULTS</b>(1) FPs could be recorded in hearts perfused for 30 to 90 min with a heart rate 90 - 120 beats/min. FP durations of both ventricular and atrial tissue were (210 +/- 78) ms and (164 +/- 58) ms, respectively and atrial ventricular conduction time was (320 +/- 150) ms. (2) The excitability of Tyrode's solution perfused tissue strips was visible for more than 2 h, and FP durations of ventricular and atrial tissue strips were (115.80 +/- 11.61) ms and (83.71 +/- 6.48) ms, respectively. (3) Spontaneous beating frequency (150 +/- 100) beats/min and FPs could be readily recorded in cardiomyocytes cultured between 2 to 72 hours.</p><p><b>CONCLUSION</b>MEAs is a sensitive, low noise and stable technique for observing local tissue action potential and activation sequence of whole heart, cardiac tissue strips and cultured cardiomyocytes.</p>