[Show abstract][Hide abstract] ABSTRACT: Background
Deceleration capacity (DC) is a newly found predictor of mortality after myocardial infarction. Age-, gender-, and circadian rhythm–related differences in DC may limit its predictive value, which should be considered in clinical settings.MethodsDC, average heart rate, and HRV parameters, including 24 hours, awaking state (15:00–20:00) and sleeping mode (00:00–05:00) strips from 24 hours Holter recordings in 636 subjects without heart diseases were examined. Heart rate variability was analyzed in time domains (standard deviation of all normal-to-normal intervals [SDNN], normal-to-normal RR intervals in all 5-minute segments [SDANN], and root mean square successive difference [RMSSD]).ResultsThe DC, SDNN, SDANN, RMSSD, and heart rate decreased with age. Deceleration capacity was significantly lower in patients greater than 50 years of age. The largest decrease of SDNN, SDANN, and RMSSD occurred in patients 30–39 years of age. The values of SDNN, SDANN, and DC of women were lower than that of men in the young and middle-aged groups, but age-related decrease of DC in men was greater than that in women. Heart rate of women was significantly higher than that of men in younger subjects, especially in a sleeping mode. There were higher values of DC and RMSSD during sleeping than that during a waking state.Conclusions
The age, gender, and circadian rhythm may be useful when evaluating cardiac autonomic function and need to be considered when evaluating DC and HRV in clinical and scientific researches.
Annals of Noninvasive Electrocardiology 08/2014; · 1.08 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The major structure elements of the AMP-activated protein kinase (AMPK) are α, β, and γ sunbunits. Mutations in γ2 subunit (PRKAG2) have been associated with a cardiac syndrome including inherited ventricular preexcitation, conduction disorder and hypertrophy mimicking hypertrophic cardiomyopathy. The aim of the present study was to identify PRKAG2 syndrome among patients presenting with left ventricular hypertrophy (LVH).
Nineteen unrelated subjects with unexplained LVH were clinically and genetically evaluated. Among 4 patients with bradycardia, manifestations of preexcitation were only found in a 19 year old male who also developed congestive heart failure 3 years later. Electrophysiological study of this case identified the coexistence of an AV accessory pathway and AV conduction defect. Histological analysis of his ventricular tissue isolated by biopsy confirmed excessive glycogen accumulation, prominent myofibrillar disarray and interstitial fibrosis. Direct sequencing of his DNA revealed a heterozygous mutation in PRKAG2 consisting of an A-to-G transition at nucleotide 1453 (c.1453A>G), predicting a substitution of a glutamic acid for lysine at highly-conserved residue 485 (p.Lys485Glu, K485E), which was absent in his unaffected family members and in 215 healthy controls. To assess the role of K485 in the structure and function of the protein, computational modeling calculations and conservation analyses were performed. Electrostatic calculations indicate that K485 forms a salt bridge with the conserved D248 residue in the AMPK β subunit, which is critical for proper regulation of the enzyme, and the K485E mutant disrupts the connection.
Our study identifies a novel de novo PRKAG2 mutation in a young, in which progression of the disease warrants close medical attention. It also underlines the importance of molecular screening of PRKAG2 gene in patients with unexplained LVH, ventricular preexcitation, conduction defect, and/or early onset of heart failure.
PLoS ONE 01/2013; 8(5):e64603. · 3.53 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To observe the effects of aspirin on nuclear factor kappaB (NF-kappaB)-DNA binding activity and on the expression of cyclooxygenase-2 (COX-2) in atherosclerotic plaque so as to explore its antiatherosclerotic mechanism.
Thirty-six New Zealand male rabbits were randomly divided into 3 equal groups: high-cholesterol (HC) group, fed with food high in cholesterol and perfused into the empty stomach daily with distilled water for 12 weeks, high-cholesterol and aspirin (HC + A) group, fed with food high in cholesterol and perfused into the empty stomach daily with aspirin solution, and normal control (NC) group, fed with normal food and perfused into the empty stomach daily with distilled water, before the experiment, and 4, 8, and 12 weeks after the beginning of experiment peripheral blood samples were collected. The serum lipids were detected with enzymatic assays; and enzyme-linked immunosorbent assay was used to detect the level of high sensitive C-reactive protein (hs-CRP). By the end of experiment the rabbits were killed to take out the specimens of aorta to observe the neointima thickness and plaque area of aorta. Electrophoretic mobility shift assay was used to detect the NF-kappaB-DNA binding activity, and immunohistochemistry and morphometry were performed to observe the expression of COX-2 protein, the neointima thickness and plaque area of aorta respectively in all three groups.
The levels of serum lipids, hs-CRP, NF-kappaB-DNA binding activity, expression of COX-2 protein, and neointima thickness and plaque area of aorta in the HC and HC + A groups were all significantly higher than those in the NC group (P < 0.05 -0.01). There was no significant differences in the serum lipids between the HC and HC + A groups (all P > 0.05), however, the levels of hs-CRP, NF-kappaB-DNA binding activity, expression of COX-2 protein, and neointima thickness and plaque area of aorta of the HC + A group were (5.14 +/- 0.32) microg/ml, (14.6 +/- 2.7) microg/ml, (0.342 +/- 0.02)A, (165 +/- 24) microm, and (24.3 +/- 7.6)% respectively, all significantly lower than those of the HC group [(9.39 +/- 0.79) microg/ml, (32.4 +/- 4.7) microg/ml, (0.572 +/- 0.061) A, (337 +/- 64) microm, and (49.5 +/- 21.3)%, all P < 0.05). By reducing the expression of COX-2.
[Show abstract][Hide abstract] ABSTRACT: In order to confirm the hypothesis that during acute hypoxia, the antiarrhythmic peptide (AAP10) could improve conductance by changing the phosphorylation state of connexin43 (Cx43), isolated perfused rat hearts were randomly divided into three groups: control, hypoxia and AAP10 (n=9 in each group). The change in Cx43 phosphorylation was tested by Western-blot; the distribution of Cx43 was observed by confocal immunofluorescence microscopy. Western-blot analysis revealed that the expression of total Cx43 protein was significantly decreased during acute hypoxia, while nonphosphorylated Cx43 (NP-Cx43) was unchanged. AAP10 could increase the expression of total Cx43 protein, but had no effects on the NP-Cx43 protein. Immunofluorescence study showed that during acute hypoxia, both total Cx43 and NP-Cx43 proteins were greatly decreased, while AAP10 only increased the expression of total Cx43 protein, but had no effect of the NP-Cx43 protein expression. These findings suggested that the decrease of intercellular communication may be associated with the reduction of phosphorylated Cx43 (p-Cx43) and translocation of NP-Cx43 from the surface of gap junction into intracellular pools during acute hypoxia. AAP10 can improve intercellular communication by enhancing phosphorylation of Cx43.
Journal of Huazhong University of Science and Technology 07/2007; 27(3):241-4. · 0.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Malignant ventricular arrhythmias can arise in a subset of congestive heart failure (CHF) patients after they undergo cardiac resynchronization therapy (CRT), thus counteracting the haemodynamic benefits typically associated with biventricular pacing. This study seeks to assess whether alteration of the ventricular transmural repolarization and conduction due to reversal of the depolarization sequence during epicardial or biventricular pacing facilitate the development of ventricular arrhythmias.
ECGs and monophasic action potential (MAP) were recorded during programmed stimulation from right ventricle (RV) endocardium (RV-Endo), left ventricle (LV) epicardium (LV-Epi), or both (biventricular, Bi-V) in 15 individuals without structural heart diseases. In patients with severe CHF and CRT (n=21), ECGs were collected during RV-Endo, LV-Epi, and Bi-V pacing. MAP duration on intracardiac electrogram, the QT, JT, and T(peak)-T(end) intervals on ECGs at different pacing sites were measured and compared. In subjects with or without structural heart disease, compared with RV-Endo pacing, LV-Epi and Bi-V pacing resulted in a longer JT (341.78+/-61.97 ms with LV-Epi, 325.86+/-59.69 ms with Bi-V vs. 286.14+/-38.68 ms with RV-Endo in CHF individuals, P<0.0001) or T(peak)-T(end) interval (121.55+/-19.88 ms with LV-Epi, 117.71+/-42.63 ms with Bi-V vs. 102.28+/-12.62 ms with RV-Endo in normal-heart subjects, P<0.0001; 199.70+/-62.44 ms with LV-Epi, 184.89+/-74.08 ms with Bi-V vs. 146.41+/-31.06 ms with RV-Endo in CHF patients, P<0.0001), in addition to prolonged myocardial repolarization time and delayed endocardial activation. During follow-up, sudden death and arrhythmia storm occurred in two CHF patients after CRT.
Epicardial and biventricular pacing prolong the time and increase the dispersion of myocardial repolarization and delay the transmural conduction. All of these should be considered as potential arrhythmogenic factors in CHF patients who receive CRT.
[Show abstract][Hide abstract] ABSTRACT: To evaluate the effects of antiarrhythmic peptide (AAP10) on ventricular arrhythmias in rabbits with healed myocardial infarction (OMI).
Thirty rabbits were randomly divided into three groups (n = 10 each): Sham group, left thoracotomy was performed without coronary ligation; OMI group and OMI + AAP10 group, the circumflex coronaries were ligated. Three months post operation, the electrophysiological and antiarrhythmic effects of AAP10 were assessed in the arterially perfused rabbit left ventricular wedge preparation. Sham and OMI group were perfused with Tyrode's solution and OMI + AAP10 group was perfused with Tyrode's solution + AAP10 (80 nmol/L). Transmembrane action potentials were recorded simultaneously from endocardium and epicardium together with a transmural ECG by use of 2 separate intracellular floating microelectrodes. The stimulus-response-interval (SRI) of the epicardium and the incidence of ventricular tachycardia (VT) were observed. Whole heart and left ventricular weights, the left ventricular thickness at infarct border zone were measured.
Whole heart and left ventricular weights as well as the left ventricular thickness at the infarct border zone significantly increased post infarction. VT was induced in 8 out of 10 rabbits in OMI group and in 2 out of 10 rabbits in OMI + AAP10 group (P < 0.05). SRI was also significantly shortened in OMI + AAP10 group compared to OMI group [SRI-1: (20.59 +/- 0.79) ms vs. (28.71 +/- 0.55) ms; SRI-2: (30.42 +/- 0.74) ms vs. (38.67 +/- 0.49) ms, all P < 0.01]. However, the action potential morphology and duration were similar between OMI and OMI + AAP10 groups.
The antiarrhythmic peptide (AAP10) can increase gap junctional intercellular conductance without affecting the action potential morphology and duration and decrease the incidence of inducible ventricular tachycardia.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 09/2006; 34(9):825-8.
[Show abstract][Hide abstract] ABSTRACT: The present study retrospectively evaluated the reliability of detecting atrial tachyarrhythmias (ATA), the efficacy of automatic atrial antitachycardia pacing (ATP) and the performance of atrial preventive pacing (APP) algorithms in an implanted antitachycardia DDDRP pacemaker for patients with sick sinus syndrome and paroxysmal ATA.
In all 24 patients, a DDDRP pacemaker (Medtronic AT500/AT501) was implanted. APP algorithms were switched on at the implanting physician's discretion. During each pacemaker follow-up, information was saved to disk and the ATA burden between those patients with APP algorithms switched "ON" and "OFF" were compared. Reliability of ATA detection was determined by reviewing the stored electrograms and ATP efficacy was also reviewed. Both the pacemaker memory data and manual EGM retrieval were used for the analysis.
Complication-free survival at (17.63 +/- 8.79) months was 100%. In 12 patients APP was not turned "ON" until the latest follow-up, in 6 patients APP was switched "ON" at their first visit after implantation, and in another 6 patients APP was switched "ON" after a median follow-up of 9.29 months. There were 97 367 episodes of ATA detected by the devices, of those with stored atrial electrograms the correct classification of ATA was (76.77 +/- 20.52)%. The percentage of atrial pacing with APP algorithms turned on was (87.95 +/- 20.93)%, which was significantly higher than that in patients with APP "OFF" (50.73 +/- 34.46)% (P < 0.01). ATP efficacy was (50.27 +/- 19.29)%. However, the ATA burden (14.73% vs 16.52%, or 7.52 hours vs 6.58 hours per week, P > 0.05) and the longest duration of single ATA episode (27.27 hours vs 20.75 hours, P > 0.05) were not significantly different between those patients with APP "ON" and "OFF". No proarrhythmic effect or major cardiovascular event was observed.
The antitachycardia DDDRP pacemaker correctly detects and diagnoses about 75% of the ATA episodes, while the ATP therapy successfully terminates atrial tachycardia or flutter in about 50% of attacks. However, there is no difference in ATA burden with the APP algorithms and high incidence of atrial pacing. As a non-curative therapy strategy, this high-cost device may only be used in strictly selected indication patients in addition to other treatments of ATA.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 04/2006; 34(4):333-7.
[Show abstract][Hide abstract] ABSTRACT: To observe the effects of simvastatin on nuclear factor kappaB (NF-kappaB)-DNA binding activity and on the expression of monocyte chemoattractant protein-1 (MCP-1) in atherosclerotic plaque in rabbits and to explore the anti-atherosclerotic properties beyond its lipid-lowering effects. Thirty-six New Zealand male rabbits were randomly divided into low-cholesterol group (LC), high-cholesterol group (HC), high-cholesterol+simvastatin group (HC+S) and then were fed for 12 weeks. At the end of the experiment, standard enzymatic assays, electrophoretic mobility shiftassay (EMSA), immunohistochemical staining, and morphometry were performed to observe serum lipids, NF-kappaB-DNA binding activity, MCP-1 protein expression, intima thickness and plaque area of aorta respectively in all three groups. Our results showed that the serum lipids, NF-kappaB-DNA binding activity, expression of MCP-1 protein, intima thickness, and plaque area of aorta in the LC and HC+S groups were significantly lower than those in the HC group (P<0.05). There was no significant difference in the serum lipids between the LC and HC+S groups (P>0.05), but the NF-kappaB-DNA binding activity, the expression of MCP-1 protein and the intima thickness and plaque area of aorta in the HC+S group were significantly decreased as compared to the LC group (P<0.05). This study demonstrated that simvastatin could decrease atherosclerosis by inhibiting the NF-kappaB-DNA binding activity and by reducing the expression of MCP-1 protein.
Journal of Huazhong University of Science and Technology 03/2006; 26(2):194-8. · 0.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The effects of amiodarone on transmural dispersion of ventricular effective refractory periods (ERPs) in the normal and hypertrophic canine heart were investigated in vivo. By using the programmed stimulation protocol, the ERPs of epicardium (Epi), midmyocardium (Mid) and endocardium (Endo) were measured by inserting specially-designed electrodes into the three myocardial layers before and after mainlining of amiodarone. No significant ERPs-dispersion was observed in the three layers before and after mainlining of amiodarone in the normal group. In contrast, ERPs of all the three layers were prolonged in the hypertrophic heart, while the ERPs-dispersion was reduced significantly after mainlining of amiodarone. The ERPs-dispersion was significantly increased in the hypertrophic heart but not in the normal heart using "long-short" and "short-long" interval stimulation technique. It was concluded that (1) the differences in ERPs-dispersion among the three layers were significant in hypertrophic heart, and differences were not significant in normal canine heart; (2) ERPs of each three-myocardial layers were significantly prolonged after using amiodarone, but the ERPs-dispersion decreased in hypertrophic heart and (3) the programmed extrastimulus technique of "long-short" and "short-long" intervals increased the transmural ERPs-dispersion in the hypertrophic heart.
Journal of Huazhong University of Science and Technology 02/2006; 26(2):182-4. · 0.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Benefits of cardiac resynchronization therapy (CRT) are well established. However, less is understood concerning its effects on myocardial repolarization and the potential proarrhythmic risk.
Healthy dogs (n = 8) were compared to a long QT interval (LQT) model (n = 8, induced by cesium chloride, CsCl) and a dilated cardiomyopathy with congestive heart failure (DCM-CHF, induced by rapid ventricular pacing, n = 5). Monophasic action potential (MAP) recordings were obtained from the subendocardium, midmyocardium, subepicardium, and the transmural dispersion of repolarization (TDR) was calculated. The QT interval and the interval from the peak to the end of the T wave (T(p-e)) were measured. All these characteristics were compared during left ventricular epicardial (LV-Epi), right ventricular endocardial (RV-Endo), and biventricular (Bi-V) pacing. In healthy dogs, TDR prolonged to 37.54 ms for Bi-V pacing and to 47.16 ms for LV-Epi pacing as compared to 26.75 ms for RV-Endo pacing (P < 0.001), which was parallel to an augmentation in T(p-e) interval (Bi-V pacing, 64.29 ms; LV-Epi pacing, 57.89 ms; RV-Endo pacing, 50.29 ms; P < 0.01). During CsCl exposure, Bi-V and LV-Epi pacing prolonged MAPD, TDR, and T(p-e) interval as compared to RV-Endo pacing. The midmyocardial MAPD (276.30 ms vs 257.35 ms, P < 0.0001) and TDR (33.80 ms vs 27.58 ms, P=0.002) were significantly longer in DCM-CHF dogs than those in healthy dogs. LV-Epi and Bi-V pacing further prolonged the MAPD and TDR in this model.
LV-Epi and Bi-V pacing result in prolongation of ventricular repolarization time, and increase of TDR accounted for a parallel augmentation of the T(p-e) interval, which provides evidence that T(p-e) interval accurately represents TDR. These effects are magnified in the LQT and DCM-CHF canine models in addition to their intrinsic transmural heterogeneity in the intact heart. This mechanism may contribute to the development of malignant ventricular arrhythmias, such as torsades de pointes (TdP) in congestive heart failure (CHF) patients treated with CRT.
Pacing and Clinical Electrophysiology 10/2005; 28(10):1098-106. · 1.25 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The current difference between male and female rabbit ventricular myocytes was investigated for elucidating the mechanism of longer QT interval and higher incidence of drug-associated torsade de pointes in female rabbits than in male rabbits. Whole cell patch clamp technique was used to record APD, Ito, IK,tail, IK1 and ICa,L of myocytes from left ventricular apex. There was no difference in the membrane capacitance between male and female rabbit myocytes. APD90 was longer in female rabbits (560.4+/-26.5 ms, n=15) than in male ones (489.0+/-20.7 ms, n = 14), P<0. 05. In female rabbit myocytes, IKtail, Ito, IK1 and ICa,L were 0.71+/-0.05 pA/pF (n=17), 8.28+/-1.03 pA/pF (n=18), 24.5+/-3.6 pA/pF (n=12) and 9.0+/-2.3 pA/pF (n=15) respectively. In male rabbit myocytes, they were 0.84+/-0.07 pA/pF (n=18), 8.60+/-1.20 pA/pF (n=18), 25.9+/-4.5 pA/pF (n=14) and 9.3+2.6 pA/pF (n=16) respectively. IK,tail in female rabbits was significantly lower than that of male rabbits (P<0.05), but there was no difference in Ito,IK1 and ICa.L between male rabbits and female rabbits (P>0.05). The lower IK.tail of female rabbit myocytes may contribute to the longer repolarization and the higher incidence of drug-associated torsade de pointes.
Journal of Huazhong University of Science and Technology 06/2005; 25(3):260-2. · 0.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To evaluate the effects of W-7, a calmodulin inhibitor, on transmural dispersion of repolarization (TDR), early after depolarization (EAD) and torsade de pointes (TdP) induction after administration of d-sotalol in isolated rabbit heart.
TdP was induced by d-sotalol (30 micromol/L), bradycardia, and hypokalemic (1.5 mmol/L)/hypomagnesaemic (0.35 mmol/L) solution in isolated female rabbit hearts. Thirty six rabbit hearts were divided into 4 groups (n = 9 each): d-sotalol alone, d-sotalol + W-7 (20 micromol/L), d-sotalol + W-7 (50 micromol/L), and d-sotalol + W-7 (100 micromol/L). Monophasic action potentials (MAPs) of the left ventricular epimyocardium (Epi), midmyocardium (M), and endomyocardium (Endo) were recorded simultaneously with ECG. The incidence of EAD and TdP were observed as well.
Treatment with d-sotalol alone prolonged ventricular MAP duration and QT interval, increased TDR, and evoked high incidence of EAD (9/9) and spontaneous TdP (7/9) in hypokalemic/hypomagnesaemic solution in female rabbit heart. W-7 concentration-dependently decreased incidence of TdP (4/9 in 20 micromol/L; 2/9 in 50 micromol/L; 1/9 in 100 micromol/L). This effect of W-7 coincided with the decreased incidence of EAD (5/9 in 20 micromol/L; 4/9 in 50 micromol/L; 1/9 in 100 micromol/L). However, the d-sotalol-induced prolongation of QT interval and TDR was not significantly altered by W-7 at the three concentration used.
In isolated female rabbit hearts, calmodulin antagonist W-7 suppresses d-sotalol-induced TdP without altering TDR but does suppress EAD. The effects observed with W-7 also suggest a possible important role for calmodulin-activated enzymes in the induction of TdP.
Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 05/2005; 33(4):364-8.
[Show abstract][Hide abstract] ABSTRACT: Clinical studies have demonstrated that hypertension is associated with a hypercoagulable state. In the present study, we evaluated the effect of hypofibrinogenemia with defibrase, a thrombin-like enzyme from snake venom, on the development of neurological deficit and kidney dysfunction in spontaneously hypertensive stroke-prone rats (SHRSP). Male eight-week-old SHRSP fed a high-salt diet was randomly divided into control (C) and defibrase-treated (DF) groups (n=12 in each group). Group DF received intravenously administered defibrase 1.5u/kg/day every 5 days. The effects of the treatments on blood pressure, body weight, proteinuria and the appearance of cerebral lesion signs and death were recorded. No significant differences were observed in body weight (225±4 g vs. 221±4 g) and blood pressure (239±9 mmHg vs. 242±6 mmHg) between group C and group DF at 12 weeks old (P>0.05). Treatment with defibrase significantly reduced fibrinogen level by 31% to 48% (P0.05) in SHRSP. After 12 weeks of age, the rats began to display neurological and behavioral signs accompanying stroke and die successively. The mean age at which any of the neurological and behavioral signs first appeared was 92.8±5.3 days in group C and 95.6±9.1 days in group DF(P>0.05). Stroke-related mortality was 75% in both defibrase-treated and control SHRSP at 14 weeks of age. Histologic examination revealed cerebrovascular lesions consistent with the occurrence of stroke in both control and defibrase-treated SHRSP. Our results do not support a possible role for the prevention of stroke and kidney dysfunction by defibrinogenation with defibrase in SHRSP.
American Journal of Hypertension 05/2005; · 3.40 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We have reported that carvedilol, a β-blocker with antioxidant activity, improved endothelial dysfunction in atherosclerotic rabbits induced by cholesterol and balloon injury (Jun Pu, et al. Atheroscler Suppl. 2003; 4:78). The present study examined the effect of carvedilol on activity of endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) in this animal model. Six rabbits received atherogenic diet alone, and six rabbits received atherogenic diet supplemented with carvedilol(10mg/kg/d). After treated for 1 week, they underwent balloon injury and remained on their respective diets for the further 10 weeks. Six sham untreated rabbits received standard diets as the normal control. At the end of the experiment, total cholesterol in serum, nitrate and nitrite (NOx) levels in plasma, and eNOS and iNOS activity in aortic segments were determined. Superoxide levels in aortic segments were measured by dihydroethidium staining using laser-scanning fluorescent confocal microscopy. Serum levels of total cholesterol, plasma levels of NOx, iNOS activity and dihydroethidium staining for superoxide in aortic segments were markedly increased whereas aortic eNOS activity was reduced in atherosclerotic control compared with normal control rabbits (P
[Show abstract][Hide abstract] ABSTRACT: To assess the value of echocardiography for detection of the flow-dependent epicardial coronary vasodilation, the changes in internal diameter of the left anterior descending coronary arteries (LAD) induced by reactive hyperemia were studied by echocardiography in 12 health anesthetized open-chest dogs. Reactive hyperemia was induced by brief occlusion of the left anterior descending coronary artery for 30 s followed by rapid release. The two- dimensional images of the left anterior descending coronary artery before and after reactive hyperemia with and without intracoronary infusion of N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS) were investigated. The internal diameter of LAD was measured and its percent change induced by reactive hyperemia was calculated. Our results showed that the internal diameter of LAD was 2.23 +/- 0.19 mm before intracoronary infusion of L-NAME (baseline). The internal diameter of LAD significantly increased to 2.52 +/- 0.24 mm (P < 0.01) after reactive hyperemia at baseline, and the percent change in internal diameter of LAD was (13.10 +/- 3.59)%. The internal diameter of LAD before and after reactive hyperemia under the condition of intracoronary infusion of L-NAME was not different from that before reactive hyperemia at baseline. The percent change in internal diameter of LAD was (1.07 +/- 2.97)%, and it was significantly lower than that at baseline (P < 0.001). We are led to conclude that the change in internal diameter of LAD responding to reactive hyperemia was detected sensitively by echocardiography, and this change was associated with endothelium-derived nitric oxide.
Journal of Huazhong University of Science and Technology 02/2005; 25(4):464-7. · 0.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To study the effect of of lidocaine and amiodarone on the transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia and to explore the mechanisms underlying the antiarrhythmic activity of lidocaine and amiodarone, rabbits were randomly divided into 4 groups: control group, ischemia group, lidocaine group and amiodarone group. By the monophasic action potential (MAP) recording technique, MAPs of epicardium, mid-myocardium and endocardium were simultaneously recorded across the left ventricular free wall in rabbit hearts perfused by low-flow ischemia (2.5 mL/min) in Langendorff method to study the transmural dispersion of repolarization (TDR) and arrhythmic induced by ischemia. Our results showed that TDR of three myocardial layers in ischemia group were significantly lengthened after ischemia. TDR was increased from 17.5 +/- 3.9 ms to 31.2 +/- 4.6 ms at the time that concided with the onset of sustained ventricle arrhythmic. Amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia, and no significant difference was found at other ischemia time points. 5 cases had ventriclar arrhythmia in ischemia group (62.5%), but no case in lidocaine group (P < 0.01) and only 1 case in amiodarone group had ventrilar arrhythmia (P < 0.01). No significant difference was found between amiodarone group and lidocaine group. It is concluded that TDR of of three myocardial layers increases significantly at ischemia and it is closely associated with development of ventricular arrhythmia, and amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia and has no effects at other ischemia time points.
Journal of Huazhong University of Science and Technology 01/2005; 25(4):400-3. · 0.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of canine in vivo was investigated. Twelve canines were divided into two groups randomly: acute ischemia (AI) group and sham operation (SO) group. By using the monophasic action potential (MAP) technique, MAP and effective refractory period (ERP) of the three layers myocardium were measured by specially designed plunge needle electrodes and the transmural dispersion of repolarization (TDR) and transmural dispersion of ERP (TDE) were analyzed. The results showed that in the AI group, MAP duration (MAPD) was shortened from 201.67 +/- 21.42 ms to 169.50 +/- 13.81 ms (P < 0.05), but ERP prolonged to varying degrees and TDE increased during ischemia. In the SO group, MAPD and ERP did not change almost. Among of the three layers myocardium of canine, MAPD was coincident in two groups. It was concluded that during acute ischemia, MAPD was shortened sharply, but there was no significant difference among of the three layers myocardium. The prolonged ERP was concomitant with increased TDE during acute ischemia, which may play an important role in the occurrence of arrhythmias induced by acute ischemia. These findings may have important implications in arrhythmogenesis.
Journal of Huazhong University of Science and Technology 01/2005; 25(5):497-500. · 0.78 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To investigate the effects of chronic treatment with imidapril on the electrophysiologic heterogeneous change of the noninfarcted myocardium of rabbits after myocardial infarction and the mechanism of its antiarrhythmic efficacy.
Rabbits with left coronary artery ligation were prepared and allowed to recover for 8 weeks. Myocytes were isolated from subendocardial, midmyocardial, and subepicardial regions of the noninfarcted left ventricular wall. Action potentials and calcium current were recorded using whole-cell patch clamp technique.
The action potential duration of repolarization 90 % (APD90) was more prolonged in midmyocardium rather than in subepicardium and subendocardium with healed myocardial infarction. The transmural dispersion of repolarization (TDR) was increased in the three ventricular regions. The amplitude of I(Ca-L) [was enhanced but its density was decreased in noninfarcted ventricular myocytes due to increased cell membrane capacitance. The increased differences of calcium currents among subepicardium, midmyocardium, and subendocardium were also discovered. Normalization of heterogeneous changes in repolarization after treatment with imidapril was observed and decrease of TDR in noninfarcted area was measured. Early after depolarization (EAD) events of noninfarcted midmyocardium were markedly decreased by imidapril.
Imidapril reduced the electrophysiologic heterogeneities in noninfarcted area in rabbits after myocardial infarction. This ability of imidapril may contribute to its antiarrhythmic efficacy.