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Objective: To investigate the effects of cardiac resynchronization therapy (CRT) on left ventricular (LV) diastolic function measured by speckle tracking imaging (STI) in patients with dilated cardiomyopathy (DCM)., Methods: CRT was performed in 21 DCM patients [15 male, mean age: 61.2 ± 11.2 (49-82) years].LV synchronization, LV systolic function and LV diastolic function were evaluated with conventional echocardiography, tissue Doppler imaging and STI before and 6 months after CRT.NYHA heart function was also assessed. Clinic Response to CRT was defined as improvement of more than 1 NYHA class.Response to CRT in echocardiography was defined as ≥ 15% reduction in LV end systolic volume at 6 months post CRT., Results: There were 16 responders and 5 non-responders at 6 months post CRT.In terms of diastolic function, conventional echocardiography derived deceleration time was both prolonged in non-responders and responders. At 6 months post CRT, STI derived LV isovolumetric diastolic strain rate [(0.19 ± 0.11) /s vs.(0.14 ± 0.09)/s, P < 0.001] was significantly increased while early diastolic mitral valve blood flow velocity/left ventricular isovolumetric diastolic strain rate (680 ± 600 vs.787 ± 690, P < 0.04) was significantly reduced in responder group while remained unchanged in non-responder group.Furthermore, left ventricular isovolumetric diastolic strain rate negatively correlated with plasma brain natriuretic peptide level (r = -0.68, P < 0.05)., Conclusion: In CRT responders of DCM patients, LV diastolic function is significantly improved and this change could be detected more effectively by STI derived LV diastolic function parameters.

Objective: To investigate the changes of open probability (Po) of large conductance Ca(2+)-activated K(+) channel (BK channel) in diabetic coronary smooth muscle cells and elucidate the underlying cellular electrophysiology mechanisms of coronary dysfunction., Methods: Rat coronary smooth muscle cells were isolated from control group and diabetic group. BK single channel currents were recorded by patch clamp technique in inside-out configuration. Open probabilities were calculated and compared between two groups. After exposure to DHS-1, a specific BK channel activator, Po at 0.2 and 1 µmol/L free Ca(2+) were compared between control and diabetic groups., Results: In the presence of 0.2 µmol/L free Ca(2+), the Po at baseline was significantly lower in diabetic rats than in control rats (0.0032 ± 0.0012 vs. 0.095 ± 0.036, P < 0.05). Cytoplasmic application of DSH-1 significantly increased the Po to 0.335 ± 0.096 (P < 0.05 vs. baseline) in control rats, whereas DSH-1 had no effect in diabetic rats (Po = 0.022 ± 0.018, P > 0.05 vs. baseline). In the presence of 1 µmol/L free Ca(2+), the Po at baseline was also significantly lower in diabetic rats than in control rats (0.210 ± 0.055 vs. 0.458 ± 0.077, P < 0.05). Cytoplasmic application of DHS-1 further robustly enhanced Po to 0.823 ± 0.019 (P < 0.05 vs. baseline) in control rats and to 0.446 ± 0.098 in diabetic rats (P < 0.05 vs. baseline of diabetic rats; P < 0.05 vs. control rats with DHS-1)., Conclusion: The decrease of Po of BK single channel in coronary smooth muscle cells may be a potential cause for coronary dysfunction in diabetic rats.

Objective: To observe the prognostic value of admission B-type natriuretic peptide (BNP) on outcome for patients with congestive heart failure (CHF)., Methods: Blood BNP levels, routine echocardiography and tissue Doppler image were obtained in 162 CHF patients [95 male, mean age: (71.8±3.7) years] at admission. Patients were divided into high BNP (BNP>1500 ng/L, n=104) and low BNP (BNP≤1500 ng/L, n=58) groups. All patients were followed up for 2 years and clinical characteristics, echocardiography including Doppler image and cardiovascular events results were analyzed. Data were also compared between patients with (n=48) or without (n=107) cardiovascular events., Results: Left ventricular ejection fractions (LVEF) was significantly lower [(40.9±5.6)% vs. (44.0±5.9)%, P<0.01] while the total cardiovascular events rate (49.1% vs. 21.0%, P<0.01) and cardiac mortality rate (25.5% vs. 9.0%, P<0.01) were significantly higher in high BNP group than in low BNP group. BNP level at admission in event group was significantly higher than in event-free group [(2875.4±325.7) ng/L vs. (1136.9±298.6) ng/L, P<0.000]. BNP level was positively related to Tei-index (r=0.793, P<0.001) and negatively correlated with LVEF (r=-0.57, P<0.001). Multiple logistic regression analysis demonstrated that BNP, LVEF, Tei-index and β-blocker use were independent risk factors for cardiovascular events. The area under the ROC curve for predicting cardiovascular death within 2 years in event group by BNP was 0.795 (95%CI 0.693-0.935, sensitivity: 72.31% and specificity: 84.62%, cut-off BNP value: 1910 ng/L). The event risk was 2.17 times higher in CHF patients with admission BNP>1910 ng/L compared CHF patients with admission BNP≤1910 ng/L (95%CI: 1.852-2.954, P=0.000)., Conclusion: Admission BNP level, LVEF, Tei-index and β-blocker use are independent risk factors for cardiovascular events in patients with CHF. Patients with higher admission BNP level (>1910 ng/L) is linked with worse prognosis in this patient cohort.

Objective: To evaluate left ventricular (LV) function and twist in patients with diabetic cardiovascular autonomic neuropathy (CAN) by two-dimensional speckle tracking imaging (STI)., Methods: STI was performed in 56 subjects with type 2 diabetes mellitus (DM) (35 with DM only: group A, 21 with CAN: group B) and 34 normal subjects (Control) from LV short-axis view. LV peak systolic, peak early (E') and peak late (A') diastolic circumferential strain in 18 myocardial segments were measured at the levels of mitral annulus, papillary muscle and apex and the rotation at mitral annulus and apex levels were also measured. LV peak systolic and the ratio of E' and A' of global and three levels, twist, untwisting rate and untwisting half-time were calculated., Results: In group A, compared with control group, LV peak systolic radial circumferential strain has no significant difference (P > 0.05), E'/A' was reduced (P < 0.05), twist at aortic valve closure and twist at mitral valve opening were significantly increased (P < 0.05), untwisting rate reduced, and untwisting half time delayed. In group B, compared with control group and group A, circumferential strain parameters [(-12.64 ± 6.49)% vs. (-19.11 ± 9.98)% and (-21.14 ± 10.13)%, P < 0.05] and E'/A' [(0.90 ± 0.35) vs. (1.24 ± 0.47) and (1.98 ± 0.63), P < 0.05] were significantly decreased, twist at aortic valve closure [(19.08 ± 5.62)° vs. (16.57 ± 2.84)° and (14.36 ± 4.06)°, P < 0.05] and twist at mitral valve opening [(13.99 ± 2.31)° vs. (11.36 ± 2.63)° and (9.04 ± 5.63)°, P < 0.05] were significantly increased, untwisting rate [(0.40 ± 0.28)%/ms vs. (0.46 ± 0.14)%/ms and (0.53 ± 0.21)%/ms, P < 0.05] reduced, and untwisting half time [(489.61 ± 97.14) ms vs. (445.21 ± 54.53) ms and (410.60 ± 50.23) ms, P < 0.05] delayed., Conclusion: Speckle tracking imaging could be used to evaluate early changes on LV twist deformation and LV systolic function in patients with type 2 diabetes mellitus.

Objective: To investigate the effects of docosahexaenoic acid (DHA) on sodium channel current (I(Na)) and transient outward potassium channel current (I(to)) in rat ventricular myocytes and to evaluate potential anti-arrhythmic mechanisms of DHA., Methods: I(Na) and I(to) of individual ventricular myocytes were recorded by patch-clamp technique in whole-cell configuration at room temperature. Effects of DHA at various concentrations (0, 20, 40, 60, 80, 100 and 120 micromol/L) on I(Na) and I(to) were observed., Results: (1) I(Na) was blocked in a concentration-dependent manner by DHA, stably inactivated curves were shifted to the left, and recover time from inactivation was prolonged while stably activated curves were not affected by DHA. At -30 mV, I(Na) was blocked to (1.51 ± 1.32)%, (21.13 ± 4.62)%, (51.61 ± 5.73)%, (67.62 ± 6.52)%, (73.49 ± 7.59)% and (79.95 ± 7.62)% in the presence of above DHA concentrations (all P < 0.05, n = 20), and half-effect concentration (EC(50)) of DHA on I(Na) was (47.91 ± 1.57)micromol/L. (2) I(to) were also blocked in a concentration-dependent manner by DHA, stably inactivated curves were shifted to the left, and recover time from inactivation was prolonged with increasing concentrations of DHA, and stably activated curves were not affected by DHA. At +70 mV, I(to) was blocked to (2.61 ± 0.26)%, (21.79 ± 4.85)%, (63.11 ± 6.57)%, (75.52 ± 7.26)%, (81.82 ± 7.63)% and (84.33 ± 8.25)%, respectively, in the presence of above DHA concentrations (all P < 0.05, n = 20), and the EC(50) of DHA on I(to) was (49.11 ± 2.68)micromol/L., Conclusion: The blocking effects of DHA on APD and I(to) may serve as one of the anti-arrhythmia mechanisms of DHA.

Objective: To investigate the mechanism of enhanced large conductance calcium-activated potassium channel currents (BK) in coronary smooth muscle cells (SMCs) by docosahexaenoic acid (DHA)., Methods: Coronary SMCs were isolated by enzyme digestion. Potassium channels in coronary SMCs were identified by applications of different potassium blockers. Effects of DHA and its metabolite 16, 17-epoxydocosapentaenoic acid (16, 17-EDP) on BK channels in the absence and presence of cytochrome P450 epoxygenase inhibitor SKF525A were studied by patch clamp in whole-cell configuration., Results: BK channels were widely distributed in SMCs, and BK currents in normal SMCs accounted for (64.2 ± 2.7)% of total potassium currents (n = 20). DHA could activate BK channels, and its 50% effective concentration (EC(50)) was (0.23 ± 0.03) µmol/L, however, the effect of DHA on BK channels was abolished after SMCs were incubated with cytochrome P450 epoxygenase inhibitor SKF525A. 16, 17-EDP, a metabolite of DHA, could reproduce the effects of DHA on BK channels, and its EC(50) was (19.7 ± 2.8) nmol/L., Conclusion: DHA and metabolites can activate BK channels and dilate coronary arteries through activating cytochrome P450 epoxygenase pathway.

Objective: To observe serum C4a and platelet aggregation rates changes in acute myocardial infarction (AMI) patients before and after percutaneous coronary intervention (PCI) and association with the development of no-reflow phenomenon., Methods: From June 2006 to August 2009, 119 AMI patients underwent PCI (28 cases of no-reflow group, 91 cases of reflow group) and 30 subjects with suspected coronary heart diseases and normal coronary angiography results (control group) were enrolled in this study. C4a and platelet aggregation rate were measured at 30 minutes before PCI, immediately after PCI, 30 minutes, 1 hour, 2 hour, and 6 months post PCI in AMI patients and at before coronary angiography in control subjects., Results: The levels of serum C4a at 30 minutes prior to PCI in control, no-reflow, and reflow groups were similar (P > 0.05). Platelet aggregation rate at 30 minutes prior to PCI was significantly higher in no-reflow group and reflow group than in control group (all P < 0.05). Serum C4a and platelet aggregation rates were significantly higher in no-reflow group at immediate, 30 minutes and 1 hour after PCI than at 30 minutes prior to PCI, two hours and 6 months after PCI (all P < 0.05), and were significantly higher than in reflow group at immediate, 30 minutes and 1 hour after PCI (all P < 0.05). Serum C4a and platelet aggregation rates were similar at different time points in reflow group (all P > 0.05). The levels of C4a in no-reflow group at immediate, 30 minutes and 1 hour after PCI were positively correlated with platelet aggregation rates (r = 0.91, 0.79, 0.60, respectively, all P < 0.01)., Conclusion: The transient increase on levels of C4a and platelet aggregation rate early post PCI are verified in no-reflow patients with AMI undergoing PCI.

Objective: To investigate the changes of large conductance Ca(2+)-activated K(+) channel (BK channel) on coronary smooth muscle cells from diabetic rats., Methods: Streptozotocin-induced rat diabetic animal model was used. Coronary smooth muscle cells were isolated by enzyme digestion. BK currents in control and diabetic groups were recorded by patch clamp technique in whole cell configuration, and BK channel protein expression was detected by Western blot. Calcium concentration was measured by fluorescence assay., Results: Compared with control group, BK current densities in diabetic group were significantly decreased when test potentials > 100 mV (P < 0.05). BK current densities were (275 ± 40) pA/pF in control group (n = 8) and (70 ± 10) pA/pF in diabetic group (n = 6) at 150 mV test potentials. α-subunit protein expression was similar between the groups (P > 0.05), however, β1-subunit protein expression was significantly reduced in diabetic group than in control group (P < 0.05). Calcium concentrations were significantly increased in diabetic group control group (151 ± 18) nmol/L (n = 6) than in control group (92 ± 7) nmol/L (n = 5, P < 0.05)., Conclusion: Observed β1-subunit downregulation, BK current density decrease and cytosolic calcium concentration increase in smooth muscle cells of diabetic coronary arteries may be associated with coronary dysfunction in diabetic rats.

Objective: To investigate the clinical features of severe chronic heart failure patients with normal B-type natriuretic peptide (BNP)., Methods: A total of 57 patients with severe chronic heart failure (New York Heart Association class III and IV) were included in this prospective control study from Dec. 2002 to Oct. 2009. Group A included 13 patients with normal BNP (< 100 ng/L) and group B included 44 patients with increased BNP (> 100 ng/L). Group A patients were followup for (19.6 ± 14.7) months and group B patients for (72.5 ± 17.1) months., Results: The baseline clinical characteristics of two groups were comparable. Left ventricular end diastolic diameter (LVEDd) of group A was larger than group B [(70.56 ± 4.33) mm vs.(63.73 ± 3.75) mm, P < 0.05], the left ventricular ejection fraction (LVEF) of group A was lower than group B [(24.16 ± 2.50)% vs. (28.49 ± 2.63)%, P < 0.05]. The number of patents tolerating metoprolol in group A is lower than in group B (7/13 vs. 39/44, P < 0.05), and the tolerant dose of metoprolol in group A is lower than in group B [(12.5 ± 6.25) mg/d vs. (24.20 ± 11.22) mg/d, P < 0.05]. The level of BNP in group B were significantly higher at acute stages than at remission stages [(962.73 ± 165.00) ng/L vs. (876.24 ± 167.70) ng/L, P < 0.05], but remained unchanged in group A [(74.03 ± 11.18) ng/L vs. (71.38 ± 11.68) ng/L, P > 0.05]. The mortality of group A was higher than group B (11/12 vs. 6/44, P < 0.05). The binary logistic regression analysis (backward) showed that normal B-type natriuretic peptide was an independent predictor of cardiovascular mortality in patients with severe chronic heart failure (OR = 45.488, 95%CI = 5.322 - 388.791)., Conclusion: Normal BNP in patients with severe chronic heart failure suggests the exhaustion of BNP secretion and associated poor prognosis.

Objective: to investigate the regulation in vascular tension of diabetic coronary artery by large conductance Ca(2+)-activated K(+) channel (BK channel) and to elucidate the mechanisms of coronary dysfunctions due to diabetes., Methods: regulation of vascular tension in normal coronary artery was evaluated by videomicroscopy system. Streptozotocin-induced rat diabetic animal model was established successfully by intraperitoneal injection. Coronary smooth muscle cells were isolated by enzyme digestion. The BK currents in control and diabetic groups were recorded by patch clamp technique in whole cell configuration. Changes of vascular tension in normal and diabetic coronary arteries were assayed by multi-wire myograph system., Results: more than 50% was contracted in inner diameters of coronary arteries when 100 nmol/L IBTX, a specific BK channel blocker, was applied. In comparison with normal group, the BK current densities in diabetic group significantly decreased when test potentials were more than 60 mV (P < 0.05). The BK current densities at 150 mV in normal group and diabetic group were (275 ± 40) pA/pF and (70 ± 10) pA/pF respectively. When 100 mmol/L KCl was washed out, vascular tensions of normal and diabetic coronary artery were (398 ± 38) mg and (390 ± 35) mg respectively (P > 0.05); however, when 100 nmol/L IBTX was added, the vascular tensions of normal and diabetic coronary artery were (395 ± 40) mg and (50 ± 7) mg (P < 0.05)., Conclusion: BK channels play an important role in the regulation of coronary vascular tension, whereas BK channels in diabetic coronary artery are dysfunction, BK currents decrease and vascular tensions increase.

Objective: To determine the feasibility on the left ventricular systolic synchronism and cardiac function evaluation in patients with permanent cardiac pacing by real-time three-dimensional echocardiography., Methods: Fifteen patients with sick sinus syndrome post dual-chamber pacemaker implantation were enrolled in this study. Pacemakers were programmed to AAI, DDD, and VVI respectively. After pacing for 5 minutes in each mode, participants were examined with real-time three-dimensional echocardiography. Images in different pacing modes were obtained and analyzed by the off-line Qlab 4.2 software. Parameters including global and 17-segmental volume-time curves (VTCs), dispersion of time to minimal regional volume for 16, 12, and 6 left ventricular segments (Tmsv16-s, Tmsv12-s, Tmsv6-s), and maximal difference of time to minimal regional volume for l6, 12 and 6 left ventricular segments (Tmsv16-dif, Tmsv12-dif, Tmsv6-dif), end diastolic volume (EDV), end systolic volume (ESV), left ventricular ejection fraction (LVEF) were measured respectively. Parameters of peak filling rate (PFR), regional end diastolic volume (rEDV), regional end systolic volume (rESV), and regional ejection fraction (rEF) were also calculated., Results: Left ventricular systolic synchronism as reflected by VTCs, Tmsv16-s, Tmsv12-s, Tmsv6-s, Tmsv16-dif, Tmsv12-dif and Tmsv6-dif as well as parameters reflecting ventricular function, i.e., LVEF, PFR were significantly better in AAI mode than in DDD and VVI models (all P < 0.05). All above indexes were similar between DDD and VVI models (all P > 0.05). rEFs of left inferior wall in base, septum in base and apex were significantly lower in DDD and VVI models compared that in AAI mode (P < 0.05)., Conclusion: Real-time three-dimensional echocardiography can objectively and accurately evaluate left ventricular systolic synchronism and cardiac function in patients with permanent cardiac pacing and AAI mode is superior to DDD and VVI models.

Objective: To investigate the effects of docosahexaenoic acid (DHA) on action potential (AP) and transient outward potassium current (I(to)) on ventricular myocytes of Sprague-Dawley rat., Methods: Calcium-tolerant ventricular myocytes were isolated by enzyme digestion. The changes of AP and I(to) with increasing DHA at concentrations of 0, 10, 20, 40, 60, 80, 100, 120 and 200 micromol/L were recorded by whole-cell patch clamp configuration., Results: (1) Action potential durations (APDs) were not affected by DHA at concentrations from 0 micromol/L to 30 micromol/L, while APDs were gradually prolonged in proportion with increasing DHA concentrations from 30 micromol/L to 200 micromol/L within 5 minutes and remained stable thereafter. APD(25), APD(50) and APD(75) were (7.7 +/- 2.0) ms, (21.2 +/- 3.5) ms, and (100.1 +/- 9.8) ms respectively at 100 micromol/L DHA. APD(25), APD(50), and APD(75) were (15.2 +/- 4.0) ms, (45.7 +/- 6.8) ms, and (215.6 +/- 15.7) ms respectively at 200 micromol/L DHA. (2) I(to) was gradually reduced with the increasing DHA concentrations from 10 micromol/L to 200 micromol/L. I(to) was blocked by DHA in a dose-dependent manner. I(to) current density was (30.1 +/- 7.2) pA/pF at DHA concentration of 60 micromol/L and its half-inhibition concentration was 58.3 micromol/L., Conclusion: APDs are gradually prolonged while I(to) reduced with increasing concentrations of DHA which might contribute to the anti-arrhythmia mechanisms of DHA.

Objective: To investigate the effects of different amlodipine isomers on L-type calcium current (ICa-L) and kinetics of rat ventricular myocytes., Methods: Rat ventricular myocytes were isolated by enzyme digestion. ICa-L, peak currents, I-V curves, steady state activation curves, steady state inactivation curves and recovery curves from inactivation with S-amlodipine, R-amlodipine and R, S-amlodipine at concentrations of 0.1, 0.5, 1, 5, and 10 micromol/L were recorded by whole-cell patch clamp configuration., Results: At the concentrations of 0.1, 0.5, 1, 5, and 10 micromol/L, ICa-L were blocked in a dose-dependent manner by S-amlodipine [(1.5 +/- 0.2)%, (25.4 +/- 5.3)%, (65.2 +/- 7.3)%, (78.4 +/- 8.1)%, and (94.2 +/- 5.0)%] and by R, S-amlodipine [(0.9 +/- 0.1)%, (10.4 +/- 3.2)%, (69.1 +/- 5.3)%, (75.2 +/- 7.0)%, and (81.6 +/- 6.4)%]. I-V curves were significantly shifted upward, steady state activation and inactivation curves were significantly shifted to left by S-amlodipine and R, S-amlodipine (0.1 micromol/L to 10 micromol/L). Recovery time from inactivation was also significantly prolonged by S-amlodipine [(210.1 +/- 19.5) ms, (225.2 +/- 21.3) ms, (241.7 +/- 20.3) ms, (252.3 +/- 24.2) ms, and (282.6 +/- 23.2) ms] and by R, S-amlodipine [(208.7 +/- 17.4) ms, (215.8 +/- 18.3) ms, (225.2 +/- 21.3) ms, (235.8 +/- 22.7) ms, and (252.3 +/- 24.2) ms] in a dose-dependent manner. The observed effects of S-amlodipine were more potent than those of R, S-amlodipine (P < 0.05). However, all these parameters were not affected by R-amlodipine at various concentrations (P > 0.05)., Conclusion: L-type calcium current of rat ventricular myocytes could be blocked by R, S-amlodipine and S-amlodipine in a dose-dependent manner.