Cardiac Electrophysiology Unit

Chiang Mai, Thailand

Cardiac Electrophysiology Unit

Chiang Mai, Thailand
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PubMed | Onze Lieve Vrouwziekenhuis Aalst, Imperial College London, Ghent University, Cardiac Electrophysiology Unit and 3 more.
Type: Journal Article | Journal: PloS one | Year: 2016

Recent efforts to increase CRT response by multiSPOT pacing (MSP) from multiple bipols on the same left ventricular lead are still inconclusive.The Left Ventricular (LV) MultiSPOTpacing for CRT (iSPOT) study compared the acute hemodynamic response of MSP pacing by using 3 electrodes on a quadripolar lead compared with conventional biventricular pacing (BiV).Patients with left bundle branch block (LBBB) underwent an acute hemodynamic study to determine the %change in LV+dP/dtmax from baseline atrial pacing compared to the following configurations: BiV pacing with the LV lead in a one of lateral veins, while pacing from the distal, mid, or proximal electrode and all 3 electrodes together (i.e. MSP). All measurements were repeated 4 times at 5 different atrioventricular delays. We also measured QRS-width and individual Q-LV durations.Protocol was completed in 24 patients, all with LBBB (QRS width 17120 ms) and 58% ischemic aetiology. The percentage change in LV+dP/dtmax for MSP pacing was 31.03.3% (MeanSE), which was not significantly superior to any BiV pacing configuration: 28.93.2% (LV-distal), 28.32.7% (LV-mid), and 29.53.0% (LV-prox), respectively. Correlation between LV+dP/dtmax and either QRS-width or Q-LV ratio was poor.In patients with LBBB MultiSPOT LV pacing demonstrated comparable improvement in contractility to best conventional BiV pacing. Optimization of atrioventricular delay is important for the best performance for both BiV and MultiSPOT pacing NTC01883141.

Marcos-Alberca P.,Hospital Clynico San Carlos | Sanchez-Quintana D.,University of Extremadura | Cabrera J.A.,Hospital Quiro | Farre J.,Cardiac Electrophysiology Unit | And 5 more authors.
European Heart Journal Cardiovascular Imaging | Year: 2014

ObjectivesThe aim of this study was to examine the feasibility of transthoracic two-dimensional (2D)-echocardiography in defining the cavo-tricuspid isthmus (CTI) anatomy and its value concerning the ease of catheter ablation of isthmic atrial flutter (AF).MethodsCTI analysis was accomplished in 39 cases: 16 necropsy specimens and 23 patients. Sixteen were patients with isthmus-dependent AF and seven controls with other supraventricular re-entrant tachycardias. Two-dimensional transthoracic echocardiography and a right atrium angiogram were performed before radiofrequency catheter ablation (RFCA).ResultsThe measurements of the CTI with angiography were compared with those taken with echocardiography and correlation was excellent (r= 0.91; P < 0.0001). In normal patients, the dimension of the vestibular thickness was successfully compared and validated with the histological examination of the necropsy specimens: histology median 6.8 mm, range 4.4-10.5 vs. echo median 6.2 mm, range 5.4-8.7; P: NS. Vestibular thickness was greater in complex than in simple RFCA (13.6 ± 1.9 mm vs. 10.0 ± 2.3 mm; P = 0.01). When vestibular thickness ≥11.5 mm, the ablation prone to be complex (sensitivity 83.3%, specificity 80%, positive predictive value 71.4%, and negative predictive value 88.9%).ConclusionsTwo- dimensional transthoracic echocardiography clearly depicts the inferior isthmus and, displaying the thickness of the tricuspid vestibule, it was related with complexity of the ablation procedure in isthmus-dependent AF. © 2013 The Author.

Pongkan W.,Chiang Mai University | Pongkan W.,Cardiac Electrophysiology Unit | Chattipakorn S.C.,Chiang Mai University | Chattipakorn N.,Chiang Mai University | Chattipakorn N.,Cardiac Electrophysiology Unit
PLoS ONE | Year: 2015

Background: Although testosterone deficiency is associated with increased risks of heart disease, the benefits of testosterone therapy are controversial. Moreover, current understanding on the cardiac effect of testosterone during cardiac ischemia-reperfusion (I/R) periods is unclear. We tested the hypothesis that testosterone replacement attenuates the impairment of left ventricular (LV) function and heart rate variability (HRV), and reduces the infarct size and arrhythmias caused by I/R injury in orchiectomized (ORX) rats. Methodology: ORX or sham-operated male Wistar rats (n = 24) were randomly divided and received either testosterone (2 mg/kg, subcutaneously administered) or the vehicle for 8 weeks. The ejection fraction (EF) and HRV were determined at baseline and the 4th and 8th week. I/R was performed by left anterior descending coronary artery ligation for 30 minutes, followed by a 120-minute reperfusion. LV pressure, arrhythmia scores, infarct size and cardiac mitochondrial function were determined. Results: Prior to I/R, EF and HRV were impaired in the ORX group, but were restored in the testosterone-treated group. During I/R, arrhythmia scores and the infarct size were greater, and cardiac mitochondrial function was impaired, whereas the time to 1st VT/VF onset and the LV end-systolic pressure were decreased in the ORX group when compared to the sham group. Testosterone replacement attenuated the impairment of these parameters in ORX rats during I/R injury, but did not show any benefit or adverse effect in non-ORX rats. Conclusions: Testosterone replacement restores cardiac function and autonomic regulation, and exerts cardioprotective effects during the I/R period via mitochondrial protection in ORX rats. © 2015 Pongkan et al.

Phrommintikul A.,Chiang Mai University | Sivasinprasasn S.,Chiang Mai University | Sivasinprasasn S.,Cardiac Electrophysiology Unit | Lailerd N.,Chiang Mai University | And 5 more authors.
European Journal of Clinical Investigation | Year: 2010

Background Despite its proposed cardioprotective effect, the role of plasma urocortin in acute myocardial infarction (AMI) remains unknown. We investigated plasma profile of urocortin in AMI patients and evaluated its long-term prognostic performance. Material and methods Sixty-six AMI patients and 21 healthy subjects were included in this study. Blood samples for urocortin were collected on days 0 (onset), 1, 3 and 5 and at 3 and 6 months. Primary endpoint was mortality within 1 year of follow-up. Secondary endpoint was combined death and nonfatal adverse cardiac events (i.e. myocardial reinfarction, urgent revascularization or hospitalization due to heart failure) within 1 year. Results During follow-up at 1 year, 38 (57·6%) patients were alive without cardiac events, nine (13·6%) had nonfatal cardiac events and 17 (25·8%) died. Plasma urocortin in AMI patients were increased on days 0, 1, 3 and 5 (P < 0·05 vs. control). The receiver-operating characteristic curve showed an area under curve (AUC) of day 0 urocortin to be 0·750 with 95% confidence interval (CI) of 0·619-0·881 (P = 0·004), whereas AUC of NT-proBNP was 0·857 (95% CI, 0·722-0·992; P = 0·003). Sensitivity values for predicting the mortality of urocortin NT-proBNP and a combined urocortin and NT-proBNP were 0·81 (95% CI, 0·54-0·95), 0·86 (95% CI, 0·42-0·99) and 1·0 (95% CI, 0·56-1·0), respectively. Conclusions Plasma urocortin level is elevated in AMI patients for 5 days from onset. High plasma urocortin within 24 h after the onset is associated with increased mortality. Combined urocortin and NT-proBNP enhance prognostic performance in AMI patients. © 2010 Stichting European Society for Clinical Investigation Journal Foundation.

Kanlop N.,Chiang Mai University | Shinlapawittayatorn K.,Chiang Mai University | Sungnoon R.,Chiang Mai University | Weerateerangkul P.,Chiang Mai University | And 3 more authors.
Canadian Journal of Physiology and Pharmacology | Year: 2010

Previous reports demonstrated that cilostazol, a phosphodiesterase 3 inhibitor, affected cellular electrophysiology and reduced episodes of ventricular fibrillation (VF) in patients with Brugada syndrome. However, its effects on VF induction and defibrillation efficacy have never been investigated. We tested the hypothesis that cilostazol increases the VF threshold (VFT) and decreases the upper limit of vulnerability (ULV) and the defibrillation threshold (DFT). A total of 48 pigs were randomly assigned to defibrillation and VF induction studies. The diastolic pacing threshold (DPT), VFT, ULV, DFT, and effective refractory period were determined before and after the infusion of cilostazol at 6 mg/kg, 3 mg/kg, or vehicle. The DPT was significantly increased after administration of 3 and 6 mg/kg cilostazol. The ULV and DFT were significantly decreased after administration of 6 mg/kg cilostazol only. The ULV in the 6 mg/kg group had 12% lower peak voltage and 25% lower total energy, and the DFT had 13% lower peak voltage and 25% lower total energy. The VFT was not altered in any experimental group. This study shows that cilostazol administration significantly increased the DPT, which was associated with significantly reduced DFT and ULV.

Semaming Y.,Chiang Mai University | Semaming Y.,Khon Kaen University | Kumfu S.,Chiang Mai University | Kumfu S.,Cardiac Electrophysiology Unit | And 5 more authors.
Journal of Endocrinology | Year: 2014

Oxidative stress has been shown to play an important role in the pathogenesis of diabetesinduced cardiac dysfunction. Protocatechuic acid (PCA) is a phenolic compound, a main metabolite of anthocyanin, which has been reported to display various pharmacological properties.We proposed the hypothesis that PCA exerts cardioprotection in type 1 diabetic (T1DM) rats. T1DM was induced in male Sprague-Dawley rats by a single i.p. injection of 50 mg/kg streptozotocin (STZ) and groups of these animals received the following treatments for 12 weeks: i) oral administration of vehicle, ii) oral administration of PCA at a dose of 50 mg/kg per day, iii) oral administration of PCA at a dose of 100 mg/kg per day, iv) s.c. injection of insulin at a dose of 4 U/kg per day, and v) a combination of PCA, 100 mg/kg per day and insulin, 4 U/kg per day. Metabolic parameters, results from echocardiography, and heart rate variability were monitored every 4 weeks, and the HbA1c, cardiac malondialdehyde (MDA), cardiac mitochondrial function, and cardiac BAX/BCL2 expression were evaluated at the end of treatment. PCA, insulin, and combined drug treatments significantly improved metabolic parameters and cardiac function as shown by increased percentage fractional shortening and percentage left ventricular ejection fraction and decreased low-frequency:high-frequency ratio inT1DMrats. Moreover, all treatments significantly decreased plasma HbA1c and cardiac MDA levels, improved cardiac mitochondrial function, and increased BCL2 expression. Our results demonstrated for the first time, to our knowledge, the efficacy of PCA in improving cardiac function and cardiac autonomic balance, preventing cardiac mitochondrial dysfunction, and increasing anti-apoptotic protein in STZ-induced T1DM rats. Thus, PCA possesses a potential cardioprotective effect and could restore cardiac function when combined with insulin treatment. These findings indicated that supplementation with PCA might be helpful for the prevention and alleviation of cardiovascular complications in T1DM. © 2014 Society for Endocrinology.

Kumphune S.,Naresuan University | Kumphune S.,Chiang Mai University | Chattipakorn S.,Chiang Mai University | Chattipakorn N.,Chiang Mai University | Chattipakorn N.,Cardiac Electrophysiology Unit
European Journal of Clinical Pharmacology | Year: 2012

The p38 mitogen-activated protein kinases (p38s) are Ser/Thr kinases that are activated as a result of cellular stresses and various pathological conditions, including myocardial ischemia/reperfusion. p38 activation has been shown to accentuate myocardial injury and impair cardiac function. Inhibition of p38 activation and its activity has been proposed to be cardioprotective by slowing the rate of myocardial damage and improving cardiac function. The growing body of evidence on the use of p38 inhibitors as therapeutic means for responding to heart problems is controversial, since both beneficial as well as a lack of protective effects on the heart have been reported. In this review, the outcomes from studies investigating the effect of p38 inhibitors on the heart in a wide range of study models, including in vitro, ex vivo, and in vivo models, are discussed. The correlations of experimental models with practical clinical usefulness, as well as the need for future studies regarding the use of p38 inhibitors, are also addressed. © Springer-Verlag 2011.

Ungprasert P.,Mahidol University | Srivali N.,Cardiac Electrophysiology Unit | Wijarnpreecha K.,Chiang Mai University | Wijarnpreecha K.,Columbia University | And 3 more authors.
Respirology | Year: 2014

A possible causal relationship between sarcoidosis and malignancy has been the subject of debates for decades.To better understand this association,we conducteda systematic review and meta-analysisof cohort studies that reported relative risk, hazard ratio or standardized incidence ratio with 95% confidence interval (CI) comparing the incidence of malignancy in patients with sarcoidosis versus non-sarcoidosis participants. Pooled risk ratios (RR) and 95% CI were calculated using a random-effect, generic inverse variance methodology.Five studies were identified and included in our data analyses. The pooled RR of malignancy in patients with sarcoidosis was 1.21 (95% CI: 1.04-1.40). However, when we performed a sensitivity analysis that included only studies that compared the incidence of malignancy after the first year of the diagnosis of sarcoidosis with the incidence of malignancy after the first year of index date for non-sarcoidosis controls, the pooled risk ratio decreased and did not reach statistical significance (RR 1.13, 95% CI: 0.97-1.32). Furthermore, analysis for publication bias has suggested that publication bias in favour of positive studies may be present.In conclusion,after accounting for possible detection bias and publication bias, there does not appear be a significant association between sarcoidosis and malignancy. © 2014 Asian Pacific Society of Respirology.

PubMed | Cardiac Electrophysiology Unit
Type: Journal Article | Journal: Journal of cardiovascular medicine (Hagerstown, Md.) | Year: 2011

Cilostazol is a selective phosphodiesterase 3 (PDE3) inhibitor approved by the Food and Drug Administration for treatment of intermittent claudication. It has also been used in bradyarrhythmic patients to increase heart rates. Recently, cilostazol has been shown to prevent ventricular fibrillation in patients with Brugada syndrome. Cilostazol is hypothesized to suppress transient outward potassium (Ito) current and increase inward calcium current, thus, maintaining the dome (phase 2) of action potential, decreasing transmural dispersion of repolarization and preventing ventricular fibrillation. Although many PDE3 inhibitors have been shown to increase cardiac arrhythmia in heart failure, cilostazol has presented effects that are different from other PDE3 inhibitors, especially adenosine uptake inhibition. Owing to this effect, cilostazol could be an effective cardioprotective drug, with its beneficial effects in preventing arrhythmia. In this review, the cardiac electrophysiological effects of cilostazol are presented and its possible cardioprotective effects, particularly in preventing ventricular fibrillation, are discussed, with emphasis on the need to further verify its clinical benefits.

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