Correlations between myocardial injury current and lead performance in His bundle pacing compared with left bundle branch area pacing and right ventricular septum pacing.

BACKGROUND: Conduction system pacing by implanting the lead in the His bundle (HBP) region or in the left bundle branch area (LBBAP) has gained popularity. Myocardial injury current (IC) is useful for predicting adequate lead fixation in right ventricular septal pacing (RVSP). OBJECTIVES AND METHODS: We compared the correlations between IC and lead performance among patients receiving HBP (n = 41), LBBAP (n = 53), and historical RVSP (n = 88). LBBAP was an alternative if optimal HBP was not achieved. A positive IC (STpost-screw-in - STpre-screw-in) was defined as > 0.2 mV or a > 25% ST elevation and prolongation of the ventricular electrograms > 10 ms from baseline. RESULTS: HBP patients with a positive IC (48%, 0.84 ± 0.4 V/0.4 ms) exhibited a similar pacing threshold to their LBBAP counterparts (76%, 0.75 ± 0.3 V/0.4 ms, p = 0.329), but a higher pacing threshold than their RVSP counterparts (67%, 0.50 ± 0.1 V/0.4 ms, p < 0.001) at implantation. The R-wave (5.70 ± 3.4 mV) and impedance (660.91 ± 140.8 Ω) were both lower than those of LBBAP (10.35 ± 6.0 mV, p = 0.002; 822.36 ± 235.8 Ω, p = 0.005) and RVSP (11.24 ± 4.9 mV, p < 0.001; 754.27 ± 126.4 Ω, p = 0.006) patients respectively at implantation. The trend of electrical parameter comparisons remained unchanged during follow-up (3.56 ± 1.4 months). Notably, HBP patients without ICs had a higher pacing threshold (1.24 ± 0.6 V/0.4 ms) compared to their LBBAP (0.73 ± 0.3 V/0.4 ms, p = 0.009) and RVSP (0.53 ± 0.1 V/0.4 ms, p < 0.001) counterparts at implantation and during follow-up. CONCLUSIONS: The detection of positive changes of myocardial ICs during HBP was associated with a better capture threshold equivalent to the LBBAP counterpart both at implantation and during short-term follow-up. Further large-scale studies with longer follow-up are necessary to confirm these findings.

First-in-human pilot trial of combined intracoronary and intravenous mesenchymal stem cell therapy in acute myocardial infarction.

Background: Acute ST-elevation myocardial infarction (STEMI) elicits a robust cardiomyocyte death and inflammatory responses despite timely revascularization. Objectives: This phase 1, open-label, single-arm, first-in-human study aimed to assess the safety and efficacy of combined intracoronary (IC) and intravenous (IV) transplantation of umbilical cord-derived mesenchymal stem cells (UMSC01) for heart repair in STEMI patients with impaired left ventricular ejection fraction (LVEF 30-49%) following successful reperfusion by percutaneous coronary intervention. Methods: Consenting patients received the first dose of UMSC01 through IC injection 4-5 days after STEMI followed by the second dose of UMSC01 via IV infusion 2 days later. The primary endpoint was occurrence of any treatment-related adverse events and the secondary endpoint was changes of serum biomarkers and heart function by cardiac magnetic resonance imaging during a 12-month follow-up period. Results: Eight patients gave informed consents, of whom six completed the study. None of the subjects experienced treatment-related serious adverse events or major adverse cardiovascular events during IC or IV infusion of UMSC01 and during the follow-up period. The NT-proBNP level decreased (1362 ± 1801 vs. 109 ± 115 pg/mL, p = 0.0313), the LVEF increased (52.67 ± 12.75% vs. 62.47 ± 17.35%, p = 0.0246), and the wall motion score decreased (26.33 ± 5.57 vs. 22.33 ± 5.85, p = 0.0180) at the 12-month follow-up compared to the baseline values. The serial changes of LVEF were 0.67 ± 3.98, 8.09 ± 6.18, 9.04 ± 10.91, and 9.80 ± 7.56 at 1, 3, 6, and 12 months, respectively as compared to the baseline. Conclusion: This pilot study shows that combined IC and IV transplantation of UMSC01 in STEMI patients with impaired LVEF appears to be safe, feasible, and potentially beneficial in improving heart function. Further phase 2 studies are required to explore the effectiveness of dual-route transplantation of UMSC01 in STEMI patients.

Usefulness of Machine Learning-Based Detection and Classification of Cardiac Arrhythmias With 12-Lead Electrocardiograms.

BACKGROUND: Deep-learning algorithms to annotate electrocardiograms (ECGs) and classify different types of cardiac arrhythmias with the use of a single-lead ECG input data set have been developed. It remains to be determined whether these algorithms can be generalized to 12-lead ECG-based rhythm classification. METHODS: We used a long short-term memory (LSTM) model to detect 12 heart rhythm classes with the use of 65,932 digital 12-lead ECG signals from 38,899 patients, using annotations obtained by consensus of 3 board-certified electrophysiologists as the criterion standard. RESULTS: The accuracy of the LSTM model for the classification of each of the 12 heart rhythms was ≥ 0.982 (range 0.982-1.0), with an area under the receiver operating characteristic curve of ≥ 0.987 (range 0.987-1.0). The precision and recall ranged from 0.692 to 1 and from 0.625 to 1, respectively, with an F1 score of ≥ 0.777 (range 0.777-1.0). The accuracy of the model (0.90) was superior to the mean accuracies of internists (0.55), emergency physicians (0.73), and cardiologists (0.83). CONCLUSIONS: We demonstrated the feasibility and effectiveness of the deep-learning LSTM model for interpreting 12 common heart rhythms according to 12-lead ECG signals. The findings may have clinical relevance for the early diagnosis of cardiac rhythm disorders.

Pulmonary vein volume and myocardial sleeve extension estimated by 3D computed tomography and voltage mapping predict arrhythmogenic triggers of paroxysmal atrial fibrillation.

PURPOSE: Relationship between pulmonary vein (PV) anatomy and the pathophysiology of paroxysmal atrial fibrillation (PAF) remains incompletely studied. The aim of this study was to determine whether PV anatomy predicts arrhythmogenic PVs. METHODS: Twenty-six consecutive PAF patients with spontaneous PAF or consistently frequent ectopic beats during electrophysiological study were enrolled. Computed tomography (CT) images for PVs were reconstructed into 3D images. The PV diameter and volume were measured based on the 3D images. The PV myocardial sleeve area was measured based on the 3D voltage mapping results. The PV myocardial sleeve area index was calculated by dividing the sleeve area of each PV by the average sleeve area of all PVs in each patient. RESULTS: The diameter and volume of the arrhythmogenic PVs were larger than those of the non-arrhythmogenic PVs (21.08 ± 4.57 mm vs. 16.47 ± 3.31 mm, P < 0.001 and 7.70 ± 3.28 cm3 vs. 4.09 ± 1.99 cm3, P < 0.001, respectively). The myocardial sleeve area and sleeve area index of the arrhythmogenic PVs were also larger than those of the non-arrhythmogenic PVs (8.62 ± 5.33 cm2 vs. 4.77 ± 3.84 cm2, P < 0.001 and 1.59 ± 0.35 vs. 0.81 ± 0.38, P < 0.001, respectively). Multivariate analysis showed the PV myocardial sleeve area index was the independent predictor for arrhythmogenic PVs (P < 0.001). CONCLUSIONS: PV size plays an important role in triggering PAF. A large myocardial sleeve extension is a powerful and independent predictor for arrhythmogenic PV, which may be useful anatomical markers to facilitate PAF ablation.

Automatic capture management may cause unnecessary battery depletion in selective his-bundle pacing.

A routine change in the automatic capture management algorithm from "adaptive" to "off or monitor" is required to conserve device longevity in a permanent pacemaker with His-bundle pacing.

Diabetes mellitus associated with an increased risk of percutaneous coronary intervention long-term adverse outcomes in Taiwan: A nationwide population-based cohort study.

AIMS: This study compared the incidence rates of patients with diabetes mellitus (DM) and patients without DM with percutaneous coronary intervention (PCI) in a national population-based cohort to determine if the patients with DM have an increased risk of adverse outcomes. METHODS: We performed a retrospective cohort study among 92,624 patients with and without DM, who underwent PCI for the first time in 2000-2008. The patients were identified from National Health Insurance Program Database through propensity score matching. Endpoints were the occurrence of PCI adverse outcomes, including myocardial infarction (MI), need for target vessel revascularization by either bypass surgery or repeat PCI, all-cause mortality or 2011/12/31. Incidence rate was calculated and hazard ratios of PCI adverse events were estimated using Cox's proportional hazard regression model. RESULTS: During the mean six-year follow up, the rates of MI (incidence rate 20.96 vs. 15.59 per 1000 person-years), bypass surgery (incidence rate 8.15 vs. 5.15 per 1000 person-years), all-cause mortality (incidence rate 6.20 vs. 4.72 per 1000 person-years), and the composite measure of MI, repeat PCI, bypass surgery, all-cause mortality (incidence rate 37.31 vs. 28.14 per 1000 person-years) were higher in patients with DM. The corresponding hazard ratios (HRs) and their 95% confidence intervals (CIs) were 1.34 (95% CI: 1.29, 1.39), 1.46 (1.38, 1.56), 1.34 (1.25, 1.44), and 1.31 (1.27, 1.35). However, the repeat PCI rate (incidence rate 2.65 vs. 2.70 per 1000 person-years); with an adjusted HR of 0.97 (0.88, 1.07) was not statistically different. CONCLUSIONS: This nationwide retrospective cohort study determined a positive correlation between PCI adverse events and DM. As the prevalence of DM and PCI continues to increase, novel treatments and intensified surveillance coronary angiography for high risk patients are needed.

Matrix metalloproteinase 1 1 G/2 G gene polymorphism is associated with acquired atrioventricular block via linking a higher serum protein level.

Limited studies are available regarding the pathophysiological mechanism of acquired atrioventricular block (AVB). Matrix metalloproteinases (MMPs) and angiotensin-converting enzyme (ACE) have been implicated in the pathogenesis of arrhythmia. However, the relationship between these molecules and acquired AVB is still unclear. One hundred and two patients with documented acquired AVB and 100 controls were studied. Gene polymorphisms of the MMP1 and ACE encoding genes were screened by the gene sequencing method or polymerase chain reaction-fragment length polymorphism assay, followed by an association study. The frequencies of the MMP1 -1607 2G2G genotype and MMP1 -1607 2 G allele were significantly higher in the AVB group than that in the controls (OR = 1.933, P = 0.027 and OR = 1.684, P = 0.012, respectively). Consistently, the level of serum MMP1 was significantly greater in acquired AVB patients than that in controls (6568.9 ± 5748.6 pg/ml vs. 4730.5 ± 3377.1 pg/ml, P = 0.019). In addition, the MMP1 2G2G genotype showed a higher MMP-1 serum level than the other genotypes (1G1G/1G2G) (7048.1 ± 5683.0 pg/ml vs. 5072.4 ± 4267.6 pg/ml, P = 0.042). MMP1 1 G/2 G gene polymorphism may contribute to determining the disease susceptibility of acquired AVB by linking the MMP serum protein level.

Inverse Correlation Between Left Atrial Appendage Function and CHA2DS2-VASc Score in Patients with Atrial Flutter.

Impaired left atrial appendage ejection fraction (LAA-EF) and peak LAA flow velocity (LAA-FV) are associated with high thromboembolic risks in patients with atrial fibrillation (AF). Herein, we examined LAA function among patients with atrial flutter (AFL) stratified by the CHA2DS2-VASc score using transesophageal echocardiography (TEE). Of 231 consecutive patients with typical AFL, 84 who fulfilled the inclusion criteria were enrolled. Among them, 57 had ongoing AFL and were divided into the isolated AFL (n = 38) and AFL with paroxysmal AF (PAF) (n = 19) groups, depending on whether they had sporadic AF before TEE. The remaining 27 patients with spontaneous sinus rhythm during TEE were designated as controls. Both the LAA-FV (31.9 cm/s vs. 51.5 cm/s, P = 0.004) and LAA-EF (28.4% vs. 36.5%, P = 0.024) measured during AFL were significantly lower in the AFL + PAF group than in the isolated AFL group. Significant inverse correlations between the CHA2DS2-VASc score and LAA-EF were identified in the AFL (P = 0.008) and AFL + PAF (P = 0.032) groups. We observed progressive LAA dysfunction in patients with AFL + PAF compared with that in patients with isolated AFL, and the LAA-EF was inversely correlated with the CHA2DS2-VASc score in these patients. Our findings may have implications on the application of thromboprophylactic therapy in patients with AFL.

Detection of Variants in Patients with Idiopathic Ventricular Fibrillation by Whole-exome Sequencing.

AIMS AND BACKGROUND: Idiopathic ventricular fibrillation (IVF) is a cause of sudden cardiac death (SCD). The frequency of mutations in disease-causing genes ranges, on average, between 16 and 48% in SCD cases. This study aimed to identify novel mutations in IVF patients without KCNQ1, KCNH2, and SCN5A mutations using whole-exome sequencing (WES). METHODS: Genomic DNA extracted from peripheral blood samples obtained from five patients with IVF and WES was used to identify mutations associated with IVF. Candidate variants were validated by Sanger sequencing. RESULTS: Four patients harbored suspected mutations in 100 inherited cardiomyopathy-and channelopathy-associated genes (e.g., TCAP, TTN, MYPN, CACNA1C, and TNNT2). All of these genetic variants have been given a dbSNP rs number; however, their clinical significance remains unknown. Bioinformatics tools predicted severe functional disruptions in the loci harboring these suspected mutations, suggesting their pivotal roles in IVF. CONCLUSIONS: This study revealed the effectiveness of WES for IVF patients without KCNQ1, KCNH2, and SCN5A mutations. Although it is difficult to interpret broad WES results, the analysis can provide insight into the etiology of a heterogeneous disease.

The Shortest QRS Duration of an Electrocardiogram Might Be an Optimal Electrocardiographic Predictor for Response to Cardiac Resynchronization Therapy.

QRS duration has been associated with the response to cardiac resynchronization therapy (CRT). However, the methods for defining QRS duration to predict the outcome of CRT have discrepancies in previous reports. The aim of this study was to determine an optimal measurement of QRS duration to predict the response to CRT.Sixty-one patients who received CRT were analyzed. All patients had class III-IV heart failure, left ventricular ejection fraction not more than 35%, and complete left bundle branch block. The shortest, longest, and average QRS durations from the 12 leads of each electrocardiogram (ECG) were measured. The responses to CRT were determined using the changes in echocardiography after 6 months. Thirty-five (57.4%) patients were responders and 26 (42.6%) patients were non-responders. The pre-procedure shortest, average, and longest QRS durations and the QRS shortening (ΔQRS) of the shortest QRS duration were significantly associated with the response to CRT in a univariate logistic regression analysis (P = 0.002, P = 0.03, P = 0.04 and P = 0.04, respectively). Based on the measurement of the area under curve of the receiver operating characteristic curve, only the pre-procedure shortest QRS duration and the ΔQRS of the shortest QRS duration showed significant discrimination for the response to CRT (P = 0.002 and P = 0.038, respectively). Multivariable logistic regression showed the pre-procedure shortest QRS duration is an independent predictor for the response to CRT.The shortest QRS duration from the 12 leads of the electrocardiogram might be an optimal measurement to predict the response to CRT.

Transforming Growth Factor-ß1 T869C Gene Polymorphism Is Associated with Acquired Sick Sinus Syndrome via Linking a Higher Serum Protein Level.

BACKGROUND: Familial sick sinus syndrome is associated with gene mutations and dysfunction of ion channels. In contrast, degenerative fibrosis of the sinus node tissue plays an important role in the pathogenesis of acquired sick sinus syndrome. There is a close relationship between transforming growth factor-ß1 mediated cardiac fibrosis and acquired arrhythmia. It is of interest to examine whether transforming growth factor-ß1 is involved in the pathogenesis of acquired sick sinus syndrome. METHODS: Overall, 110 patients with acquired SSS and 137 age/gender-matched controls were screened for transforming growth factor-ß1 and cardiac sodium channel gene polymorphisms using gene sequencing or restriction fragment length polymorphism methods. An enzyme-linked immunosorbent assay was used to determine the serum level of transforming growth factor-ß1. RESULTS: Two transforming growth factor-ß1 gene polymorphisms (C-509T and T+869C) and one cardiac sodium channel gene polymorphism (H588R) have been identified. The C-dominant CC/CT genotype frequency of T869C was significantly higher in acquired sick sinus syndrome patients than in controls (OR 2.09, 95% CI 1.16-3.75, P = 0.01). Consistently, the level of serum transforming growth factor-ß1 was also significantly greater in acquired sick sinus syndrome group than in controls (5.3±3.4 ng/ml vs. 3.7±2.4 ng/ml, P = 0.01). In addition, the CC/CT genotypes showed a higher transforming growth factor-ß1 serum level than the TT genotype (4.25 ± 2.50 ng/ml vs. 2.71± 1.76 ng/ml, P = 0.028) in controls. CONCLUSION: Transforming growth factor-ß1 T869C polymorphism, correlated with high serum transforming growth factor-ß1 levels, is associated with susceptibility to acquired sick sinus syndrome.

Prospective randomized study to assess the efficacy of site and rate of atrial pacing on long-term progression of atrial fibrillation in sick sinus syndrome: Septal Pacing for Atrial Fibrillation Suppression Evaluation (SAFE) Study.

BACKGROUND: Atrial-based pacing is associated with lower risk of atrial fibrillation (AF) in sick sinus syndrome compared with ventricular pacing; nevertheless, the impact of site and rate of atrial pacing on progression of AF remains unclear. We evaluated whether long-term atrial pacing at the right atrial (RA) appendage versus the low RA septum with (ON) or without (OFF) a continuous atrial overdrive pacing algorithm can prevent the development of persistent AF. METHODS AND RESULTS: We randomized 385 patients with paroxysmal AF and sick sinus syndrome in whom a pacemaker was indicated to pacing at RA appendage ON (n=98), RA appendage OFF (n=99), RA septum ON (n=92), or RA septum OFF (n=96). The primary outcome was the occurrence of persistent AF (AF documented at least 7 days apart or need for cardioversion). Demographic data were homogeneous across both pacing site (RA appendage/RA septum) and atrial overdrive pacing (ON/OFF). After a mean follow-up of 3.1 years, persistent AF occurred in 99 patients (25.8%; annual rate of persistent AF, 8.3%). Alternative site pacing at the RA septum versus conventional RA appendage (hazard ratio=1.18; 95% confidence interval, 0.79-1.75; P=0.65) or continuous atrial overdrive pacing ON versus OFF (hazard ratio=1.17; 95% confidence interval, 0.79-1.74; P=0.69) did not prevent the development of persistent AF. CONCLUSIONS: In patients with paroxysmal AF and sick sinus syndrome requiring pacemaker implantation, an alternative atrial pacing site at the RA septum or continuous atrial overdrive pacing did not prevent the development of persistent AF. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. UNIQUE IDENTIFIER: NCT00419640.

Comparing Survival between peritoneal dialysis and hemodialysis patients with subclinical peripheral artery disease: a 6-year follow-up.

Peripheral artery disease (PAD) is known to be an increased mortality risk in patients with end-stage renal disease (ESRD). The aim of this study was to compare patient survival between patients with subclinical PAD undergoing peritoneal dialysis (PD) and hemodialysis (HD). Subclinical peripheral artery was defined as an ankle-brachial index of less than 0.9. This study was conducted from April 2005, and the observation period ended on 30 June 2011. At the end of the follow-up, the status of all patients was assessed and data on mortality were obtained for the entire cohort. A total of 91 patients (61 HD and 30 PD) were included for analyses in this study. Mortality rate was 60.0% (18/30) for PD and 52.5% (32/61) for HD. Kaplan-Meier estimate demonstrate that PD patients had a higher mortality rate than those underwent HD (log-rank p = 0.0039). Cox regression model demonstrated that PD was an independent predictor for further mortality in ESRD patients with subclinical peripheral artery disease.(p = 0.012, HR: 1.776, 95% CI: 1.136-2.775). In multivariate analysis, the HD group still had a greater survival than PD group (p = 0.005, HR:1.916, 95% CI: 1.218-3.015). In patients with subclinical peripheral artery disease, the patient survival is better in HD patients as compared with PD patients.

Promoter polymorphism G-6A, which modulates angiotensinogen gene expression, is associated with non-familial sick sinus syndrome.

BACKGROUND: It is well known that familial sick sinus syndrome (SSS) is caused by functional alterations of ion channels and gap junction. Limited information is available on the mechanism of age-related non-familial SSS. Although evidence shows a close link between arrhythmia and the renin-angiotensin system (RAS), it remains to be determined whether the RAS is involved in the pathogenesis of non-familial SSS. METHODS: In this study, 113 patients with documented non-familial SSS and 125 controls were screened for angiotensinogen (AGT) and gap junction protein-connexin 40 (Cx40) promoter polymorphisms by gene sequencing, followed by an association study. A luciferase assay was used to determine the transcriptional activity of the promoter polymorphism. The interaction between nuclear factors and the promoter polymorphism was characterized by an electrophoretic mobility shift assay (EMSA). RESULTS: Association study showed the Cx40 -44/+71 polymorphisms are not associated with non-familial SSS; however, it indicated that four polymorphic sites at positions -6, -20, -152, and -217 in the AGT promoter are linked to non-familial SSS. Compared to controls, SSS patients had a lower frequency of the G-6A AA genotype (OR 2.88, 95% CI 1.58-5.22, P = 0.001) and a higher frequency of the G allele at -6 position (OR 2.65, 95% CI 1.54-4.57, P = 0.0003). EMSA and luciferase assays confirmed that nucleotide G at position -6 modulates the binding affinity with nuclear factors and yields a lower transcriptional activity than nucleotide A (P<0.01). CONCLUSION: G-6A polymorphism, which modulates the transcriptional activity of the AGT promoter, may contribute to non-familial SSS susceptibility.

Usefulness of pre-procedure cavotricuspid isthmus imaging by modified transthoracic echocardiography for predicting outcome of isthmus-dependent atrial flutter ablation.

BACKGROUND: Anatomic characteristics of the cavotricuspid isthmus (CTI) have been reported to be related to the outcome of atrial flutter ablation therapy. However, preprocedural evaluation of CTI anatomy using modified transthoracic echocardiography to guide atrial flutter ablation has not been well described. METHODS: Transthoracic echocardiography was prospectively performed before atrial flutter ablation in 42 patients with typical CTI-dependent atrial flutter. A modified apical long-axis view was designed to visualize and evaluate anatomic characteristics of the CTI and Eustachian ridge (ER). A prominent ER, extending from the inferior vena cava to the interatrial septum, is defined as an extensive ER. RESULTS: Twenty-eight patients had straightforward ablation procedures, and 14 patients had difficult ablation procedures. Two patients with difficult procedures had unsuccessful ablation. Multivariate analysis (using CTI length, the presence of a pouch or recess, ER morphology, and significant tricuspid regurgitation as variables) showed that the presence of extensive ER was the only independent predictor of a difficult ablation procedure. The ablation time in patients with extensive ER (n = 13) was significantly longer than in those patients with nonextensive ER (n = 29) (1,638.4 ± 1,548.3 vs 413.8 ± 195.5 sec, P = .015). The incidence of difficulty in achieving bidirectional isthmus block was also higher in patients with extensive ER (10 of 13 vs four of 29, P < .001). CONCLUSION: Preprocedural transthoracic echocardiography using a modified apical long-axis view is useful to characterize the morphology of the CTI and the ER. An extensive ER is a strong predictor for difficult ablation of CTI-dependent atrial flutter.

Atrial fibrillation linked to vascular access thrombosis in chronic hemodialysis patients.

AIM: Atrial fibrillation (AF) is characterized by the development of thromboembolic events and is more prevalent among end-stage renal disease patients than in the general population. Vascular access thrombosis (VAT) is a major morbidity in chronic hemodialysis (HD) patients; however, the association between AF and VAT is unknown. METHODS: We retrospectively reviewed chronic HD patients with functional vascular access between 1997 and 2006. The association between AF and the development of VAT was analyzed using Kaplan-Meier analysis and multivariate Cox proportional hazards regression. RESULTS: A total of 568 chronic HD patients, including 55 (9.7%) patients with AF, were reviewed and 154 (27.1%) patients developed at least one episode of VAT. Patients with AF had worse VAT-free survival than patients without AF (p< 0.001). In Cox regression, age, type of vascular access, atrial fibrillation, diabetes, hypertension, and C-reactive protein were independently linked to the development of VAT ( p= 0.049, < 0.001, < 0.001, 0.001, 0.028 and 0.045). The hazard ratios were 2.1 (95% CI: 1.00-1.03) for arteriovenous graft, 2.47 (95% CI: 1.66-3.69) for AF, 1.72 (95% CI: 1.25-2.39) for diabetes and 1.09 (95% CI: 1.00-1.18) for serum C-reactive protein (every 1 mg/dL increase), respectively. CONCLUSION: Atrial fibrillaiton is linked to the development of vascular access thrombosis in chronic hemodialysis patients and is independent of traditional VAT risk factors.

Green tea extract given before regional myocardial ischemia-reperfusion in rats improves myocardial contractility by attenuating calcium overload.

There is evidence for a negative correlation between green tea consumption and cardiovascular diseases. The aim of the present study was to examine whether green tea extract (GTE) given before regional myocardial ischemia could improve depression of myocardial contractility by preventing cytosolic Ca(2+) overload. Regional ischemia-reperfusion (IR) was induced in rats by ligating the left anterior descending branch for 20 min, then releasing the ligature. Ligation induced ventricular arrhythmias in rats without GTE pretreatment, but decreased arrhythmogenesis was seen in rats pretreated 30 min earlier with GTE (400 mg/kg). During reperfusion, arrhythmias only occurred during the initial 5 min, and GTE pretreatment had no effect. After overnight recovery, serum cTnI levels were greatly increased in control post-IR rats but only slightly elevated in GTE-pretreated post-IR rats. Myocardial contractility measured by echocardiography was still depressed after 3 days in control post-IR rats, but not in GTE-pretreated post-IR rats. No myocardial ischemic injury was seen in post-IR rats with or without GTE pretreatment. Using freshly isolated single heart myocytes, GTE was found to attenuate the post-IR injury-associated cytosolic Ca(2+) overload and modulate changes in the levels and distribution of myofibril, adherens junction, and gap junction proteins. In summary, GTE pretreatment protects cardiomyocytes from IR injury by preventing cytosolic Ca(2+) overload, myofibril disruption, and alterations in adherens and gap junction protein expression and distribution.