Predictors of pacing-induced cardiomyopathy detection and outcomes demonstration after conduction system pacing upgrade on patients with long-term persistent atrial fibrillation.

OBJECTIVE: To identify the predictors of pacing-induced cardiomyopathy (PICM) and illustrate the safety and feasibility of conduction system pacing (CSP) upgrade on patients with long-term persistent atrial fibrillation (AF). METHODS: All patients with long-term persistent AF and normal left ventricular ejection fraction (LVEF) ≥50% were consecutively enrolled from January 2008 to December 2017, and all the patients with atrioventricular block (AVB) and high right ventricular pacing (RVP) percentage of at least 40%. The predictors of PICM were identified, and patients with PICM were followed up for at least 1 year regardless of CSP upgrade. Cardiac performances and lead outcomes were investigated in all patients before and after CSP upgrade. RESULTS: The present study included 139 patients, out of which 37 (26.62%) developed PICM, resulting in a significant decrease in the left ventricular ejection fraction (LVEF) from 56.11 ± 2.56% to 38.10 ± 5.81% (p< .01). The median duration for the development of PICM was 5.43 years. Lower LVEF (≤52.50%), longer paced QRS duration (≥175 ms), and higher RVP percentage (≥96.80%) were identified as independent predictors of PICM. Furthermore, the morbidity of PICM progressively increased with an increased number of predictors. The paced QRS duration (183.90 ± 22.34 ms vs. 136.57 ± 20.71 ms, p < .01), LVEF (39.35 ± 2.71% vs. 47.50 ± 7.43%, p < .01), and left ventricular end-diastolic diameter (LVEDD) (55.53 ± 5.67 mm vs. 53.20 ± 5.78 mm, p = .03) improved significantly on patients accepting CSP upgrade. CSP responses and complete reverse remodeling (LVEF ≥50% and LVEDD < 50 mm) were detected in 80.95% (17/21) and 42.9% (9/21) of patients. The pacing threshold (1.52 ± 0.78 V/0.4 ms vs. 1.27 ± 0.59 V/0.4 ms, p = .16) was stable after follow-up. CONCLUSION: PICM is very common in patients with long-term persistent AF, and CSP upgrade was favorable for better cardiac performance in this patient population.

Brady-arrhythmias in patients with atrial fibrillation and heart failure of reduced ejection fraction: is his-bundle pacing superior to biventricular pacing？.

OBJECTIVE: To investigate the efficacy and safety of His-bundle pacing (HBP) compared with the traditional biventricular pacing (BVP) on patients with brady-arrhythmias, who suffer from permanent atrial fibrillation (AF) and heart failure with reduced ejection fraction (HFrEF). METHODS: All patients with brady-arrhythmias, permanent AF and HFrEF were continuously enrolled from January 2017 to July 2019 and followed up for at least 12 months. The differences in QRS duration (QRSd), New York Heart Association (NYHA) classification, left ventricular ejection fraction (LVEF), tricuspid regurgitation grade, mitral regurgitation grade, left ventricular end-diastolic diameter (LVEDD), and left atrial size were compared. RESULTS: A total of 52 patients were enrolled: 37 patients were with HBP and 15 patients with BVP. There was no electrode dislodged, perforation, infection or thrombosis during the follow-up of 18.12 ± 4.45 months. The success rate for HBP implantation was 88.10%. The capture threshold of his-bundle and the threshold of the left ventricular lead remained stable during follow-up. LVEF increased to higher than 50% in 11 patients with HBP (29.73%). The NYHA classification (both p < .001), LVEF (both p < .001) and LVEDD improved significantly during the follow-up in both groups. NYHA (p = .030), LVEF (p = .013), and LVEDD (p = .003) improved in patients with HBP compared with BVP. CONCLUSION: HBP was safe and more effective in improving the cardiac function and remodeling in patients with brady-arrhythmias, permanent AF and HFrEF compared with BVP.

Comparison of cryoballoon ablation for atrial fibrillation guided by real-time three-dimensional transesophageal echocardiography vs. contrast agent injection.

BACKGROUND: Pulmonary vein (PV) occlusion generally depends on repetitive contrast agent injection when cryoballoon ablation for atrial fibrillation (AF). The present study was to compare the effect of cryoballoon ablation for AF guided by transesophageal echocardiography (TEE) vs. contrast agent injection. METHODS: Eighty patients with paroxysmal AF (PAF) were enrolled in the study. About 40 patients underwent cryoballoon ablation without TEE (non-TEE group) and the other 40 underwent cryoballoon ablation with TEE for PV occlusion (TEE group). In the TEE group during the procedure, PVs were displayed in 3-dimensional images to guide the balloon to achieve PV occlusion. The patients were followed up at regularly scheduled visits every 2 months. RESULTS: No differences were identified between the groups in regard to the procedure time and cryoablation time for each PV. The fluoroscopy time (6.7 ±â€Š4.2 min vs. 17.9 ±â€Š5.9 min, P < 0.05) and the amount of contrast agent (3.0 ±â€Š5.1 mL vs.18.1 ±â€Š3.4 mL, P < 0.05) in the TEE group were both less than the non-TEE group. At a mean of 13.0 ±â€Š3.3 mon follow-up, success rates were similar between the TEE group and non-TEE group (77.5% vs. 80.0%, P = 0.88). CONCLUSIONS: Cryoballoon ablation with TEE for occlusion of the PV is both safe and effective. Less fluoroscopy time and a lower contrast agent load can be achieved with the help of TEE for PV occlusion during procedure.

Preprodynorphin gene mutation causes progressive cardiac conduction disease: A whole-exome analysis of a pedigree.

AIMS: Progressive cardiac conduction disease (PCCD) is a rare heart disease that usually shows familial inheritance. Potential genetic risk factors for PCCD have been mostly limited to genes that encode ion channels, cardiac transcription factors, T-box transcription factors, gap junction proteins, energy metabolism regulators and structural proteins. MAIN METHODS: Subjects in the present study came from a family who exhibited the autosomal dominant inheritance of PCCD. The primary proband had syncope and an electrocardiogram typical for PCCD, which started in the left bundle branch block, and passed to the atrioventricular block. The patient received a permanent pacemaker in 2013. Pathogenic mutations in the proband's family were identified using whole-exome sequencing and Sanger sequencing. KEY FINDINGS: The results for the family members were verified using Sanger sequencing, while the results for healthy unrelated individuals were verified using SNaPShot. All patients in the family shared two adjacent missense mutations in the preprodynorphin (PDYN) gene (c.581A > T, c.580G > C; p.D194L). SIGNIFICANCE: The PDYN double mutation c.581A > T and c.580G > C (p.D194L) may be linked to the onset of familial PCCD. The effects of these mutations on electrophysiology require further investigation.

Serum and salivary ferritin and Hepcidin levels in patients with chronic periodontitis and type 2 diabetes mellitus.

BACKGROUND: Iron disorder and abnormal expression of hepcidin play important roles in many diseases, but it is still unclear in chronic periodontitis (CP) and type 2 diabetes mellitus (T2DM). We aimed to assess ferritin and hepcidin levels in serum and saliva of CP patients with or without T2DM. METHODS: Serum and unstimulated whole saliva samples were collected from 88 participants, who were categorized into 4 groups based on the presence or absence of CP or T2DM. Demographics and general health parameters were recorded. Full-mouth clinical periodontal parameters including probing pocket depth, clinical attachment loss, bleeding index, and plaque index were recorded. Chemiluminescence microparticle immunoassay and enzyme-linked immunosorbent assay were used to detect ferritin and hepcidin concentrations, respectively, in serum and saliva. RESULTS: Serum ferritin and hepcidin levels in the CP and CP with T2DM groups were higher than in the control group (P < 0.05). Serum hepcidin and serum ferritin are linear correlated (P < 0.001). Serum hepcidin/ferritin values in the CP with T2DM group were significantly lower than those in the T2DM and control groups. Moreover, salivary ferritin levels in the CP and T2DM groups were higher than those in the control group (P < 0.05). There was positively correlation between salivary ferritin and serum ferritin (P = 0.017). Hepcidin concentrations were relatively low in saliva. CONCLUSIONS: These results suggest that iron overload and hepcidin inadequacy existed in CP with T2DM patients. Salivary ferritin might provide a reference for body iron load. TRIAL REGISTRATION: ChiCTR-ROC-17012780.

Novel Role for the Immunoproteasome Subunit PSMB10 in Angiotensin II-Induced Atrial Fibrillation in Mice.

Angiotensin II (Ang II) and inflammation are associated with pathogenesis of atrial fibrillation (AF), but the underlying molecular mechanisms of these events remain unknown. The immunoproteasome has emerged as a critical regulator of inflammatory responses. Here, we investigated its role in Ang II-induced AF in immunosubunit PSMB10 (also known as ß2i or LMP10) knockout (KO) mice. AF was induced by Ang II infusion (2000 ng/min per kg). PSMB10 expression and trypsin-like activity were increased in atrial tissues and serum from Ang II-treated mice or serum from patients with AF. Moreover, Ang II-infused wild-type (WT) mice had a higher AF and increased atrial fibrosis, reactive oxygen species production, and inflammation compared with saline-treated WT animals. These effects were attenuated in PSMB10 KO mice but were aggravated in recombinant adeno-associated virus serotype 9-PSMB10-treated mice. Administration of IKKß-specific inhibitor IMD 0354 reduced Ang II-induced AF, reactive oxygen species production, inflammation, and NF-kB (nuclear factor-kB) activation. Mechanistically, Ang II infusion upregulated PSMB10 expression to promote PTEN (phosphatase and tensin homolog deleted on chromosome ten) degradation and AKT1 activation, which not only activated TGF-ß-Smad2/3 signaling leading to cardiac fibrosis but also induced IKKß activation and ubiquitin-mediated degradation of IkBα ultimately resulting in activation of NF-kB target genes (IL [interleukin]-1ß, IL-6, NOX [NADPH oxidase] 2, NOX4, and CX43 [connexin 43]). Overall, our study identifies immunosubunit PSMB10 as a novel regulator that contributes to Ang II-induced AF and suggests that inhibition of PSMB10 may represent a potential therapeutic target for treating hypertensive AF.

Elevated Circulating Fibrocytes Is a Marker of Left Atrial Fibrosis and Recurrence of Persistent Atrial Fibrillation.

BACKGROUND: In atrial fibrillation (AF), a more extensively fibrotic left atrium (LA) provides a substrate for arrhythmias and increases risk of relapse following ablation. Fibrocytes are bone marrow-derived circulating mesenchymal progenitors that have been identified in the atrium of patients with AF who have valvular diseases. The present study investigates the associations between circulating fibrocytes and LA fibrosis or the prevalence of recurrence after ablation in patients with persistent AF. METHODS AND RESULTS: We measured the proportion, differentiation, and migration of circulating fibrocytes from patients with persistent AF (n=40), those with paroxysmal AF (n=30), and sinus rhythm controls (n=30). LA low-voltage (fibrosis) area was identified by an electroanatomic mapping system, and patients were followed up for 1 year after ablation. The relationship between circulating fibrocyte percentage and LA low-voltage area or recurrence was assessed by multivariate regression analysis. Circulating fibrocyte percentage positively associated with LA low-voltage area in the persistent AF group, and circulating fibrocyte (≥4.05%) was a significant predictor of 1-year recurrence after ablation. Cultured fibrocytes exhibited enhanced potential of differentiation in the persistent AF group (67.58±1.54%) versus the paroxysmal AF group (56.67±1.52%) and sinus rhythm controls (48.43±1.79%). Furthermore, expression of fibroblast activation markers and cell migratory ability were also elevated in differentiated fibrocytes from patients with persistent AF. Transforming growth factor ß1 and stromal cell-derived factor 1 were elevated in the plasma of patients with persistent AF and were shown to promote fibrocyte differentiation and migration, respectively. CONCLUSIONS: In patients with persistent AF, increased circulating fibrocytes served as a marker of LA fibrosis and recurrence.

Genetic and Pharmacologic Inhibition of the Chemokine Receptor CXCR2 Prevents Experimental Hypertension and Vascular Dysfunction.

BACKGROUND: The recruitment of leukocytes to the vascular wall is a key step in hypertension development. Chemokine receptor CXCR2 mediates inflammatory cell chemotaxis in several diseases. However, the role of CXCR2 in hypertension development and the underlying mechanisms remain unknown. METHODS: Angiotensin II (490 ng·kg-1·min-1) or deoxycorticosterone acetate (DOCA) salt-induced mouse hypertensive models in genetic ablation, pharmacologic inhibition of CXCR2, and adoptive bone marrow transfer mice were used to determine the role of CXCR2 in hypertension (measured by radiotelemetry and tail-cuff system), inflammation (verified by flow cytometry and quantitative real-time polymerase chain reaction [PCR] analysis), vascular remodeling (studied by haematoxylin and eosin and Masson's trichrome staining), vascular dysfunction (assessed by aortic ring), and oxidative stress (indicated by nicotinamide adenine dinucleotide phosphate [NADPH] oxidase activity, dihydroethidium staining, and quantitative real-time PCR analysis). Moreover, the blood CXCR2+ cells in normotensive controls and hypertension patients were analyzed by flow cytometry. RESULTS: Angiotensin II significantly upregulated the expression of CXCR2 mRNA and protein and increased the number of CD45+ CXCR2+ cells in mouse aorta (n=8 per group). Selective CXCR2 knockout (CXCR2-/-) or pharmacological inhibition of CXCR2 markedly reduced angiotensin II- or DOCA-salt-induced blood pressure elevation, aortic thickness and collagen deposition, accumulation of proinflammatory cells into the vascular wall, and expression of cytokines (n=8 per group). CXCR2 inhibition also ameliorated angiotensin II-induced vascular dysfunction and reduced vascular superoxide formation, NADPH activity, and expression of NADPH oxidase subunits (n=6 per group). Bone marrow reconstitution of wild-type mice with CXCR2-/- bone marrow cells also significantly abolished angiotensin II-induced responses (n=6 per group). It is important to note that CXCR2 blockade reversed established hypertension induced by angiotensin II or DOCA-salt challenge (n=10 per group). Furthermore, we demonstrated that CXCR2+ proinflammatory cells were higher in hypertensive patients (n=30) compared with normotensive individuals (n=20). CONCLUSIONS: Infiltration of CXCR2+ cells plays a pathogenic role in arterial hypertension and vascular dysfunction. Inhibition of CXCR2 pathway may represent a novel therapeutic approach to treat hypertension.

Circulating E3 ligases are novel and sensitive biomarkers for diagnosis of acute myocardial infarction.

Ubiquitin ligase (E3) is a decisive element of the ubiquitin-proteasome system (UPS), which is the main pathway for intracellular protein turnover. Recently, circulating E3 ligases have been increasingly considered as cancer biomarkers. In the present study, we aimed to determine if cardiac-specific E3 ligases in circulation can serve as novel predictors for early diagnosis of acute myocardial infarction (AMI). By screening and verifying their tissue expression patterns with microarray and real-time PCR analysis, six of 261 E3 ligases, including cardiac-specific Rnf207 and cardiac- and muscle-enriched Fbxo32/atrogin-1, Trim54/MuRF3, Trim63/MuRF1, Kbtbd10/KLHL41, Asb11 and Asb2 in mouse heart, were selected for the present study. In the AMI rats, the levels of five E3 ligases including Rnf207, Fbxo32, Trim54, Trim63 and Kbtbd10 in the plasma were significantly increased compared with control animals. Especially, the plasma levels of Rnf207 was markedly increased at 1 h, peaked at 3 h and decreased at 6-24 h after ligation. Further evaluation of E3 ligases in AMI patients confirmed that plasma Rnf207 level increased significantly compared with that in healthy people and patients without AMI, and showed a similar time course to that in AMI rats. Simultaneously, plasma level of cardiac troponin I (cTnI) was measured by ELISA assays. Finally, receiver operating characteristic (ROC) curve analysis indicated that Rnf207 showed a similar sensitivity and specificity to the classic biomarker troponin I for diagnosis of AMI. Increased cardiac-specific E3 ligase Rnf207 in plasma may be a novel and sensitive biomarkers for AMI in humans.

The impact of hypertension on the electromechanical properties and outcome of catheter ablation in atrial fibrillation patients.

BACKGROUND: Although hypertension is associated with atrial fibrillation (AF), the impact of hypertension on the electromechanical properties and outcome of catheter ablation in AF patients is unclear. METHODS: AF patients [n=213, 136 paroxysmal AF (PAF) patients and 77 persistent AF patients] undergoing circumferential pulmonary vein (PV) isolation guided by CARTO mapping were enrolled, and then were divided into normotension group and hypertension group. Several left atrial (LA) electroanatomical parameters determined by the CARTO system were compared between groups. RESULTS: The LA bipolar voltage was lower in PAF patients with than without hypertension (1.44±1.09 vs. 1.92±0.76 mV, P=0.048); a significant difference was also observed in persistent AF patients. Hypertension significantly increased the size of the LA scar and low-voltage zones (LVZs) in both PAF and persistent AF patients. However, hypertension did not significantly affect recurrence in either PAF or persistent AF patients. The LA bipolar voltage was higher in PAF patients without recurrence than in those with recurrence (1.77±1.01 vs. 1.29±0.93 mV, P=0.048); a significant difference was also observed in persistent AF patients. PAF and persistent AF patients with AF recurrence had significantly larger LA scar and LVZs than patients without recurrence. CONCLUSIONS: Hypertension has a significant impact on the LA electromechanical properties in AF patients, and the LA substrate has an important influence on the outcome of catheter ablation.

[Long term outcome of atrial fibrillation patients with KCNA5 and NPPA mutations post circumferential pulmonary vein ablation].

OBJECTIVE: The outcome of atrial fibrillation patients with genetic mutations post ablation was not well evaluated. METHODS AND RESULTS: Three atrial fibrillation patients with evidence of mutations in KCNA5 and NPPA post successful circumferential pulmonary vein ablation were included. Mutation in KCNA5 was found in one male patient with paroxysmal atrial fibrillation. He was free of atrial fibrillation post ablation after 46 months follow-up. Mutations in NPPA were found in two male patients with persistent atrial fibrillation and they were free from atrial fibrillation after 64 months and 38 months follow-up post circumferential pulmonary vein ablation, roof line and mitral isthmus line ablation. CONCLUSION: Satisfactory long term results are observed in atrial fibrillation patients with KCNA5 and NPPA mutations post circumferential pulmonary vein ablation.

Effect of ventricular leads position on the clinic outcome of cardiac resynchronization therapy.

The RV lead position, either RVA or RVHS appears to make no difference in the response to CRT but the LV lead placement play a vital role.9,30 The latest activated regions of LV or areas without transmural myocardial scar for an optimal CRT are preferred. Currently, data demonstrate that no significant difference of clinical outcomes in posterior, anterior, and lateral LV lead position was found, while the ideal pacing site of the LV should be avoided in the apex position as suggested in COMPANION trial and MADIT-CRT trial. And dual-site LV CRT, which is a new technique, is also still in progress and we are looking forward to getting more updates from that.

Left ventricular 12 segmental strain imaging predicts response to cardiac resynchronization therapy.

BACKGROUND: The number of non-responders to cardiac resynchronization therapy (CRT) exposes the need for better patient selection criteria for CRT. This study aimed to identify echocardiographic parameters that would predict the response to CRT. METHODS: Forty-five consecutive patients receiving CRT-D implantation for heart failure (HF) were included in this prospective study. New York Heart Association (NYHA) class, 6-minute walk distance, electrograph character, and multi echocardiographic parameters, especially in strain patterns, were measured and compared before and six months after CRT in the responder and non-responder groups. Response to CRT was defined as a decrease in left ventricular endsystolic volume (LVESV) of 15% or more at 6-month follow up. RESULTS: Twenty-two (48.9%) patients demonstrated a response to CRT at 6-month follow-up. Significant improvement in NYHA class (P < 0.01), left ventricular end-diastolic volume (LVEDV) (P < 0.01), and 6-minute walk distance (P < 0.01) was shown in this group. Although there was an interventricular mechanical delay determined by the difference between left and right ventricular pre-ejection intervals ((42.87 ± 19.64) ms vs. (29.43 ± 18.19) ms, P = 0.02), the standard deviation of time to peak myocardial strain among 12 basal, mid and apical segments (Tε-SD) ((119.97 ± 43.32) ms vs. (86.62 ± 36.86) ms, P = 0.01) and the non-ischemic etiology (P = 0.03) were significantly higher in responders than non-responders, only the Tε-SD (OR = 1.02, 95% CI = 1.01 - 1.04, P = 0.02) proved to be a favorable predictor of CRT response after multivariate Logistic regression analysis. CONCLUSION: The left ventricular 12 segmental strain imaging is a promising echocardiographic parameter for predicting CRT response.

Substrate of complex fractionated atrial electrograms: evidence by pathologic analysis.

BACKGROUND: Ablation of complex fractionated atrial electrograms (CFAE) is an important adjunctive therapy in atrial fibrillation (AF). The present study was to elucidate the substrate underlying CFAE. METHODS: Nine adult mongrel dogs were involved in the present study. AF was induced through rapid atrial pacing with vagosympathetic nerve stimulation. CFAE was recorded during AF. Ablation was performed at CFAE sites. Based on the location of the ablation scar, the atrial specimens were divided into CFAE and non-CFAE sites. Serial sections of the atrium were stained respectively with hematoxylin-eosin (HE) and the general neural marker protein gene product 9.5 (PGP9.5). We compared the characteristics of the myocardium and the ganglionated plexus (GPs) distribution between the CFAE and non-CFAE sites. RESULTS: The myocardium of non-CFAE sites was well-organized with little intercellular substance. However, the myocardium in the CFAE site was disorganized with more interstitial tissue ((61.7 ± 24.3)% vs. (34.1 ± 9.2)%, P < 0.01). GPs in the CFAE site were more abundant than in non-CFAE sites ((34.45 ± 37.46) bundles/cm(2) vs. (6.73 ± 8.22) bundles/cm(2), P < 0.01). CONCLUSION: The heterogeneity of the myocardium and GPs distribution may account for the substrate of CFAE and serve as a potential target of ablation.

Left ventricular lead position for cardiac resynchronization: a comprehensive cinegraphic, echocardiographic, clinical, and survival analysis.

AIMS: We sought to determine the clinical and survival outcomes of cardiac resynchronization therapy (CRT) associated with left ventricular (LV) lead location. The lateral left ventricle has been considered the optimal LV lead location for CRT. METHODS AND RESULTS: Left ventricular lead cinegrams taken in 30° right and left anterior oblique views were evaluated in 457 recipients of CRT with a pacemaker or a defibrillator from 1 January 2002 to 31 December 2008 in this retrospective study. Left ventricular lead placement was prioritized at implantation into posterolateral (PL), anterolateral (AL), middle cardiac, and anterointerventricular coronary veins. Using echocardiographic LV 16-segment analysis, we grouped the leads as anterior, AL, PL, and posterior locations. New York Heart Association (NYHA) class and echocardiography were assessed before and after CRT. Clinical and survival outcomes after CRT were compared among the four LV lead locations.  Patient baseline demographic characteristics were similar among these four groups. Improvement in NYHA class was significantly greater in the AL (P= 0.04) and PL (P= 0.03) locations than in the anterior location. There was a tendency for greater improvement in LV ejection fraction among the AL (P= 0.11) and PL (P= 0.08) locations than the anterior location. Kaplan-Meier survival estimate at 4 years varied for location: AL, 72%; anterior, 48%; PL, 62%; and posterior, 72% (P= 0.003). CONCLUSION: Cardiac resynchronization therapy recipients are profiting from all lead positions. However, LV lead placed in the AL and PL positions is more preferential for achieving optimal CRT benefit than leads placed in the anterior position.

Lack of cardiac nerve sprouting after intramyocardial transplantation of bone marrow-derived stem cells in a swine model of chronic ischemic myocardium.

Previous experimental studies suggested that mesenchymal stem cell transplantation causes cardiac nerve sprouting; however, whether bone marrow (BM)-derived mononuclear cells (MNC) and endothelial progenitor cells (EPC) can also lead to cardiac nerve sprouting and alter gap junction expression remains unclear. We investigated the effect of electroanatomical mapping-guided direct intramyocardial transplantation of BM-MNC (n = 8) and CD31+EPC (n = 8) compared with saline control (n = 8) on cardiac nerve sprouting and gap junction expression in a swine model of chronic ischemic myocardium. At 12 weeks after transplantation, the distribution and density of cardiac nerve sprouting were determined by staining of tyrosine hydroxylase (TH) and growth associated protein 43(GAP-43) and expression of connexin 43 in the targeted ischemic and remote normal myocardium. After 12 weeks, no animal developed sudden death after the transplantation. There were no significant differences in the number of cells with positive staining of TH and GAP-43 in the ischemic and normal myocardium between three groups. Furthermore, expression of connexin 43 was also similar in the ischemic and normal myocardia in each group of animals (P > 0.05). The results of this study demonstrated that intramyocardial BM-derived MNC or EPC transplantation in a large animal model of chronic myocardial ischemia was not associated with increased cardiac nerve sprouting over the ischemic myocardium.

[Predictive value of HATCH score on atrial fibrillation recurrence post radiofrequency catheter ablation].

OBJECTIVE: To determine the predictive value of HATCH score on recurrence of atrial fibrillation (AF) after radiofrequency catheter ablation (RFCA). METHODS: The data of 123 consecutive AF patients (74 paroxysmal and 49 persistent AF) who underwent RFCA between April 2009 and December 2010 in our department were retrospectively analyzed. Of theses patients, 65 (52.9%) patients had HATCH score = 0, 41 (33.3%) patients had HATCH score = 1, and 17 (13.8%) patients had HATCH score ≥ 2 (HATCH = 2 in 11 patients, HATCH = 3 in 5 patients, HATCH = 4 in 1 patient). The recurrence was defined as atrial tachyarrhythmia lasting more than 30 seconds after 3 months post RFCA. The patients were divided into recurrence group and no recurrence group. Relationship between HATCH score and recurrence was observed. RESULTS: There were 43 cases in recurrence group and 80 cases in no recurrence group. After 12 months follow-up, HATCH score was significant higher in recurrence group than in non-recurrence group [(0.91 ± 0.94) score vs. (0.53 ± 0.80) score, P < 0.05]. The ratio of patients with HATCH ≥ 2 in recurrence group was higher than in non-recurrence group [23.3% (10/43) vs. 8.8% (7/80), P < 0.01]. The sensitivity and specificity of HATCH ≥ 2 to define the risk of recurrence was 25.0%, 92.4% respectively. Cumulative non-recurrence rate of patients with HATCH score ≥ 2 was lower than patients with HATCH score = 0 and 1 (P < 0.05). CONCLUSION: Higher HATCH score is associated with increased risk of AF recurrence post RFCA.

[Effects of ventricular demand and dual-chamber pacing models on the long-term clinical outcome and cardiac remodeling in patients with symptomatic bradycardia].

OBJECTIVE: To assess the effects of VVI (ventricular demand) and DDD (dual-chamber) pacing models on cardiac remodeling and the long-term clinical outcome of patients with symptomatic bradycardia. METHODS: All patients with DDD and VVI pacing models at our hospital from January 1991 to January 2003 were retrospectively analyzed. RESULTS: After a follow-up period of over 8 years in DDD and VVI groups (97 ± 27, 107 ± 44 months), left atrial diameter [(45 ± 12) mm vs (39 ± 12) mm, P < 0.01] and left ventricular end-diastolic diameter [(53 ± 11) mm vs (50 ± 9) mm, P = 0.01] in 57 patients with VVI pacing model were markedly enlarged than those at pre-implantation. And tricuspid regurgitation increased (42.4% vs 16.9%, P < 0.05). But in 59 patients with DDD pacing model, except for increased tricuspid regurgitation (42.1% vs 10.5%, P < 0.01), left atrial diameter [(37 ± 5) mm vs. (35 ± 5) mm, P = 0.07] and left ventricular end-diastolic diameter [(47 ± 7) mm vs (47 ± 5) mm, P = 0.32] were not significantly different. Mitral regurgitation significantly increased only in the VVI group (P < 0.01). The increases of left ventricular end-diastolic diameter (P = 0.04), mitral valve (P = 0.02) and tricuspid regurgitation (P < 0.01) were much more pronounced in the VVI group than those in the DDD group. Left ventricular ejection fraction (LVEF) showed no difference with that at pre-implantation (P = 0.11 in DDD group, P = 0.05 in VVI group). But the LVEF value was lower (P = 0.04) while the incidence of thrombosis was higher (P = 0.03) in the VVI group than those in the DDD group at post-implantation. However, the incidence of atrial fibrillation (P = 0.14), hospitalization (P = 0.08) and survival (P = 0.77) showed no significant difference between two groups. CONCLUSION: DDD pacing offers more benefits over VVI pacing through improving cardiac functions and arresting left ventricular remodeling. However, neither groups showed any difference in decreasing mortality rate and hospitalization. Moreover, both pacing modes fail to reverse cardiac electrical and anatomical remodeling. It is imperative to explore more physiological pacing site and rational atrioventricular (AV) interval to improve the prognosis of patients.

Genome-wide association identifies a susceptibility locus for coronary artery disease in the Chinese Han population.

Coronary artery disease (CAD) causes more than 700,000 deaths each year in China. Previous genome-wide association studies (GWAS) in populations of European ancestry identified several genetic loci for CAD, but no such study has yet been reported in the Chinese population. Here we report a three-stage GWAS in the Chinese Han population. We identified a new association between rs6903956 in a putative gene denoted as C6orf105 on chromosome 6p24.1 and CAD (P = 5.00 × 10⁻³, stage 2 validation; P = 3.00 × 10⁻³, P = 1.19 × 10⁻8 and P = 4.00 × 10⁻³ in three independent stage 3 replication populations; P = 4.87 × 10⁻¹², odds ratio = 1.51 in the combined population). The minor risk allele A of rs6903956 is associated with decreased C6orf105 mRNA expression. We report the first GWAS for CAD in the Chinese Han population and identify a SNP, rs6903956, in C6orf105 associated with susceptibility to CAD in this population.