Evaluation of the safety and efficacy of transcatheter aortic valve implantation in patients with a severe stenotic bicuspid aortic valve in a Chinese population.

OBJECTIVE: The purpose of this study is to evaluate the safety and efficacy of transcatheter aortic valve implantation (TAVI) in patients with a severe stenotic bicuspid aortic valve (BAV) in a Chinese population. While several groups have reported the feasibility, efficacy, and safety of TAVI for patients with a BAV, worldwide experience of the technique is still limited, especially in China. METHODS: From March 2013 to November 2014, high surgical risk or inoperable patients with symptomatic severe aortic stenosis (AS) who had undergone TAVI at our institution were selected for inclusion in our study. RESULTS were compared between a BAV group and a tricuspid aortic valve (TAV) group. RESULTS: Forty patients were included in this study, 15 (37.5%) of whom were identified as having a BAV. In the BAV group, the aortic valve area was smaller ((0.47±0.13) vs. (0.59±0.14) cm(2)), the ascending aortic diameter was larger ((40.4±4.4) vs. (36.4±4.3) mm), and the concomitant aortic regurgitation was lower. No significant differences were found between the groups in the other baseline characteristics. No differences were observed either in the choice of access or valve size. The procedural success achieved in this study was 100%. There were no differences between groups in device success (86.7% vs. 88.0%), 30-d mortality (6.7% vs. 8.0%), or 30-d combined end point (13.3% vs. 12.0%). The incidences of new pacemaker implantation, paravalvular regurgitation and other complications, recovery of left ventricle ejection fraction and heart function were similar in both groups. CONCLUSIONS: Patients with a severely stenotic BAV can be treated with TAVI, and their condition after treatment should be similar to that of people with a TAV.

Dissociated pulmonary vein rhythm may predict the acute pulmonary vein reconnection post-isolation in patients with paroxysmal atrial fibrillation.

AIMS: Dissociated pulmonary vein rhythm (PVD) has been taken as a signal of PV isolation, but has been questioned recently; we assessed the relationship between PVD and acute PV reconnection after PV isolation in this study. METHODS AND RESULTS: Eighty-five consecutive patients (52 males; mean age 59±11 years) were referred for catheter ablation of drug-refractory paroxysmal AF. Following PV isolation, the presence and cycle length of PVD were recorded. Pulmonary veins were classified into veins with PVD (Group 1) and veins without PVD (Group 2). Adenosine triphosphate (ATP) was then injected during isoproterenol infusion to reveal dormant conduction gap(s), and PVs were further remapped at 30 min post-isolation. Totally, PVD was observed in 68% (58 of 85) of patients and 34.7% (112 of 323) of PVs. Seventy-nine (24.5%) PVs were found acutely reconnected, including 48 veins revealed by ATP induction [ATP(+)PV] and 64 veins by reassessment after 30 min post-isolation [Time(+)PV]. Time(+)PVs were observed more frequently in Group 1 than those in Group 2 (31.3 vs. 13.7%, P<0.01), but no significant difference was found in the occurrence of ATP(+)PVs between Group 1 and Group 2 (17.9 vs. 13.3%, P=0.27). The sequences of the PVD and the acutely reconnected PV potential were similar in 87.5% of veins. After PV re-isolation, 70% (28 of 40) of previously documented PVD disappeared. CONCLUSION: The occurrence of PVD after PV isolation was closely related to the acute PV reconnection after 30 min post-isolation.

Early detection of pulmonary vein reconnection after isolation in patients with paroxysmal atrial fibrillation: a comparison of ATP-induction and reassessment at 30 minutes postisolation.

INTRODUCTION: Catheter ablation for paroxysmal AF (PAF) is limited by an unacceptable recurrence rate, mainly due to pulmonary vein (PV) reconnection. Strategies to minimize reconnection include adenosine infusion and also a waiting period of 30 minutes after PV isolation. The aim of the present study was to assess whether these two strategies revealed the same conduction gap. METHODS AND RESULTS: In total, 88 consecutive patients (54 males, mean age of 60 years) with drug refractory PAF underwent circumferential PV isolation (CPVI). After isolation of ipsilateral PVs, with entry and exit block checked using a circular mapping catheter, 20 mg ATP was injected during isoproterenol infusion to reveal dormant conduction gap(s). Unless the reconnection revealed by ATP persisted, PVs were further remapped with the circular mapping catheter at 30 minutes postisolation. Totally, PV reconnection was observed in 56 (64%) patients. 24.3% veins (80/329) were found reconnected. Reassessment at 30 minutes postablation was more efficient as compared to ATP induction (19.8% vs 14.6% for ATP). The agreement between these 2 methods is moderate (kappa value = 0.50). In veins that transiently reconnected after ATP administration and later observed at 30 minutes postablation, 94% (17 of 19) of them were found being reconnected with the same gap. CONCLUSION: Acute PV reconnection is common, occurring in 64% of patients, as detected by adenosine infusion and waiting time. Each shows a unique quality as compared to one another. The combined use of these 2 methods may reduce the AF recurrence rate after CPVI.

Knockout of the tumor necrosis factor a receptor 1 gene can up-regulate erythropoietin receptor during myocardial ischemia-reperfusion injury in mice.

BACKGROUND: Tumor necrosis factor a receptor 1 (TNFalphaR1) plays an important role in the signal pathway of apoptosis. The objective of this study was to investigate the effects of TNFalphaR1 knockout on the up-regulation of erythropoietin receptor (Epo-R) and the coordinated anti-apoptosis functions during myocardial ischemia-reperfusion injury in mice. METHODS: The ischemia-reperfusion injury model for cardiomyocytes was performed by ligating the left circumflex branch artery of TNFalphaR1 knockout (P55(-/-)) C17 B6 mice, as well as wild-type (P55(+/+)) C17 B6 mice. Triphenyltetrazolium chloride (TTC) staining was performed to observe the damaged area of the heart. TUNEL staining and DNA fragmentation were used to identify apoptosis. Mitochondrial Bcl-2 and Bax as well as expression of Epo-R and its downstream genes (Jak-2, stat-5, Akt, IkB-alpha, HIF-1alpha) were measured by Western blotting. The gene knockout mice were assigned into those undergoing the apoptosis surgical model group (KO group), and those subjected to sham operation (KOs group). Similarly, wild-type mice were either exposed to the surgical model (WT group) or subject to a sham operation (WTs group). RESULTS: The myocardial damage ratio of the wild-type group after the operation was significantly higher than that of the knockout group, (50.5 +/- 6.4)% vs (36.9 +/- 6.9)%, P < 0.01. Similarly, TUNEL positive ratio of the wild-type group was significantly higher than that of the knockout group, (63.1 +/- 5.6)% vs (42.1 +/- 4.7)%, P < 0.01. The gray value ratios of Epo-R, Jak-2, stat-5, Akt, IkB-alpha, HIF-1 and mitochondrial Bcl-2 in the KO group were significantly higher than those of the WT group, P < 0.05; however, mitochondrial Bax was significantly lower than that of the WT group significantly (P < 0.05). CONCLUSIONS: Using the ischemia-reperfusion injury model in mice, cardiomyocytes of TNFalphaR1 knockouts exhibited anti-apoptotic characteristics. This information could be used to coordinate the prevention of myocardial apoptosis by up-regulating and activating the Epo-R pathway.

[Mechanism and re-ablation strategy for postablation atrial tachyarrhythmia in atrial fibrillation patients].

OBJECTIVE: To investigate the mechanism and re-ablation strategy of recurrent atrial tachyarrhythmia (ATA) following circumferential ablation of pulmonary veins (PV) in patients with atrial fibrillation (AF). METHODS: Fifteen patients with recurrent ATA following first AF ablation procedure were included in this study. Under CARTO guidance, PVs were remapped and ablated subsequently for relapse of left atrium to PV conduction. The whole atrium was then remapped and individualized ablation was made to eliminate inducible ATA. RESULTS: Left atrium to PV conduction relapses were evidenced in 14 patients. After re-ablation, there were no inducible ATA in 9 patients, inducible left atrial macro-reentry tachycardia in 3 patients and all were terminated by further linear ablation on the roof and left atrial isthmus, inducible atrial focal tachycardia from left atrial isthmus in 1 patient and was eliminated after additional focal ablation, inducible right atrial macro-reentry tachycardia in 2 patients and were eliminated by right isthmus linear ablation. During 1 - 16 (5.5 +/- 4.4) months follow-up, ATA was disappeared in 13 patients and reduced in another 2 patients. CONCLUSIONS: Relapse of left atrium to PV conduction is one of the main mechanisms for postablation ATA in patients with AF. Atrial macro-reentry tachycardia and focal atrial tachycardia were less common mechanisms for postablation ATA. Re-ablation focused on closing the PV gaps and additional individualized focal and lineal ablation strategies were helpful for treating postablation ATA in AF patients.

[A prospective, randomized, controlled trial of autologous mesenchymal stem cells transplantation for dilated cardiomyopathy].

OBJECTIVE: Recent experimental and clinical observations have suggested that cell transplantation could be of therapeutic value for the treatment of heart failure. This study was performed to explore the efficacy and safety of intracoronary autologous mesenchymal stem cells (MSCs) transplantation for treating patients with idiopathic dilated cardiomyopathy. METHOD: Twenty-four consecutive patients with idiopathic dilated cardiomyopathy received standard drug therapy were randomly divided into intracoronary injection of autologous mesenchymal stem cells (treated, n = 12) or saline (control, n = 12) groups. Serum IL-6, TNF-alpha and CRP, plasma brain natriuretic peptides (BNP) were determined and echocardiography, Holter electrocardiogram monitoring and six minutes walk test were performed at baseline, 3 and 6 months post injection. RESULTS: IL-6, TNF-alpha and CRP remained unchanged after MSCs transplantation. Plasma BNP levels at 3 months and 6 months post MSCs injection were significantly higher than that of pre-injection (378.10 +/- 147.47, 420.40 +/- 148.50 vs. 292.40 +/- 148.54 ng/L, respectively, P < 0.05) but were significantly lower than that in control group at comparable time points (3 months: 378.10 +/- 147.47 vs. 473.10 +/- 106.31 ng/L; 6 months: 420.40 +/- 148.50 vs. 544.60 +/- 93.11 ng/L, P < 0.05). Six-minute-walking distance significantly increased at 6 months after MSCs injection compared with pre-injection level and which is also higher than that in control patients (519.00 +/- 43.28 vs. 396.33 +/- 42.19 and 464.00 +/- 76.5 m, respectively, P < 0.05). Left ventricular ejection fraction and LVEDd remained unchanged post MSCs injection. No malignant arrhythmias and severe side effects could be observed around transplantation and during six months follow-up. Survival was similar between the two groups during six months follow-up. CONCLUSION: Percutaneous coronary autologous mesenchymal stem cells transplantation can attenuate the increase of plasma BNP, increase six-minute-walking capacity in patients with idiopathic dilated cardiomyopathy.

Human bone marrow-derived mesenchymal stem cells transplanted into damaged rabbit heart to improve heart function.

OBJECTIVE: The present study was designed to test whether transplantation of human bone marrow-derived mesenchymal stem cells (hMSCs) in New Zealand rabbits with myocardial infarction can improve heart function; and whether engrafted donor cells can survive and transdifferentiated into cardiomyocytes. METHODS: Twenty milliliters bone marrow was obtained from healthy men by bone biopsy. A gradient centrifugation method was used to separate bone marrow cells (BMCs) and red blood cells. BMCs were incubated for 48 h and then washed with phosphate-buffered saline (PBS). The culture medium was changed twice a week for 28 d. Finally, hematopoietic cells were washed away to leave only MSCs. Human MSCs (hMSCs) were premarked by BrdU 72 h before the transplantation. Thirty-four New Zealand rabbits were randomly divided into myocardial infarction (MI) control group and cell treated group, which received hMSCs (MI+MSCs) through intramyocardial injection, while the control group received the same volume of PBS. Myocardial infarction was induced by ligation of the left coronary artery. Cell treated rabbits were treated with 5 x 10(6) MSCs transplanted into the infarcted region after ligation of the coronary artery for 1 h, and the control group received the same volume of PBS. Cyclosporin A (oral solution; 10 mg/kg) was provided alone, 24 h before surgery and once a day after MI for 4 weeks. Echocardiography was measured in each group before the surgery and 4 weeks after the surgery to test heart function change. The hearts were harvested for HE staining and immunohistochemical studies after MI and cell transplantation for 4 weeks. RESULTS: Our data showed that cardiac function was significantly improved by hMSC transplantation in rabbit infarcted hearts 4 weeks after MI (ejection fraction: 0.695+/-0.038 in the cell treated group (n=12) versus 0.554+/-0.065 in the control group (n=13) (P<0.05). Surviving hMSCs were identified by BrdU positive spots in infarcted region and transdifferentiated into cardiomyocytes characterized with a positive cardiac phenotype: troponin I. CONCLUSION: Transplantation of hMSCs could transdifferentiate into cardiomyocytes and regenerate vascular structures, contributing to functional improvement.

Allograftic bone marrow-derived mesenchymal stem cells transplanted into heart infarcted model of rabbit to renovate infarcted heart.

OBJECTIVE: To investigate the directed transplantation of allograftic bone marrow-derived mesenchymal stem cells (MSCs) in myocardial infarcted (MI) model rabbits. MATERIALS AND METHODS: Rabbits were divided into 3 groups, heart infarcted model with MSCs transplanted treatment (MSCs group, n = 12), heart infarcted model with PBS injection (control group, n = 20), sham operation with PBS injection (sham group, n = 17). MSCs labelled by BrdUrd were injected into the MI area of the MSCs group. The same volume of PBS was injected into the MI area of the control group and sham group. The mortality, LVIDd, LVIDs and LVEF of the two groups were compared 4 weeks later. Tropomyosin inhibitory component (Tn I) and BrdUrd immunohistochemistry identified the engrafted cells 4 weeks after transplantation. RESULT: The mortality of the MSCs group was 16.7% (2/12), and remarkably lower than the control group's mortality [35% (7/20) (P < 0.05)]. Among the animals that survived for 4 weeks, the LVIDd and LVIDs of the MSCs group after operation were 1.17+/-0.21 cm and 0.74+/-0.13 cm, and remarkably lower than those of the model group, which were 1.64+/-0.14 cm and 1.19+/-0.12 cm (P < 0.05); the LVEF of the MSCs group after operation was 63+/-6%, and remarkably higher than that of the model group, which was 53+/-6% (P < 0.05). Among the 10 cases of animals that survived for 4 weeks in the MSCs group, in 8 cases (80%), the transplanted cells survived in the non MI, MI region and its periphery, and even farther away; part of them differentiated into cardiomyocytes; in 7 cases (70%), the transplanted cells participated in the formation of blood vessel tissue in the MI region. CONCLUSION: Transplanted allograftic MSCs can survive and differentiate into cardiomyocytes, form the blood vessels in the MI region. MSCs transplantation could improve the heart function after MI.