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1.

Objective

Arch obstruction after the Norwood procedure is common and contributes to mortality. We determined the prevalence, associated factors, and practice variability of arch reintervention and assessed whether arch reintervention is associated with mortality.

Methods

From 2005 to 2017, 593 neonates in the Congenital Heart Surgeons' Society Critical Left Heart Obstruction cohort underwent a Norwood procedure. Median follow-up was 3.7 years. Multivariable parametric models, including a modulated renewal analysis, were performed.

Results

Of the 593 neonates, 146 (25%) underwent 218 reinterventions for arch obstruction after the Norwood procedure: catheter-based (n = 168) or surgical (n = 50) at a median age of 4.3 months (quartile 1-quartile 3, 2.6-5.7). Interdigitation of the distal aortic anastomosis was protective against arch reintervention. Development of ≥ moderate tricuspid valve regurgitation and right ventricular dysfunction at any point was associated with arch reintervention. Nonsignificant variables for arch reintervention included shunt type and preoperative aortic measurements. Surgical arch reintervention was protective against arch reintervention, but transcatheter reintervention was associated with increased reintervention. Arch reintervention was not associated with increased mortality. There was wide institutional variation in incidence of arch reintervention (range, 0-40 reinterventions per 100 years patient follow-up) and in preintervention gradient (range, 0-64 mm Hg).

Conclusions

Interdigitation of the distal aortic anastomosis during the Norwood procedure decreased the risk of arch reintervention. Surgical arch reintervention is more definitive than transcatheter. Arch reintervention after the Norwood procedure is not associated with increased mortality. Serial surveillance for arch obstruction, integrated with changes in right ventricular function and tricuspid valve regurgitation, is recommended after the Norwood procedure to improve outcomes.  相似文献   
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目的观察愈心梗液保护大鼠急性心肌梗死(AMI)后状动脉造成实验性AMI心力衰竭模型,并使之长期存活。造模成心力衰竭心肌细胞及线粒体超微结构和抗氧化的作用。方法结扎Wistar大鼠冠功后,大鼠随机分为7组,每组10只,即空白组、假手术(只穿刺不结扎)组、模型组、开搏通组、愈心梗液大、中、小剂量组。各给药组于手术即日起开始灌胃给药,连续4周。4周后麻醉处死大鼠.心脏组织切片处理后通过电镜和光镜观察心肌细胞及线粒体的形态结构及测定心肌细胞的横截面积、周长,同时测定大鼠心肌组织和血清中丙二醛(MDA)和超氧化物歧化酶(SOD)的含量。结果动物造模4周后,大鼠心肌细胞中心肌纤维排列杂乱,图像系统测量显示心肌细胞横截面积增大、周长增加。与模型组比较,愈心梗液大、中剂量可显著降低大鼠心肌细胞横截面积、周长和直径(和模型比较,P〈0.01)。减少大鼠心肌组织和血清中MDA的含量和升高SOD的含量。结论愈心梗液可抑制大鼠AMI后心肌细胞的代偿性增大,保护线粒体结构的相对完整性,提高大鼠的抗氧化能力,干预AMI大鼠心室重构VR的病理过程,有改善AMI后心力衰竭的作用。  相似文献   
4.
The delayed rectifier potassium current (I K) is known to be important in action potential repolarisation and may contribute to the diastolic pacemaker depolarisation in pacemaker cells from the heart. In this study, using whole-cell patch clamp, we investigated the characteristics of I K in morphologically normal cells from the atrioventricular node (AVN) and ventricle of the rabbit heart. Cells were held at −40 mV and 5 μM external nifedipine was used to block L-type calcium current (I Ca,L). Significant I K was observed with pulses to potentials more positive than −30 mV. The steady-state activation curve in both cell types showed maximal activation at between + 10 and + 20 mV. Half-maximal activation of I K occurred at −4.9 and −4.1 mV with slope factors of 8.3 and 12.4 mV in ventricular and AVN cells, respectively. Using pulses of increasing duration, significant I K tails after repolarisation from + 40 mV were observed with pulses of 20 ms and increased with pulses up to 100–120 ms in both cell types. Pulses of longer duration did not activate further I K and this suggested that only the rapid component of I K, called I Kr, was present in either cell type. Moreover, I K tails after pulses to all potentials were blocked completely by E-4031, a selective blocker of I Kr. The reversal potential of I K varied with the concentration of external K. Superfusion of AVN cells with medium containing 4, 15 and 40 mM [K+]o resulted in reversal potentials of −81, −56 and −32 mV, respectively, which are close to values predicted if the I K channel were highly selective for K. The time constants for deactivation of I K in ventricle and AVN on return to −40 mV after a 500-ms activating pulse to + 60 mV were 480 ms and 230 ms, respectively. The faster deactivation of I K in AVN cells was a distinguishing feature and suggests that there may be differences in the I Kr channel protein between ventricular and AVN cells. Received: 24 July 1995 /Received after revision: 20 October 1995 /Accepted: 23 October 1995  相似文献   
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目的:通过人工套接大鼠右侧颈动静脉,造成左向右分流,导致大鼠右心室压力容量负荷增加,从多个不同层面研究大鼠右心室重塑过程中细胞间质的变化。方法:设4个实验组与4个对照组,每组10只体重、性别相匹配的近交系Wistar大鼠。实验组无菌手术套接大鼠右侧颈总动脉与颈外静脉,造成左向右分流,于术后1、2、4、8周分别测定动物体重(BW),右心室与左心室加室间隔质量之比[R/(L+S)]及右心室质量与体重之比(RV mg/BW g);右心室组织切片,普通光镜下观察组织学的改变,并利用计算机形态学分析软件分析细胞与间质的改变;提取右心室心肌组织中mRNA,应用RT PCR法测定Ⅰ、Ⅲ型胶原、纤维结合素Ⅰ基因表达量的变化。对照组手术操作同试验组,唯不套接动静脉,同样条件饲养。结果:术后第1周开始,试验组大鼠右心室压力即明显高于对照组,术后第1、2、4、8周之间相比,无统计学意义。试验组大鼠(RV mg/BW g)在术后8周时有统计学意义(0.64±0.05 vs 0.43±0.03,P<0.01); R/(L+S)至第8周时也有类似变化(0.36±0.04 vs 0.21±0.02,P<0.05 );所有试验大鼠均未发生心衰现象,与对照组相比,Ⅰ、Ⅲ型胶原mRNA表达量在第1、4、8周时改变不明显,第2周时有统计学意义(Ⅰ型胶原:0.93±0.18 vs 0.79±0.07,P<0.05;Ⅲ型胶原:0.43±0.07 vs 0.36±0.07,P<0.05。平均光密度法)。纤维结合素Ⅰ第1周时即可检测到mRNA表达量升高,与对照组相比有统计学意义(0.26±0.06 vs 0.20±0.05,P<0.05);第2、4、8周时与对照相比无统计学差异。结论:①压力容量负荷改变能够引起大鼠右心室的重塑,包括心肌细胞和细胞周围基质,不同的改变可以有不同的时间特征,并和右心室压力有明显相关性;②反映细胞周围基质改变的Ⅰ型胶原、Ⅲ型胶原、纤维结合素Ⅰ基因在改变的早期出现明显改变,说明右心室重塑是机体对外界环境改变积极适应的结果。  相似文献   
7.
目的:观察神经内分泌因子对扩张型心肌病(DCM)心室重构及心力衰竭的影响。方法:DCM患者120例,按心功能分级分为3组,心功能Ⅱ级组34例,心功能Ⅲ级组45例,心功能Ⅳ级组41例。另选取80例心功能正常者作为对照组。所有患者人院第2天均检测去甲肾上腺素(NE)、血管紧张素Ⅱ(AngⅡ)、细胞肿瘤坏死因-α(TNT-α)、白介素-6(IL-6)、细胞可溶性凋亡因子(sFas)。结果:DCM心功能Ⅱ~Ⅳ级患者与正常组对照,NE,AngⅡ、TNF-α、IL-6、sFas水平明显升高,且随着心功能恶化逐渐增强(P〈0.01)。DCM组中不同功能级别者与对照组相比差异有统计学意义(P〈0.05或P〈0.01〉。结论:DCM患者其NE,AngⅡ、TNF-α、IL-6、sFas常过度表达,通过影响心肌收缩力,引起心肌肥大,诱导心肌凋亡、纤维化,加重心室重构和心力衰竭发生、发展。  相似文献   
8.
Muscarinic acetylcholine receptors (mAChRs) mediate their main cardiac effects via pertussis toxin-sensitive G-proteins. Physiological effects differ considerably between atrium and ventricle, and it is unknown to which extent these differences derive from selective receptor-G-protein coupling or further downstream events. We have characterized specific coupling between mAChRs and Gi/Go-protein isoforms in atrial and ventricular myocardium by agonist-dependent photoaffinity labeling with [(32)P]azidoanilido GTP (aaGTP) and immunoprecipitation in sarcolemmal membranes from terminally failing human hearts. The total amount of mAChRs, as determined by specific binding of [(3)H]QNB, was significantly higher in right-atrial (RA +/- SEM, 959 +/- 68 fmol/mg, n = 4) than in left-ventricular membranes (LV, 582 +/- 53 fmol/mg, n = 6). Standardized immunoblots revealed that Gialpha-2 was the predominant subtype in both regions. A 40-kDa splice variant of Goalpha (Goalpha-1 and/or Goalpha-3) was almost exclusively detectable in RA. Levels of Gialpha-3 and a 39-kDa splice variant of Goalpha (Goalpha-2) were also higher in RA. Basal aaGTP binding was higher in RA than in LV for all Gialpha/Goalpha subtypes. The carbachol (10 micromol/l)-induced increase in aaGTP binding was significantly higher in RA than in LV for Goalpha-1/3 (336 +/- 95% of LV, n = 4) and for Gialpha-3 (211 +/- 83%), lower for Gialpha-2 (42 +/- 5%), and was similar in both regions for Goalpha-2 (130 +/- 62%). The differential coupling of mAChRs in human RA and LV suggests that the initiation of different physiological responses to mAChR stimulation starts with signal sorting at the receptor-G-protein level.  相似文献   
9.
In normal adult-ventricular myocardium, Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR) is activated via Ca2+ entry through L-type Ca2+ channels. However, embryonic-ventricular myocytes have a prominent T-type Ca2+ current (ICa,T). In this study, the contribution of ICa,T to CICR was determined in chick-ventricular development. Electrically stimulated Ca2+ transients were examined in myocytes loaded with fura-2 and Ca2+ currents with perforated patch-clamp. The results show that the magnitudes of the Ca2+ transient, L-type Ca2+ current (ICa,L) and ICa,T, decline with development with the majority of the decline of transients and ICa,L occurring between embryonic day (ED) 5 and 11. Compared to controls, the magnitude of the Ca2+ transient in the presence of nifedipine was reduced by 41% at ED5, 77% at ED11, and 78% at ED15. These results demonstrated that the overall contribution of ICa,T to the transient was greatest at ED5, while ICa,L was predominate at ED11 and 15. This indicated a decline in the contribution of ICa,T to the Ca2+ transient with development. Nifedipine plus caffeine was added to deplete the SR of Ca2+ and eliminate the occurrence of CICR due to ICa,T. Under these conditions, the transients were further reduced at all three developmental ages, which indicated that a portion of the Ca2+ transients present after just nifedipine addition was due to CICR stimulated by ICa,T. These results indicate that Ca2+ entry via T-type channels plays a significant role in excitation-contraction coupling in the developing heart that includes stimulation of CICR.  相似文献   
10.
We report a patient born with a Holmes heart who was later diagnosed with pheochromocytoma in her teenage years. A review of the literature showed only two such cases reported. The findings of these two rare conditions simultaneously in several individuals is suggestive of an association.  相似文献   
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