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Aims: The prevalence of heart failure in New Zealand is increasing. A small number of select patients with predicted poor short-term survival are candidates for advanced heart failure therapies such as transplantation and durable mechanical circulatory support (MCS). The aim of our study was to introduce left ventricular assist devices (LVADs) to the wider clinicians and highlight their role in managing patients with advanced heart failure in New Zealand., Method: A retrospective audit of all ventricular assist device (VAD) recipients from January 2005 to December 2022 was conducted. Data were collated using electronic medical and paper records. The primary outcome was survival to transplantation or successful explant of VAD., Results: Thirty-nine patients received VADs; 32 were male and seven female. Mean age was 45 years (range 10-64 years). Most recipients were NZ European (25), six were Māori, four were Pacific peoples and four were of other ethnicities. The majority of LVADs were implanted for those with dilated cardiomyopathy (67%). At the time of data collection, 24 (62%) had survived to heart transplantation, seven (18%) died while on VAD support, five from right ventricular failure and two from strokes, one patient had their VAD explanted due to recovery and seven (18%) VAD recipients continue on support awaiting transplant., Conclusion: This audit has provided an opportunity to inform New Zealand clinicians of our durable MCS programme and the expanding role of VAD support in patients with advanced heart failure. The programme will need to continue to audit and report its practice in order to provide equitable allocation of this very limited resource to a growing population in need., Competing Interests: Nil., (© PMA.)

The natural history of a systemic right ventricle after an atrial switch procedure has yet to be fully characterised. We describe the case of the longest surviving patient at our institution who underwent a Mustard Baffle correction for dextro-transposition of great arteries in childhood. Over following decades he was reviewed regularly with deteriorating systemic right ventricle function. At around 50 years of age he developed worsening heart failure on maximal medical therapy. He was subsequently assessed for cardiac transplantation which he underwent successfully at the age of 55 years., (© 2019 Royal Australasian College of Physicians.)

Heart failure (HF) is defined by compromised contractile function and is associated with changes in excitation-contraction (EC) coupling and cardiomyocyte organisation. Tissue level changes often include fibrosis, while changes within cardiomyocytes often affect structures critical to EC coupling, including the ryanodine receptor (RyR), the associated protein junctophilin-2 (JPH2) and the transverse tubular system architecture. Using a novel approach, we aimed to directly correlate the influence of structural alterations with force development in ventricular trabeculae from failing human hearts. Trabeculae were excised from explanted human hearts in end-stage failure and immediately subjected to force measurements. Following functional experiments, each trabecula was fixed, sectioned and immuno-stained for structural investigations. Peak stress was highly variable between trabeculae from both within and between failing hearts and was strongly correlated with the cross-sectional area occupied by myocytes (MCSA), rather than total trabecula cross-sectional area. At the cellular level, myocytes exhibited extensive microtubule densification which was linked via JPH2 to time-to-peak stress. Trabeculae fractional MCSA variability was much higher than that in adjacent free wall samples. Together, these findings identify several structural parameters implicated in functional impairment in human HF and highlight the structural variability of ventricular trabeculae which should be considered when interpreting functional data.

Aims: In heart failure transverse-tubule (t-tubule) remodelling disrupts calcium release, and contraction. T-tubules in human failing hearts exhibit increased labelling by wheat germ agglutinin (WGA), a lectin that binds to the dystrophin-associated glycoprotein complex. We hypothesized changes in this complex may explain the increased WGA labelling and contribute to t-tubule remodelling in the failing human heart. In this study we sought to identify the molecules responsible for this increased WGA labelling., Methods and Results: Confocal and super-resolution fluorescence microscopy and proteomic analyses were used to quantify left ventricle samples from healthy donors and patients with idiopathic dilated cardiomyopathy (IDCM). Confocal microscopy demonstrated both WGA and dystrophin were located at t-tubules. Super-resolution microscopy revealed that WGA labelling of t-tubules is largely located within the lumen while dystrophin was restricted to near the sarcolemma. Western blots probed with WGA reveal a 5.7-fold increase in a 140 kDa band in IDCM. Mass spectrometry identified this band as type VI collagen (Col-VI) comprised of α1(VI), α2(VI), and α3(VI) chains. Pertinently, mutations in Col-VI cause muscular dystrophy. Western blotting identified a 2.4-fold increased expression and 3.2-fold increased WGA binding of Col-VI in IDCM. Confocal images showed that Col-VI is located in the t-tubules and that their diameter increased in the IDCM samples. Super-resolution imaging revealed Col-VI was restricted to the t-tubule lumen where increases were associated with displacement in the sarcolemma as identified from dystrophin labelling. Samples were also labelled for type I, III, and IV collagen. Both confocal and super-resolution imaging identified that these collagens were also present within t-tubule lumen., Conclusion: Increased expression and labelling of collagen in IDCM samples indicates fibrosis may contribute to t-tubule remodelling in human heart failure., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2017. For permissions, please email: journals.permissions@oup.com.)

Background: The cardiac myocyte t-tubular system ensures rapid, uniform cell activation and several experimental lines of evidence suggest changes in the t-tubular system and associated excitation-contraction coupling proteins may occur in heart failure., Methods and Results: The organization of t-tubules, L-type calcium channels (DHPRs), ryanodine receptors (RyRs) and contractile machinery were examined in fixed ventricular tissue samples from both normal and failing hearts (idiopathic (non-ischemic) dilated cardiomyopathy) using high resolution fluorescent imaging. Wheat germ agglutinin (WGA), Na-Ca exchanger, DHPR and caveolin-3 labels revealed a shift from a predominantly transverse orientation to oblique and axial directions in failing myocytes. In failure, dilation of peripheral t-tubules occurred and a change in the extent of protein glycosylation was evident. There was no change in the fractional area occupied by myofilaments (labeled with phalloidin) but there was a small reduction in the number of RyR clusters per unit area. The general relationship between DHPRs and RyR was not changed and RyR labeling overlapped with 51±3% of DHPR labeling in normal hearts. In longitudinal (but not transverse) sections there was an ∼30% reduction in the degree of colocalization between DHPRs and RyRs as measured by Pearson's correlation coefficient in failing hearts., Conclusions: The results show that extensive remodelling of the t-tubular network and associated excitation-contraction coupling proteins occurs in failing human heart. These changes may contribute to abnormal calcium handling in heart failure. The general organization of the t-system and changes observed in failure samples have subtle differences to some animal models although the general direction of changes are generally similar.

Background: Some patients continue to have significant heart failure symptoms despite optimal medical therapy., Methods: We describe a first-in-human experience with an implantable non-blood-contacting extra-ascending aortic counterpulsation heart assist system (C-Pulse) in 5 end-stage heart failure patients, aged 54 to 73 years., Results: All patients improved by 1 NYHA class and improvements in invasive hemodynamics were documented in 3 patients. Three of 5 patients (60%) had infectious complications. Two patients were explanted at 5 and 7 weeks, respectively, as a result of mediastinal infection related to the implant procedure. One patient was successfully transplanted at 1 month and 1 remained hemodynamically improved on the device at 6 months but suffered infective complications. The device and protocol have been modified as a result of this pilot study with a further multicenter safety study underway., Conclusions: Although feasibility of this device is suggested by this pilot study, safety and efficacy will need to be examined in a larger cohort with longer follow-up., (Copyright © 2010 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.)

Aim: To report the results of transcatheter atrial septal defect (ASD) closure with the Amplatzer septal occluder (ASO) from the single centre providing interventions for congenital heart disease in New Zealand., Methods: A single centre retrospective review of all patients 1997-2004 inclusive, undergoing planned transcatheter ASD closure was undertaken. Implantation success, complications and latest patient follow-up are described., Results: Percutaneous ASD closure was planned in 227 adults and children. (55% had additional medical co-morbidities.) The mean ASD size was 22+/-6 mm, and device size ranged from 5 to 40 mm. Closure was successful in 93%, unsuccessful in 5% and not attempted in 2%. There were two device embolisations, one immediately post-release and one within 24h. Minor procedural complications occurred in 5% of patients. There were no cases of suspected or proven device erosion. Ninety-two percent had documented follow-up beyond 6 months. At latest follow-up the closure rate was 98.5%. There was no significant change in the degree of mitral regurgitation. Sixteen of 24 with pre-closure arrhythmias resolved while 10 remained in atrial fibrillation. Six patients developed new arrhythmias but these were well controlled medically., Conclusion: There is a high implantation and closure rate using transcatheter ASD closure with the Amplatzer septal occluder in children and adults avoiding the need for cardiac surgery. Follow-up at one year shows there is no progression of mitral regurgitation, and supraventricular arrhythmias have usually resolved.

Purpose: The purpose of this study is to describe the first experience of implanting a new left ventricular assist device in pediatric patients with end-stage heart failure., Description: In two recent prospective, international, multicenter clinical trials, three children (aged

A 37-year-old man presented with severe dilated cardiomyopathy secondary to occult aortic coarctation. He was successfully managed with combined orthotopic heart transplantation and aortic coarctation repair.

Evidence from animal models suggest that t-tubule changes may play an important role in the contractile deficit associated with heart failure. However samples are usually taken at random with no regard as to regional variability present in failing hearts which leads to uncertainty in the relationship between contractile performance and possible t-tubule derangement. Regional contraction in human hearts was measured by tagged cine MRI and model fitting. At transplant, failing hearts were biopsy sampled in identified regions and immunocytochemistry was used to label t-tubules and sarcomeric z-lines. Computer image analysis was used to assess 5 different unbiased measures of t-tubule structure/organization. In regions of failing hearts that showed good contractile performance, t-tubule organization was similar to that seen in normal hearts, with worsening structure correlating with the loss of regional contractile performance. Statistical analysis showed that t-tubule direction was most highly correlated with local contractile performance, followed by the amplitude of the sarcomeric peak in the Fourier transform of the t-tubule image. Other area based measures were less well correlated. We conclude that regional contractile performance in failing human hearts is strongly correlated with the local t-tubule organization. Cluster tree analysis with a functional definition of failing contraction strength allowed a pathological definition of ‘t-tubule disease’. The regional variability in contractile performance and cellular structure is a confounding issue for analysis of samples taken from failing human hearts, although this may be overcome with regional analysis by using tagged cMRI and biopsy mapping. [ABSTRACT FROM AUTHOR]