The GORE CARDIOFORM atrial septal defect (ASD) Occluder (GCA) is composed of a platinum-filled nitinol wire frame covered with expanded polytetrafluoroethylene, making it softer and more conformable compared with nitinol mesh devices. After the ASSURED clinical study confirmed the efficacy and safety of the device, it received U.S. Food and Drug Administration approval and a European conformity mark. Our aim was to understand the learning curve implicated in using the GCA for ASD closure in paediatric and adult patients as well as to study the early outcomes. To this end, a review of ASD device closures with GCA in 4 UK centres was conducted between January 2020 and January 2023. Implantation success was the primary outcome; the secondary outcomes were serious adverse events, including new onset arrhythmia. In all, 135 patients were included, and 128 (95%) had successful ASD device closure with GCA. The median patient age was 49 years, the median defect size was 18 mm, and the median device size was 37 mm. The median follow-up time was 6 months (interquartile range 1-14). One device embolisation occurred, and 15 patients (12% of GCA implantations) developed new onset arrhythmia - this was not related to patient age, defect diameter or device oversizing but was positively associated with device size. With growing experience using GCA, the device can be applied to a wide variety of ASD sizes and morphologies. Given the number of successful implantations with an absence of aortic erosion, as well as the ability to perforate through the device should procedures be required in the left atrium, the GCA device is an important addition for interventionists who close atrial septal defects.
Transcatheter aortic valve implantation (TAVI) is a relatively new procedure, currently for those in whom conventional surgery is too high risk. Preliminary data has been encouraging and a number o...
Aims Patients with sickle cell disease have significant morbidity and mortality. Pulmonary hypertension is suggested to be an important contributor but its nature and severity in these patients and how best to non-invasively assess it are controversial. We hypothesised that a high-output state rather than primary pulmonary vascular pathology may be the major abnormality in sickle cell disease. This study aimed to evaluate the characteristics and severity of pulmonary hypertension in patients with sickle cell disease using detailed echocardiography. Methods and Results We undertook a prospective study in 122 consecutive stable outpatients with sickle cell disease and 30 age, gender and ethnicity-matched healthy controls. Echocardiographic evaluation included 3D ventricular volumes, sphericity, tissue Doppler, and non-invasive estimation of pulmonary vascular resistance. 36% of patients had a tricuspid regurgitant velocity ≥2.5 m.s-1 but only 2% had elevated pulmonary vascular resistance and the prevalence of right ventricular dysfunction was very low. Patients with raised tricuspid regurgitant velocity had significantly elevated biventricular volumes and globular left ventricular remodelling, related primarily to anaemia. In a subgroup of patients who underwent cardiac catheterization, invasive pulmonary haemodynamics confirmed the echocardiographic findings. Conclusions Elevated cardiac output and left ventricular volume overload secondary to chronic anaemia may be the dominant factor responsible for abnormal cardiopulmonary haemodynamics in patients with sickle cell disease. 3D echocardiography with non-invasive estimation of pulmonary vascular resistance represents a valuable approach for initial evaluation of cardiopulmonary haemodynamics in sickle cell disease.
A patent foramen ovale is a relatively common finding in the general population and is associated with a number of conditions, including cryptogenic stroke. In 2014, percutaneous patent foramen ovale (PFO) closure is a frequently performed procedure; the bulk of these procedures being carried out for secondary prevention of cryptogenic stroke, along with other indications, such as prevention of decompression illness, platypnoea-orthodeoxia syndrome and migraine. Of these conditions the largest body of evidence available is for cryptogenic stroke and there is ongoing debate of the benefit of PFO closure over medical therapy. This article will review the available evidence of PFO closure in each of these contexts, with a particular focus on randomised controlled trials, and endeavour to outline in whom the evidence suggests closure should be considered.
Treatment of degenerative aortic stenosis has been transformed by transcatheter aortic valve implantation (TAVI) over the past 10–15 years. The success of various technologies has led operators to attempt to broaden the indications, and many patients with native valve aortic regurgitation have been treated ‘off label’ with similar techniques. However, the alterations in the structure of the valve complex in pure native aortic regurgitation are distinct to those in degenerative aortic stenosis, and there are unique challenges to be overcome by percutaneous valves. Nevertheless some promise has been shown with both non-dedicated and dedicated devices. In this article, the authors explore some of these challenges and review the current evidence base for TAVI for aortic regurgitation.
AbstractBackground: Reduced exercise capacity in patients with repaired Tetralogy of Fallot cannot be explained wholly by severe pulmonary regurgitation alone. We investigated the effect of pulmonary regurgitation and other measures of left and right ventricular function to identify the principal determinants of exercise performance. Methods: 100 patients with TOF were evaluated, 60 with severe PR and 40 with no or minimal PR. Patients underwent cardiopulmonary exercise testing with concurrent echocardiography. Echocardiography was performed at rest and during exercise (both at low and high intensity for the appropriate parameters). Contractile reserve was expressed as the percentage increase at the relevant time point. Univariate and multivariate linear regression was used to generate a predictive model for exercise function. Results: There was no difference in exercise performance between those with and without pulmonary regurgitation when judged by peak absolute oxygen consumption VO2 (1695±627vs1744±521, ml/min, p>0.05), or a range of other submaximal cardiopulmonary parameters. Right ventricular volumes were higher in those with pulmonary regurgitation while left ventricular long axis function was reduced. There were no associations between exercise measures with the degree of pulmonary regurgitation and right ventricular volume at rest or during exercise. There was lower contractile reserve of the right ventricle in those with pulmonary regurgitation (fractional area change 20±15 % vs 23±16 %, p<0.05) balanced by improved reserve of the left ventricle. Augmentation of the left ventricular global longitudinal strain and right ventricular fractional area curve together showed the strongest association with peak VO2. Conclusions: There was an overall marked reduction in exercise capacity in patients with repaired tetralogy of Fallot, but no difference between those with and without PR. The degree of exercise limitation is more dependent upon the ability of right and left ventricles.