Background Covered stent correction of sinus venosus ASDs (SVASD) is a relatively new technique. Challenges include anchoring a sufficiently long stent in a nonstenotic superior vena cava (SVC) and expanding the stent at the wider SVC‐RA junction without obstructing the anomalous right upper pulmonary vein (RUPV). The 10‐zig covered Cheatham‐platinum (CCP) stent has the advantage of being available in lengths of 5–11 cm and dilatable to 34 mm in diameter. Methods An international registry reviewed the outcomes of 10‐zig CCP stents in 75 patients aged 11.4–75.9 years (median 45.4) from March 2016. Additional stents were used to anchor the stent in the SVC or close residual shunts in 33/75. An additional stent was placed in 4/5 (80%) with 5/5.5 cm CCPs, 18/29 (62%) with 6 cm CCPs, 5/18 (28%) with 7 cm CCPs, 5/22 (23%) with 7.5/8 cm CCPs and 0/1 with an 11 cm CCP. A “protective” balloon catheter was inflated in the RUPV in 17. Results Early stent embolization in two patients required surgical removal and defect repair and tamponade was drained in one patient. The CT at 3 months showed occlusion of the RUPV in one patient. Follow up is from 2 months to 5.1 years (median 1.8 years). QP:QS has reduced from 2.5 ± 0.5 to 1.2 ± 0.36 (p < .001) and RVEDVi from 149.1 ± 35.4 to 95.6 ± 21.43 ml/m2 (p < .001). Conclusions Ten‐zig CCPs of 7–8 cm appear to provide reliable SVASD closure with a low requirement for additional stents. Careful selection of patients and meticulous attention to detail is required to avoid complications.

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Objectives To describe a multi‐center experience of percutaneous transcatheter pulmonary valve replacement (TPVR) using the Edwards Sapien S3 Valve. Background Off‐label use of the Sapien S3 valve can allow for TPVR in patients with congenital heart disease (CHD) and large diameter dysfunctional right ventricular outflow tract (RVOT). The initial experience at five centers with the SAPIEN S3 valve for TPVR is presented with a focus on procedural techniques, success, complications, and efficacy. Methods A retrospective review was performed of all patients with CHD and dysfunctional RVOT who underwent TPVR using Sapien S3 valve. Imaging data, procedural elements, and clinical follow‐up data were collected to evaluate acute and short‐term results. Results A total of 50 patients underwent percutaneous placement of the Sapien S3 in the pulmonary position. Of these, 38 were placed into “native RVOTs”, measuring 24–32 mm in diameter, as assessed by compliant balloon sizing. In all cases, the valve was implanted after introduction and there were no cases of valve embolization. On follow up (range 1–9 months, median 3 months), no patients had significant obstruction or regurgitation through or around the valve requiring intervention. There were no procedural deaths. Major complications included severe aortic compression (n = 1) and tricuspid valve (TV) injury related to valve placement (n = 2) and prestenting (n = 1). Conclusions TPVR in patients with large diameter dysfunctional RVOTs can be effectively performed with the Sapien S3. All procedures were technically successful with no embolizations, no perivalvular leaks, and excellent short‐term valve function. Tricuspid valve injury from implantation of an uncovered valve was a serious procedural complication.

turbo-field-echo sequence-4 chamber view). No focal fibrosis was detected in late gadolinium enhancement sequences (Figure 1c, single-shot inversion recovery sequence-4 chamber view). Global edema in T2 weighted images was visible (Figure 1d, T2 [short tau inversion recovery] sequence-3 chamber view) as well as globally elevated T2 (56 ms, referent 48 § 3 ms) (Figure 1e, T2 mapping-short-axis view) and T1 (1,090 ms, referent 989 § 28 ms) (Figure 1f, T1 mapping -short-axis view) mapping times, suggesting acute myocardial injury. On March 26, 2020, hypoxic respiratory failure (saturation of 80%) required mechanical ventilation. The patient improved and was extubated, and the level of cardiac biomarkers declined (N-terminal proBtype natriuretic peptide 631 ng/liter, troponin 61 ng/liter) in due course.Cardiac MRI with its unique accuracy in defining cardiac morphology and function and its ability to provide tissue characterization makes it well suited to study cardiac involvement in COVID-19. Recently, Inciardi et al 3 proved severe biventricular myocardial injury with edema and late gadolinium enhancement. In the absence of epicardial coronary artery stenosis, sub-clinical myocardial dysfunction in COVID-19 may be a consequence of an impairment of microcirculatory endothelial function observed during the early stages of the systemic inflammatory response to the infection, which portends a poor prognosis in patients with established cardiovascular disease and impaired microcirculatory endothelial function. 4 In addition, direct COVID-19-mediated infection of endothelial cells might contribute to cardiac injury. 5 In summary, we show that elevated biomarkers of cardiac injury were associated with generalized myocardial edema without late gadolinium enhancement in cardiac MRI despite a normal echocardiogram during COVID-19.