Background—Prospective data on the medium-term safety and effectiveness of the AMPLATZER Septal Occluder in clinical practice are not available. The objective of this study was to prospectively evaluate the risk of hemodynamic compromise and obtain medium-term survival data on patients implanted with the AMPLATZER Septal Occluder for percutaneous closure of secundum atrial septal defects.Methods and Results—Subjects were enrolled prospectively at 50 US sites and followed for 2 years. Between 2008 and 2012, atrial septal defect closure with the AMPLATZER Septal Occluder was attempted in 1000 patients (aged 0.3–83.6 years, mean 21±22 years). Procedural closure occurred in 97.9%, with 1-month and 2-year closure 98.5% and 97.9%, respectively. Hemodynamic compromise occurred in 6 subjects (0.65%), because of dysrhythmia in 2, device embolization in 1, and cardiac erosion in 3. The rate of cardiac erosion was 0.3% (average 83, range 12–171 days from implant).Conclusions—Closure of atrial septal defect with the AMPLATZER Septal Occluder is safe and effective. The rate of hemodynamic compromise and cardiac erosion is rare. The risk factors for cardiac erosion after device closure are not yet clear.Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT00650936.

Background The practice of coiling APCs before Fontan completion is controversial and published data are limited. We sought to compare outcomes in subjects with and without pre-Fontan coil embolization of aortopulmonary collaterals (APCs) using the Pediatric Heart Network (PHN) Fontan Cross-Sectional Study database which enrolled survivors of prior Fontan palliation. Methods We compared hospital length of stay (LOS) after Fontan in 80 subjects who underwent APC coiling with 459 subjects who did not. Secondary outcomes included post-Fontan complications and assessment of health status and ventricular performance at cross-sectional evaluation (mean 8.6±3.4 years after Fontan). Results Centers varied markedly in frequency of pre-Fontan APC coiling (range 0-30% of subjects, p<0.001). The coil group was older at Fontan (p=0.004), and more likely to have single right ventricular morphology (p=0.054) and pre-Fontan atrioventricular valve regurgitation (p=0.03). The coil group underwent Fontan surgery more recently (p<0.001), was more likely to have a prior superior cavopulmonary anastomosis (p<0.001), and more likely to undergo extracardiac Fontan connection (p<0.001) and surgical fenestration (p<0.001). In multivariable analyses, APC coiling was not associated with LOS (hazard ratio (HR) for remaining in-hospital 0.91, 95% CI 0.70-1.18, p=0.48) or postoperative complications, except more post-Fontan catheter interventions (HR 1.74, 95% CI 1.04-2.91, p=0.03), primarily additional APC coils. The groups had similar outcomes at cross-sectional evaluation. Conclusion Management of APCs before Fontan shows marked practice variation. We did not find an association between pre-Fontan coiling of APCs and shorter post-operative hospital stay or with better late outcomes. Prospective studies of this practice are needed.

The study illustrates a profile of characteristics, medical history, functional health state, and markers of ventricular performance in patients with heterotaxy after the Fontan procedure. Despite obvious anatomic differences, and some differences in echocardiography and heart rhythm, there were no important differences in exercise performance or functional health state between these patients and other survivors of the Fontan procedure.

Background Little is known about the contemporary mortality experience among adults with congenital heart disease (CHD). The objectives of this study were to assess the age at death, presence of cardiovascular comorbidities, and most common causes of death among adults with CHD in a contemporary cohort within the United States. Methods and Results Patients with CHD who had a healthcare encounter between 2008 and 2013 at 1 of 5 comprehensive CHD centers in North Carolina were identified by International Classification of Diseases, Ninth Revision ( ICD‐9 ), code. Only patients who could be linked to a North Carolina death certificate between 2008 and 2016 and with age at death ≥20 years were included. Median age at death and underlying cause of death based on death certificate data were analyzed. The prevalence of acquired cardiovascular risk factors was determined from electronic medical record data. Among the 629 included patients, the median age at death was 64.2 years. Those with severe CHD (n=157, 25%), shunts (n=202, 32%), and valvular lesions (n=174, 28%) had a median age at death of 46.0, 65.0, and 73.3 years, respectively. Cardiovascular death was most common in adults with severe CHD (60%), with 40% of those deaths caused by CHD. Malignancy and ischemic heart disease were the most common causes of death in adults with nonsevere CHD. Hypertension and hyperlipidemia were common comorbidities among all CHD severity groups. Conclusions The most common underlying causes of death differed by lesion severity. Those with severe lesions most commonly died from underlying CHD, whereas those with nonsevere disease more commonly died from non‐CHD causes.

Background Myocardial injury is associated with excess mortality in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, and the mechanisms of injury are diverse. Coagulopathy associated with this infection may have unique cardiovascular implications. Case summary We present a case of 62-year-old male who presented after experiencing syncope and cardiac arrest. Given the clinical presentation and electrocardiographic findings, there was concern for acute coronary syndrome. However, coronary angiogram did not reveal significant coronary obstruction. Due to the unclear nature of his presentation, a bedside echocardiogram was rapidly performed and was indicative of right ventricular strain. Due to these findings, a pulmonary angiogram was performed that revealed massive pulmonary embolism. He successfully underwent catheter-directed thrombolysis and, after a prolonged hospital stay, was discharged home on lifelong anticoagulation. Discussion The impact of coronavirus disease-2019 (COVID-19) on the cardiovascular system has been prominent and multifaceted. COVID-19 can have wide-ranging effects on the cardiovascular system due to coagulopathy with resultant venous and arterial thrombo-embolism. Due to the critical condition of many patients affected by COVID-19, imaging for thrombo-embolic events is often delayed. With the use of bedside echocardiogram, observation of right ventricular strain may be critical in raising suspicion for pulmonary embolism, especially when atypical features are noted on electrocardiogram.

Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is commonly associated with myocardial injury and heart failure. The pathophysiology behind this phenomenon remains unclear, with many diverse and multifaceted hypotheses. To contribute to this understanding, we describe the underlying cardiac findings in fifty patients who died with coronavirus disease 2019 (COVID-19). Methods Included were autopsies performed on patients with a positive SARS-CoV-2 reverse-transcriptase-polymerase-chain reaction test from the index hospitalization. In the case of out-of-hospital death, patients were included if post-mortem testing was positive. Complete autopsies were performed according to a COVID-19 safety protocol, and all patients underwent both macroscopic and microscopic examination. If available, laboratory findings and echocardiograms were reported. Results The median age of the decedents was 63.5 years. The most common comorbidities included hypertension (90.0%), diabetes (56.0%) and obesity (50.0%). Lymphocytic inflammatory infiltrates in the heart were present in eight (16.0%) patients, with focal myocarditis present in two (4.0%) patients. Acute myocardial ischemia was observed in eight (16.0%) patients. The most common findings were myocardial fibrosis (80.0%), hypertrophy (72.0%), and microthrombi (66.0%). The most common causes of death were COVID-19 pneumonia in 18 (36.0%), COVID-19 pneumonia with bacterial superinfection in 12 (24.0%), and COVID-19 pneumonia with pulmonary embolism in 10 (20.0%) patients. Conclusions Cardiovascular comorbidities were prevalent, and pathologic changes associated with hypertensive and atherosclerotic cardiovascular disease were the most common findings. Despite markedly elevated inflammatory markers and cardiac enzymes, few patients exhibited inflammatory infiltrates or necrosis within cardiac myocytes. A unifying pathophysiologic mechanism behind myocardial injury in COVID-19 remains elusive, and additional autopsy studies are needed.

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