Embolism from the heart or the thoracic aorta often leads to clinically significant morbidity and mortality due to transient ischemic attack, stroke or occlusion of peripheral arteries. Transthoracic and transesophageal echocardiography are the key diagnostic modalities for evaluation, diagnosis, and management of stroke, systemic and pulmonary embolism. This document provides comprehensive American Society of Echocardiography guidelines on the use of echocardiography for evaluation of cardiac sources of embolism. It describes general mechanisms of stroke and systemic embolism; the specific role of cardiac and aortic sources in stroke, and systemic and pulmonary embolism; the role of echocardiography in evaluation, diagnosis, and management of cardiac and aortic sources of emboli including the incremental value of contrast and 3D echocardiography; and a brief description of alternative imaging techniques and their role in the evaluation of cardiac sources of emboli. Specific guidelines are provided for each category of embolic sources including the left atrium and left atrial appendage, left ventricle, heart valves, cardiac tumors, and thoracic aorta. In addition, there are recommendation regarding pulmonary embolism, and embolism related to cardiovascular surgery and percutaneous procedures. The guidelines also include a dedicated section on cardiac sources of embolism in pediatric populations.

Despite having a normal fractional shortening, children exposed to anthracyclines have subclinical derangement of their left ventricular deformation as measured by decreases in strain and strain rate in both the circumferential and longitudinal axis. In particular, there was a profound decrease in diastolic strain rate following anthracycline exposure compared with controls. Whether the decline of strain or strain rate can predict future risk of developing cardiomyopathy requires further investigation.

RVSW can be estimated in children with PAH, and is significantly associated with abnormal WHO class, the need for septostomy, as well as mortality. Indices accounting for RV performance as well as ventricular-vascular coupling may be useful in the prognosis and, hence, management of children with PAH.

Background Mortality for infants undergoing complex cardiac surgery is >10% with a 30% to 40% risk of complications. Early identification and treatment of high‐risk infants remains challenging. Metabolites are small molecules that determine the minute‐to‐minute cellular phenotype, making them ideal biomarkers for postsurgical monitoring and potential targets for intervention. Methods and Results We measured 165 serum metabolites by tandem mass spectroscopy in infants ≤120 days old undergoing cardiopulmonary bypass. Samples were collected prebypass, during rewarming, and 24 hours after surgery. Partial least squares–discriminant analysis, pathway analysis, and receiver operator characteristic curve analysis were used to evaluate changes in the metabolome, assess altered metabolic pathways, and discriminate between survivors/nonsurvivors as well as upper/lower 50% intensive care unit length of stay. Eighty‐two infants had preoperative samples for analysis; 57 also had rewarming and 24‐hour samples. Preoperation, the metabolic fingerprint of neonates differed from older infants ( R 2 =0.89, Q 2 =0.77; P <0.001). Cardiopulmonary bypass resulted in progressive, age‐independent metabolic disturbance ( R 2 =0.92, Q 2 =0.83; P <0.001). Multiple pathways demonstrated changes, with arginine/proline ( P =1.2×10 −35 ), glutathione ( P =3.3×10 −39 ), and alanine/aspartate/glutamate ( P =1.4×10 −26 ) metabolism most affected. Six subjects died. Nonsurvivors demonstrated altered aspartate ( P =0.007) and nicotinate/nicotinamide metabolism ( P =0.005). The combination of 24‐hour aspartate and methylnicotinamide identified nonsurvivors versus survivors (area under the curve, 0.86; P <0.01), as well as upper/lower 50% intensive care unit length of stay (area under the curve, 0.89; P <0.01). Conclusions The preoperative metabolic fingerprint of neonates differed from older infants. Large metabolic shifts occurred after cardiopulmonary bypass, independent of age. Nonsurvivors and subjects requiring longer intensive care unit length of stay showed distinct changes in metabolism. Specific metabolites, including aspartate and methylnicotinamide, may differentiate sicker patients from those experiencing a more benign course.

The transplanted heart experiences numerous hemodynamic changes during and after cardiac transplantation. This study sought to evaluate the left ventricular myocardial mechanics in the pediatric heart transplant population using Velocity Vector Imaging (VVI). This study retrospectively evaluated 28 heart transplant recipients by echocardiography 12 months after transplantation. Echocardiograms from 28 age- and gender-matched subjects were used as a control group. Peak global longitudinal and circumferential left ventricular strain, systolic strain rate, and diastolic strain rate were obtained. Student's t tests were used to assess differences between the two groups (defined as p ≤ 0.05). The peak global left ventricular longitudinal strain was lower in the transplant group (17.21%) than in the control group (22.14%). The transplant and control groups did not differ significantly in terms of their peak global circumferential strain (20.28% vs. 20.79%, respectively). Similar results were observed for longitudinal and circumferential systolic and diastolic strain rates. The transplant patients showed statistically significant reductions in all peak global longitudinal measures compared with those of the control subjects. Circumferential myocardial deformation appears to be preserved in transplant recipients. This could suggest evidence of ischemia given the known myocardial fiber arrangement of longitudinal fibers toward the endocardial surface, which is also more distal in the coronary arterioles.

No abstract

No abstract

Transplant coronary artery vasculopathy (TCAV) is the primary cause of late graft loss in pediatric heart transplant recipients. TCAV is diagnosed using angiography or intravascular ultrasound; however, noninvasive methods remain elusive. We sought to define patterns of myocardial mechanics in patients with TCAV and to determine whether this can detect TCAV before invasive methods. In this retrospective study, we queried our heart transplant database to identify all recipients with TCAV since 2006 (n = 41). Echoes were reviewed from the last normal catheterization and at TCAV diagnosis, and from time-matched transplant controls (n = 33) without TCAV. Peak global circumferential and longitudinal strain and systolic and diastolic strain rate (SSR and DSR) of the left ventricle were derived using velocity vector imaging. T tests were used to compare both groups longitudinally and between groups at both time points. Longitudinal strain, SSR, and DSR were diminished in the TCAV group compared to the transplant control group at both time points. No differences were found across time points in either group. Retrospective modeling using a longitudinal strain cutoff of 15 % on echoes 2 years prior to TCAV diagnosis predicted development or exclusion of TCAV with sensitivity of 53 %, specificity of 89 % with an area under the curve of 0.8. Decreases in longitudinal strain measurements demonstrate that alterations in myocardial mechanics occur in patients with TCAV at least 2 years prior to invasive diagnosis. These early changes may be due to microvascular disease. This modality could aid in earlier treatment and intervention for this challenging problem .