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.