Contrast-enhanced ultrasound in pediatric echocardiography.

The safety and benefits of cardiac contrast-enhanced ultrasound (CEUS) have been demonstrated in children and adolescents for a variety of clinical indications, including congenital heart disease. Cardiac CEUS is performed with US and the intravenous administration of ultrasound contrast agents (UCAs). It improves transthoracic echocardiography, which can be challenging in children and adults with acoustic window limitations (e.g., from obesity) and alterations in chest wall and cardiac geometry (e.g., from prior surgical procedures). Cardiac CEUS is also used to evaluate ischemia in the follow-up of congenital and acquired heart disease. In 2019, the United States Food and Drug Administration (FDA) approved a UCA for pediatric echocardiography. This article focuses on the clinical applications of UCAs in pediatric and adult echocardiography, outlining its diagnostic value, safety and potential for future applications.

Expecting the unexpected: Echo laboratory preparedness in the time of COVID-19.

COVID-19 poses a unique set of challenges to the healthcare system due to its rapid spread, intensive resource utilization, and relatively high morbidity and mortality. Healthcare workers are at especially high risk of exposure given the viruses spread through close contact. Reported cardiac complications of COVID-19 include myocarditis, acute coronary syndrome, cardiomyopathy, pericardial effusion, arrhythmia, and shock. Thus, echocardiography is integral in the timely diagnosis and clinical management of COVID-19 patients. Rush University Medical Center has been at the forefront of the COVID-19 response in Illinois with high numbers of cases reported in Chicago and surrounding areas. The echocardiography laboratory at Rush University Medical Center (RUMC) proactively took numerous steps to balance the imaging needs of a busy, nearly 700-bed academic medical center while maintaining safety.

Pulmonary hypertension: diagnosis, imaging techniques, and novel therapies.

Pulmonary hypertension (PH), defined as the elevation of mean pulmonary arterial pressure (mPAP) above 25 mmHg, has numerous causes, which the World Health Organization (WHO) has divided into five distinct categories based upon the underlying mechanism of action. This review will explore the pathophysiology, diagnostic testing, and treatment of PH. Identification of PH depends on a strong clinical suspicion, a detailed history, and a thorough physical exam. We review the evidence supporting experimental and clinical laboratory parameters for diagnosis and monitoring of PH. Transthoracic echocardiogram (TTE) is the initial screening test of choice. This review will detail specific echocardiographic techniques for the assessment and classification of PH. Furthermore, the importance of advanced imaging, including computed tomography (CT) and magnetic resonance imagining (MRI) is explored. New developments in pharmacology, percutaneous intervention, and surgical approaches are summarized. Finally, we will address the tools available to predict morbidity and mortality.

HCN channelopathy in external globus pallidus neurons in models of Parkinson's disease.

Parkinson's disease is a common neurodegenerative disorder characterized by a profound motor disability that is traceable to the emergence of synchronous, rhythmic spiking in neurons of the external segment of the globus pallidus (GPe). The origins of this pathophysiology are poorly defined for the generation of pacemaking. After the induction of a parkinsonian state in mice, there was a progressive decline in autonomous GPe pacemaking, which normally serves to desynchronize activity. The loss was attributable to the downregulation of an ion channel that is essential in pacemaking, the hyperpolarization and cyclic nucleotide-gated (HCN) channel. Viral delivery of HCN2 subunits restored pacemaking and reduced burst spiking in GPe neurons. However, the motor disability induced by dopamine (DA) depletion was not reversed, suggesting that the loss of pacemaking was a consequence, rather than a cause, of key network pathophysiology, a conclusion that is consistent with the ability of L-type channel antagonists to attenuate silencing after DA depletion.