Publications
Department of Medicine faculty members published more than 3,000 peer-reviewed articles in 2022.
2021
2021
PURPOSE OF REVIEW
Cardiomyopathy with underlying left ventricular (LV) dysfunction is a heterogenous group of disorders that may be present with, and/or secondary to, coronary artery disease (CAD). The purpose of this review is to demonstrate, via case illustrations, the benefits offered by cardiac positron-emission tomography (PET) stress testing with coronary flow capacity (CFC) in the evaluation and treatment of patients with left ventricular (LV) dysfunction and CAD.
RECENT FINDINGS
CFC, a metric that is increasing in prominence, represents the integration of several absolute perfusion metrics into clinical strata of CAD severity. Our prior work has demonstrated improvement in regional perfusion metrics as a result of revascularization to territories with severe reduction in CFC. Conversely, when CFC is adequate, there is no change in regional perfusion metrics following revascularization, despite angiographically severe stenosis. Furthermore, Gould et al. demonstrated decreased rates of myocardial infarction and death following revascularization of myocardium with severely reduced CFC, with no clinical benefit observed following revascularization of patients with preserved CFC. In a series of cases, we present pre-revascularization and post-revascularization PET scans with perfusion metrics in patients with LV dysfunction and CAD. In these examples, we demonstrate improvement in LV function and perfusion metrics following revascularization only in cases where baseline CFC is severely reduced. PET with CFC offers unique guidance regarding revascularization in patients with reduced LV function and CAD.
View on PubMed2021
Severe cases of coronavirus disease 2019 (COVID-19), caused by infection with SARS-CoV-2, are characterized by a hyperinflammatory immune response that leads to numerous complications. Production of proinflammatory neutrophil extracellular traps (NETs) has been suggested to be a key factor in inducing a hyperinflammatory signaling cascade, allegedly causing both pulmonary tissue damage and peripheral inflammation. Accordingly, therapeutic blockage of neutrophil activation and NETosis, the cell death pathway accompanying NET formation, could limit respiratory damage and death from severe COVID-19. Here, we demonstrate that synthetic glycopolymers that activate signaling of the neutrophil checkpoint receptor Siglec-9 suppress NETosis induced by agonists of viral toll-like receptors (TLRs) and plasma from patients with severe COVID-19. Thus, Siglec-9 agonism is a promising therapeutic strategy to curb neutrophilic hyperinflammation in COVID-19.
View on PubMed2021
2021
2021
2021