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Coronary Artery Disease: HELP
Articles by Steven M. Holland
Based on 4 articles published since 2008
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Between 2008 and 2019, Steven M. Holland wrote the following 4 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Review Hyper IgE syndrome: an update on clinical aspects and the role of signal transducer and activator of transcription 3. 2008

Paulson, Michelle L / Freeman, Alexandra F / Holland, Steven M. ·Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, USA. ·Curr Opin Allergy Clin Immunol · Pubmed #18978467.

ABSTRACT: PURPOSE OF REVIEW: Hyper IgE syndrome (HIES) is a primary immunodeficiency characterized by eczema, recurrent skin and lung infections, elevated serum IgE, and connective tissue and skeletal abnormalities. We present newly recognized aspects of the clinical phenotype and discuss recent genetic and immunologic findings. RECENT FINDINGS: In 2007, mutations in signal transducer and activator of transcription 3 (STAT3) were determined to be the cause of autosomal-dominant HIES. Mutations lead to disruption of STAT3-dependent pathways, which are crucial for signaling of many cytokines, including IL-6 and IL-10. On the one hand, cells from STAT3-defective patients have a proinflammatory profile with elevated TNFalpha and IFNgamma; on the other hand, STAT3 mutations result in the inability to produce IL-17 or form Th17 cells. SUMMARY: HIES was previously defined on the basis of clinical manifestations and laboratory markers that were not specific to the disease. With the identification of STAT3 mutations as the cause of HIES, we can definitively characterize the disease at molecular and immunologic levels. Future study of HIES and STAT3 will help us understand eczema, IgE regulation, infection susceptibility, coronary artery disease, scoliosis, and bronchiectasis as well as provide mechanistic insights into treatment.

2 Article Coronary atherosclerosis and dilation in hyper IgE syndrome patients: Depiction by magnetic resonance vessel wall imaging and pathological correlation. 2017

Abd-Elmoniem, Khaled Z / Ramos, Nadine / Yazdani, Saami K / Ghanem, Ahmed M / Holland, Steven M / Freeman, Alexandra F / Gharib, Ahmed M. ·National Institute of Diabetes and Digestive and Kidney Diseases, Biomedical and Metabolic Imaging Branch, United States. · University of South Alabama, United States. · National Institute of Diabetes and Digestive and Kidney Diseases, Biomedical and Metabolic Imaging Branch, United States; Electrical Engineering Department, Suez Canal University, Ismailia, Egypt. · National Institute of Allergy and Infectious Diseases, United States. · National Institute of Diabetes and Digestive and Kidney Diseases, Biomedical and Metabolic Imaging Branch, United States. Electronic address: agharib@mail.nih.gov. ·Atherosclerosis · Pubmed #28167354.

ABSTRACT: BACKGROUND AND AIMS: Autosomal dominant hyper-IgE (AD-HIES) is a primary immunodeficiency caused by mutations in STAT3. Elevated levels of IgE, an ineffective immune response, connective tissue abnormalities, and coronary arterial dilation and tortuosity characterize AD-HIES. To date, coronary artery evaluation in AD-HIES patients has been limited to lumenography measurements. Direct in vivo coronary vessel wall (VW) imaging may allow for better interrogation of coronary vessel abnormalities. The goal of this prospective study was to evaluate the coronary VW of AD-HIES patients using Magnetic Resonance Imaging (MRI) and histology. VW image findings were compared in healthy subjects and subjects with coronary atherosclerotic disease (CAD). METHODS: A total of 28 subjects (10 with AD-HIES, 8 healthy, 10 with CAD) were studied by coronary VW MRI imaging. Additionally, a post-mortem coronary artery from one VW imaged AD-HIES patient was examined. RESULTS: Coronary VW in AD-HIES was thicker than in healthy controls but not significantly different from VW thickness in CAD subjects. AD-HIES coronaries showed increased VW area compared to healthy controls and CAD subjects. On histology, the AD-HIES coronary artery had findings consistent with atherosclerotic plaque, but had minimal luminal narrowing, deficient adventitia thickening and absence of both internal and external elastic laminae. CONCLUSIONS: This is the first study to demonstrate subclinical coronary atherosclerosis in AD-HIES patients on VW imaging by MRI. Histologic evaluation confirmed the presence of atherosclerosis with lack of supportive adventitial thickening and elastic components. These findings suggest mechanisms for coronary dilation in AD-HIES and thereby help direct clinical management.

3 Article Assessment of atherosclerosis in chronic granulomatous disease. 2014

Sibley, Christopher T / Estwick, Tyra / Zavodni, Anna / Huang, Chiung-Yu / Kwan, Alan C / Soule, Benjamin P / Long Priel, Debra A / Remaley, Alan T / Rudman Spergel, Amanda K / Turkbey, Evrim B / Kuhns, Douglas B / Holland, Steven M / Malech, Harry L / Zarember, Kol A / Bluemke, David A / Gallin, John I. ·From the Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center (C.T.S., A.Z., A.C.K., E.B.T., D.A.B.), Laboratory of Host Defenses (T.E., P.B.S., A.K.R.S., H.L.M., K.A.Z., J.I.G.), Biostatistics Research Branch (C.-Y.H.), and Laboratory of Clinical Infectious Diseases (S.M.H.), National Institute of Allergy and Infectious Diseases and National Heart, Lung, and Blood Institute (A.T.R.), National Institutes of Health, Bethesda, MD. · From the Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center (C.T.S., A.Z., A.C.K., E.B.T., D.A.B.), Laboratory of Host Defenses (T.E., P.B.S., A.K.R.S., H.L.M., K.A.Z., J.I.G.), Biostatistics Research Branch (C.-Y.H.), and Laboratory of Clinical Infectious Diseases (S.M.H.), National Institute of Allergy and Infectious Diseases and National Heart, Lung, and Blood Institute (A.T.R.), National Institutes of Health, Bethesda, MD. jgallin@cc.nih.gov. ·Circulation · Pubmed #25239440.

ABSTRACT: BACKGROUND: Patients with chronic granulomatous disease (CGD) experience immunodeficiency because of defects in the phagocyte NADPH oxidase and the concomitant reduction in reactive oxygen intermediates. This may result in a reduction in atherosclerotic injury. METHODS AND RESULTS: We prospectively assessed the prevalence of cardiovascular risk factors, biomarkers of inflammation and neutrophil activation, and the presence of magnetic resonance imaging and computed tomography quantified subclinical atherosclerosis in the carotid and coronary arteries of 41 patients with CGD and 25 healthy controls in the same age range. Univariable and multivariable associations among risk factors, inflammatory markers, and atherosclerosis burden were assessed. Patients with CGD had significant elevations in traditional risk factors and inflammatory markers compared with control subjects, including hypertension, high-sensitivity C-reactive protein, oxidized low-density lipoprotein, and low high-density lipoprotein. Despite this, patients with CGD had a 22% lower internal carotid artery wall volume compared with control subjects (361.3±76.4 mm(3) versus 463.5±104.7 mm(3); P<0.001). This difference was comparable in p47(phox)- and gp91(phox)-deficient subtypes of CGD and independent of risk factors in multivariate regression analysis. In contrast, the prevalence of coronary arterial calcification was similar between patients with CGD and control subjects (14.6%, CGD; 6.3%, controls; P=0.39). CONCLUSIONS: The observation by magnetic resonance imaging and computerized tomography of reduced carotid but not coronary artery atherosclerosis in patients with CGD despite the high prevalence of traditional risk factors raises questions about the role of NADPH oxidase in the pathogenesis of clinically significant atherosclerosis. Additional high-resolution studies in multiple vascular beds are required to address the therapeutic potential of NADPH oxidase inhibition in cardiovascular diseases. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01063309.

4 Article Coronary artery abnormalities in Hyper-IgE syndrome. 2011

Freeman, Alexandra F / Avila, Elizabeth Mannino / Shaw, Pamela A / Davis, Joie / Hsu, Amy P / Welch, Pamela / Matta, Jatin R / Hadigan, Colleen / Pettigrew, Roderic I / Holland, Steven M / Gharib, Ahmed M. ·Immunopathogenesis Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), 10 Center Drive, Bethesda, MD 20892-1899, USA. freemaal@mail.nih.gov ·J Clin Immunol · Pubmed #21494893.

ABSTRACT: OBJECTIVE: Hyper-IgE syndrome (HIES) is a rare primary immunodeficiency caused by autosomal dominant STAT3 mutations resulting in recurrent infections and connective tissue abnormalities. Coronary artery abnormalities have been reported infrequently. We aimed to determine the frequency and characteristics of coronary artery abnormalities. DESIGN: STAT3-mutated HIES patients (n=38), ranging in age from 8 to 57 years, underwent coronary artery imaging by computed tomography or magnetic resonance imaging. Images were evaluated for tortuosity, dilation, and aneurysm. Charts were reviewed for cardiac risk factors. To allow blinded image interpretation, an age- and gender-matched non-HIES group was also evaluated (n=33). RESULTS: Coronary artery tortuosity or dilation occurred in 70% of HIES patients, with aneurysms present in 37%, incidences much higher than in the literature and in our non-HIES group, in which 21% had tortuosity or dilation and 3% had aneurysms. Hypertension was more common in the HIES group than in the general population and was associated with vessel abnormalities. Atherosclerosis was uncommon and mild. CONCLUSIONS: Coronary artery aneurysms and tortuosity are common in HIES, despite a paucity of atherosclerosis, suggesting that STAT3 plays an integral role in human vascular remodeling and atherosclerosis.