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Coronary Artery Disease: HELP
Articles by Judith L. Meadows
Based on 4 articles published since 2010
(Why 4 articles?)

Between 2010 and 2020, Judith Meadows wrote the following 4 articles about Coronary Artery Disease.
+ Citations + Abstracts
1 Editorial Role of Imaging in the Management of Stable Ischemic Heart Disease: An Evolving Paradigm Shift. 2017

Boden, William E / Meadows, Judith L. ·VA Boston Healthcare System and the Massachusetts Veterans Epidemiology, Research, and Informatics Center, Boston University School of Medicine, Boston, Massachusetts. Electronic address: william.boden@va.gov. · VA Connecticut Health Care System, Yale University School of Medicine, Division of Cardiology, New Haven, Connecticut. ·JACC Cardiovasc Imaging · Pubmed #28279381.

ABSTRACT: -- No abstract --

2 Review Imaging Atherosclerotic Plaque Calcification: Translating Biology. 2016

Bailey, Grant / Meadows, Judith / Morrison, Alan R. ·Department of Internal Medicine (Section of Cardiovascular Medicine), Yale Cardiovascular Research Center, Yale University School of Medicine, New Haven, CT, 06511, USA. · VA Connecticut Healthcare System, 950 Campbell Avenue, West Haven, CT, 06516, USA. · Department of Internal Medicine (Section of Cardiovascular Medicine), Alpert Medical School at Brown University, Providence, RI, 02903, USA. alan_morrison@brown.edu. · Providence VA Medical Center, 830 Chalkstone Avenue, Providence, RI, 02908, USA. alan_morrison@brown.edu. ·Curr Atheroscler Rep · Pubmed #27339750.

ABSTRACT: Calcification of atherosclerotic lesions was long thought to be an age - related, passive process, but increasingly data has revealed that atherosclerotic calcification is a more active process, involving complex signaling pathways and bone-like genetic programs. Initially, imaging of atherosclerotic calcification was limited to gross assessment of calcium burden, which is associated with total atherosclerotic burden and risk of cardiovascular mortality and of all cause mortality. More recently, sophisticated molecular imaging studies of the various processes involved in calcification have begun to elucidate information about plaque calcium composition and consequent vulnerability to rupture, leading to hard cardiovascular events like myocardial infarction. As such, there has been renewed interest in imaging calcification to advance risk assessment accuracy in an evolving era of precision medicine. Here we summarize recent advances in our understanding of the biologic process of atherosclerotic calcification as well as some of the molecular imaging tools used to assess it.

3 Clinical Trial Stress cardiac magnetic resonance imaging provides effective cardiac risk reclassification in patients with known or suspected stable coronary artery disease. 2013

Shah, Ravi / Heydari, Bobak / Coelho-Filho, Otavio / Murthy, Venkatesh L / Abbasi, Siddique / Feng, Jiazhuo H / Pencina, Michael / Neilan, Tomas G / Meadows, Judith L / Francis, Sanjeev / Blankstein, Ron / Steigner, Michael / di Carli, Marcelo / Jerosch-Herold, Michael / Kwong, Raymond Y. ·Noninvasive Cardiovascular Imaging Section, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis St, Boston, MA 02115, USA. ·Circulation · Pubmed #23804252.

ABSTRACT: BACKGROUND: A recent large-scale clinical trial found that an initial invasive strategy does not improve cardiac outcomes beyond optimized medical therapy in patients with stable coronary artery disease. Novel methods to stratify at-risk patients may refine therapeutic decisions to improve outcomes. METHODS AND RESULTS: In a cohort of 815 consecutive patients referred for evaluation of myocardial ischemia, we determined the net reclassification improvement of the risk of cardiac death or nonfatal myocardial infarction (major adverse cardiac events) incremental to clinical risk models, using guideline-based low (<1%), moderate (1% to 3%), and high (>3%) annual risk categories. In the whole cohort, inducible ischemia demonstrated a strong association with major adverse cardiac events (hazard ratio=14.66; P<0.0001) with low negative event rates of major adverse cardiac events and cardiac death (0.6% and 0.4%, respectively). This prognostic robustness was maintained in patients with previous coronary artery disease (hazard ratio=8.17; P<0.0001; 1.3% and 0.6%, respectively). Adding inducible ischemia to the multivariable clinical risk model (adjusted for age and previous coronary artery disease) improved discrimination of major adverse cardiac events (C statistic, 0.81-0.86; P=0.04; adjusted hazard ratio=7.37; P<0.0001) and reclassified 91.5% of patients at moderate pretest risk (65.7% to low risk; 25.8% to high risk) with corresponding changes in the observed event rates (0.3%/y and 4.9%/y for low and high risk posttest, respectively). Categorical net reclassification index was 0.229 (95% confidence interval, 0.063-0.391). Continuous net reclassification improvement was 1.11 (95% confidence interval, 0.81-1.39). CONCLUSIONS: Stress cardiac magnetic resonance imaging effectively reclassifies patient risk beyond standard clinical variables, specifically in patients at moderate to high pretest clinical risk and in patients with previous coronary artery disease. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01821924.

4 Article Rac2 Modulates Atherosclerotic Calcification by Regulating Macrophage Interleukin-1β Production. 2017

Ceneri, Nicolle / Zhao, Lina / Young, Bryan D / Healy, Abigail / Coskun, Suleyman / Vasavada, Hema / Yarovinsky, Timur O / Ike, Kenneth / Pardi, Ruggero / Qin, Lingfen / Qin, Li / Tellides, George / Hirschi, Karen / Meadows, Judith / Soufer, Robert / Chun, Hyung J / Sadeghi, Mehran M / Bender, Jeffrey R / Morrison, Alan R. ·From the Department of Internal Medicine (Section of Cardiovascular Medicine), VA Connecticut Healthcare System, West Haven (N.C., L.Z., A.H., L.Q., G.T., J.M., R.S., M.M.S., A.R.M.) · Department of Medicine and Division of Cardiology, Providence VA Medical Center, RI (A.H., A.R.M.) · Department of Internal Medicine (Section of Cardiovascular Medicine), Yale Cardiovascular Research Center, Yale University School of Medicine, New Haven, CT (N.C., L.Z., B.D.Y., A.H., S.C., H.V., T.O.Y., K.I., L.Q., L.Q., G.T., K.H., J.M., R.S., H.J.C., M.M.S., J.R.B, A.R.M.) · Department of Internal Medicine (Section of Cardiovascular Medicine), Alpert Medical School at Brown University, Providence, RI (A.H., A.R.M.) · and Department of Molecular Pathology, Universita Vita Salute School of Medicine, San Raffaele Scientific Institute, Milan, Italy (R.P.). ·Arterioscler Thromb Vasc Biol · Pubmed #27834690.

ABSTRACT: OBJECTIVE: The calcium composition of atherosclerotic plaque is thought to be associated with increased risk for cardiovascular events, but whether plaque calcium itself is predictive of worsening clinical outcomes remains highly controversial. Inflammation is likely a key mediator of vascular calcification, but immune signaling mechanisms that promote this process are minimally understood. APPROACH AND RESULTS: Here, we identify Rac2 as a major inflammatory regulator of signaling that directs plaque osteogenesis. In experimental atherogenesis, Rac2 prevented progressive calcification through its suppression of Rac1-dependent macrophage interleukin-1β (IL-1β) expression, which in turn is a key driver of vascular smooth muscle cell calcium deposition by its ability to promote osteogenic transcriptional programs. Calcified coronary arteries from patients revealed decreased Rac2 expression but increased IL-1β expression, and high coronary calcium burden in patients with coronary artery disease was associated with significantly increased serum IL-1β levels. Moreover, we found that elevated IL-1β was an independent predictor of cardiovascular death in those subjects with high coronary calcium burden. CONCLUSIONS: Overall, these studies identify a novel Rac2-mediated regulation of macrophage IL-1β expression, which has the potential to serve as a powerful biomarker and therapeutic target for atherosclerosis.