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Coronary Artery Disease: HELP
Articles by Prediman K. Shah
Based on 13 articles published since 2010
(Why 13 articles?)
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Between 2010 and 2020, P. K. Shah wrote the following 13 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Editorial Temporal Change in CAC Score and Prognosis: Follow-Up Score Is Simpler and as Good as a Change in Score. 2016

Shah, Prediman K. ·Oppenheimer Atherosclerosis Research Center, Cedars Sinai Heart Institute, Los Angeles, California. Electronic address: Shahp@cshs.org. ·JACC Cardiovasc Imaging · Pubmed #27372020.

ABSTRACT: -- No abstract --

2 Editorial Can carotid plaque predict coronary plaque? 2013

Shah, Prediman K. ·Division of Cardiology and Oppenheimer Atherosclerosis Research Center, Cedars-Sinai Heart Institute, Department of Medicine, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, California. Electronic address: shahp@cshs.org. ·JACC Cardiovasc Imaging · Pubmed #24229769.

ABSTRACT: -- No abstract --

3 Editorial Jekyll and Hyde of HDL: a lipoprotein with a split personality. 2013

Shah, Prediman K. ·Division of Cardiology and Oppenheimer Atherosclerosis Research Center, Cedars Sinai Heart Institute and Department of Medicine at Cedars Sinai Medical Center and UCLA, CA, USA. ·Eur Heart J · Pubmed #24062336.

ABSTRACT: -- No abstract --

4 Review Biomarkers of plaque instability. 2014

Shah, P K. ·Division of Cardiology, Atherosclerosis Prevention and Treatment Center, Oppenheimer Atherosclerosis Research Center, Cedars Sinai Heart Institute, 127 South San Vicente Blvd: Suite A3307, Los Angeles, CA, 90048, USA, shahp@cshs.org. ·Curr Cardiol Rep · Pubmed #25326730.

ABSTRACT: Atherosclerosis is the proximate cause of arterial thrombosis, leading to acute occlusive cardiovascular syndromes. Thrombosis in atherosclerosis usually results from rupture of the fibrous cap of atherosclerotic plaques with a smaller proportion resulting from superficial endothelial erosion. Ruptured plaques are often associated with intimal and adventitial inflammation, increased size of lipid-rich necrotic core with thinned out collagen-depleted fibrous cap, outward remodeling, increased plaque neovascularity, intraplaque hemorrhage, and microcalcification. By inference, non-ruptured plaques with similar compositional features are considered to be at risk for rupture and hence are labeled vulnerable plaques or high-risk plaques. Identification of vulnerable plaques may help in predicting the risk of acute occlusive syndromes and may also allow targeting for aggressive systemic and possibly local therapies. Plaque rupture is believed to result from extracellular matrix (which comprises the protective fibrous cap) dysregulation due to excessive proteolysis in the context of diminished matrix synthesis. Inflammation is believed to play a key role by providing matrix-degrading metalloproteinases and also by inducing death of matrix-synthesizing smooth muscle cells. Systemic markers of inflammation are thus the most logical forms of potential biomarkers which may predict the presence of vulnerable or high-risk plaques. Several studies have suggested the potential prognostic value of a variety of systemic markers, but regrettably, their overall clinical predictive value is modestly incremental at best, especially for individual subjects compared to groups of patients. Nevertheless, continued investigation of reliable, cost-effective biomarkers that predict the presence of a high-risk plaque and future athero-thrombotic cardiovascular events with greater sensitivity and specificity is warranted.

5 Review The role of non-HDL cholesterol in risk stratification for coronary artery disease. 2012

Rana, Jamal S / Boekholdt, S Matthijs / Kastelein, John J P / Shah, Prediman K. ·Division of Cardiology and Oppenheimer Atherosclerosis Research Center, Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA. jamal.rana@cshs.org ·Curr Atheroscler Rep · Pubmed #22203405.

ABSTRACT: Despite aggressive lipid-lowering therapy, patients continue to be at significant risk of coronary heart disease (CHD). Assessment of non-high-density lipoprotein cholesterol (non-HDL-C) provides a measure of cholesterol contained in all atherogenic particles. In the third Adult Treatment Panel (ATP III) guidelines of the US National Cholesterol Education Program, non-HDL-C was introduced as a secondary target of therapy in persons with triglycerides ≥200 mg/dL. A recent meta-analysis of the relationship between non-HDL-C reduction and CHD risk showed non-HDL-C as an important target of therapy for CHD prevention. Most lipid-modifying drugs used as monotherapy have a 1:1 relationship between percent non-HDL-C lowering and percent CHD reduction. In the EPIC-Norfolk prospective population study, 21,448 participants without diabetes or CHD between 45 and 79 years of age were followed for 11.0 years. Participants with high non-HDL-C levels were at increased CHD risk independently of their LDL-C levels. Also, compared to apolipoprotein B, non-HDL-C appears to be a better choice given the fact that no additional tests or costs are needed and established cut points are already available. Future guidelines should emphasize the importance of non-HDL-C for guiding cardiovascular prevention strategies with an increased need to have non-HDL-C reported on routine lipid panels.

6 Review Evolving concepts on benefits and risks associated with therapeutic strategies to raise HDL. 2010

Shah, Prediman K. ·Division of Cardiology, Oppenheimer Atherosclerosis Research Center, Cedars Sinai Heart Institute, Los Angeles, California 90048, USA. shahp@cshs.org ·Curr Opin Cardiol · Pubmed #20827180.

ABSTRACT: PURPOSE OF REVIEW: To provide an update on high-density lipoprotein (HDL) biology and emerging new HDL-based therapies for athero-thrombosis. RECENT FINDINGS: Atherosclerotic cardiovascular disease remains a major public health threat despite a significant decline over the past three decades. Although current medical therapies, specifically low-density lipoprotein lowering with statins, reduce cardiovascular events by about 25-35%, a substantial residual risk remains, leading to a search for additional therapeutic interventions. In this regard, HDL has emerged as one important target because of epidemiologic evidence linking HDL levels inversely to cardiovascular events, known vascular protective actions of HDL and experimental and clinical research supporting athero-protective actions of HDL. However, complexities of HDL composition, particle size, and metabolism have suggested that HDL functionality, and how HDL is increased, may be important determinants of its protective effects. SUMMARY: Thus the possibility that HDL modification could address the residual risk has brought renewed focus on an old HDL-raising drug, niacin, and a number of newer strategies to exploit the vascular benefits of HDL.

7 Article Sex as a Determinant of Responses to a Coronary Artery Disease Self-Antigen Identified by Immune-Peptidomics. 2020

Lio, Wai Man / Cercek, Bojan / Yano, Juliana / Yang, Wei / Ghermezi, Jonathan / Zhao, Xiaoning / Zhou, Jianchang / Zhou, Bo / Freeman, Michael R / Chyu, Kuang-Yuh / Shah, Prediman K / Dimayuga, Paul C. ·Oppenheimer Atherosclerosis Research Center, Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States. · Division of Cancer Biology and Therapeutics, Departments of Surgery and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, United States. ·Front Immunol · Pubmed #32373127.

ABSTRACT: A significant body of work implicates the adaptive immune response in atherosclerosis, the main underlying cause of coronary artery disease (CAD), yet specific antigens involved remain to be fully identified. The pathobiology of CAD is influenced by sex with many factors that may be involved in the underlying mechanisms. Given the reported sexual dimorphic nature of immune-inflammatory responses, we investigated the influence of sex on potential CAD self-antigens from acute coronary syndrome (ACS) patients using immune-precipitation of soluble HLA Class-I/peptide complexes and mass spectrometry. Relevance of identified self-antigens to atherosclerosis, the major underlying cause of CAD, was tested in the apoE-/- atherosclerotic mouse model. Soluble HLA Class-I complexes from ACS patients and self-reported controls were immune-precipitated and subjected to elution, denaturation and size-exclusion to obtain HLA-bound peptides. Peptides were then subjected to mass spectrometry and patient-unique self-peptides were grouped as common to both female and male, or unique to either sex. Three peptides common to both female and male patients (COL6A1, CDSN, and SAA2), and 2 peptides each unique to female (COL1A1 and COL5A2) or male (SAA1 and KRT 9) patients were selected and mouse homologs of the peptides were screened for self-reactive immune responses in apoE-/- mice. The screening step revealed potential sex-influenced immune responses which was associated with differential immune profiles. Based on the frequency in patient plasma, COL6A1, COL5A2, and KRT 9 peptides were then tested in immunization studies. Neither COL5A2 nor KRT 9 peptide immunization resulted in significant effects on atherosclerosis compared to controls. On the other hand, female mice immunized with COL6A1 peptide had significantly reduced atherosclerosis whereas male mice had significantly increased atherosclerosis, associated with differential immune profiles. Our study identified potential self-antigens involved in atherosclerosis using the immune peptidome of CAD patients. Altering self-reactive immune responses to COL6A1 in apoE-/- mice resulted in differential effects on atherosclerosis burden with sex as a determinant of outcome.

8 Article Keratin 8 is a potential self-antigen in the coronary artery disease immunopeptidome: A translational approach. 2019

Mihailovic, Peter M / Lio, Wai Man / Herscovici, Romana / Chyu, Kuang-Yuh / Yano, Juliana / Zhao, Xiaoning / Zhou, Jianchang / Zhou, Bo / Freeman, Michael R / Yang, Wei / Shah, Prediman K / Cercek, Bojan / Dimayuga, Paul C. ·Oppenheimer Atherosclerosis Research Center, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States of America. · Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia. · Division of Cancer Biology and Therapeutics, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California, United States of America. · Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, California, United States of America. ·PLoS One · Pubmed #30811493.

ABSTRACT: BACKGROUND: Inflammation is an important risk factor in atherosclerosis, the underlying cause of coronary artery disease (CAD). Unresolved inflammation may result in maladaptive immune responses and lead to immune reactivity to self-antigens. We hypothesized that inflammation in CAD patients would manifest in immune reactivity to self-antigens detectable in soluble HLA-I/peptide complexes in the plasma. METHODS: Soluble HLA-I/peptide complexes were immuno-precipitated from plasma of male acute coronary syndrome (ACS) patients or age-matched controls and eluted peptides were subjected to mass spectrometry to generate the immunopeptidome. Self-peptides were ranked according to frequency and signal intensity, then mouse homologs of selected peptides were used to test immunologic recall in spleens of male apoE-/- mice fed either normal chow or high fat diet. The peptide detected with highest frequency in patient plasma samples and provoked T cell responses in mouse studies was selected for use as a self-antigen to stimulate CAD patient peripheral blood mononuclear cells (PBMCs). RESULTS: The immunopeptidome profile identified self-peptides unique to the CAD patients. The mouse homologs tested showed immune responses in apoE-/- mice. Keratin 8 was selected for further study in patient PBMCs which elicited T Effector cell responses in CAD patients compared to controls, associated with reduced PD-1 mRNA expression. CONCLUSION: An immunopeptidomic strategy to search for self-antigens potentially involved in CAD identified Keratin 8. Self-reactive immune response to Keratin 8 may be an important factor in the inflammatory response in CAD.

9 Article Coronary Atherosclerosis T 2017

Xie, Yibin / Kim, Young-Jin / Pang, Jianing / Kim, Jung-Sun / Yang, Qi / Wei, Janet / Nguyen, Christopher T / Deng, Zixin / Choi, Byoung Wook / Fan, Zhaoyang / Bairey Merz, C Noel / Shah, Prediman K / Berman, Daniel S / Chang, Hyuk-Jae / Li, Debiao. ·Biomedical Imaging Research Institute, Cedars Sinai Medical Center, Los Angeles, California; Department of Bioengineering, University of California, Los Angeles, California. · Department of Radiology, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. · Biomedical Imaging Research Institute, Cedars Sinai Medical Center, Los Angeles, California. · Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, South Korea. · Heart Institute, Cedars Sinai Medical Center, Los Angeles, California. · Biomedical Imaging Research Institute, Cedars Sinai Medical Center, Los Angeles, California; Heart Institute, Cedars Sinai Medical Center, Los Angeles, California. · Division of Cardiology, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, South Korea; Biomedical Imaging Institute, Yonsei University College of Medicine, Seoul, South Korea. Electronic address: hjchang@yuhs.ac. · Biomedical Imaging Research Institute, Cedars Sinai Medical Center, Los Angeles, California; Department of Bioengineering, University of California, Los Angeles, California. Electronic address: debiao.li@cshs.org. ·JACC Cardiovasc Imaging · Pubmed #27743950.

ABSTRACT: OBJECTIVES: The aim of this work is the development of coronary atherosclerosis T BACKGROUND: T METHODS: CATCH acquired dark-blood T RESULTS: Per-subject analysis showed none of the 13 reference control subjects had coronary hyperintensive plaques (CHIP) in either pre-contrast or post-contrast CATCH. Five patients had CHIP on pre-contrast CATCH and 5 patients had CHIP on post-contrast CATCH. Patients with CHIP had greater lipid abnormality than those without. Per-segment analysis showed elevated pre- and post-contrast plaque to myocardium signal ratio in the lesions with HRPF versus those without. Positive correlation was observed between plaque to myocardium signal ratio and OCT HRPF scoring. CHIP on pre-contrast CATCH were associated with significantly higher stenosis level than non-CHIP on invasive coronary angiography. CONCLUSIONS: CATCH provided accelerated whole heart coronary plaque characterization with simultaneously acquired anatomical reference. CHIP detected by CATCH showed positive association with high-risk plaque features on invasive imaging studies.

10 Article Extensive thoracic aortic calcification is an independent predictor of development of coronary artery calcium among individuals with coronary artery calcium score of zero. 2015

Brodov, Yafim / Gransar, Heidi / Rozanski, Alan / Hayes, Sean W / Friedman, John D / Thomson, Louise E J / Dey, Damini / Slomka, Piotr J / Min, James K / Shaw, Leslee J / Shah, P K / Germano, Guido / Berman, Daniel S. ·Department of Cardiac Imaging (Division of Nuclear Medicine), The Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Cardiology, The Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: yafim.brodov@gmail.com. · Department of Cardiac Imaging (Division of Nuclear Medicine), The Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Cardiology, The Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA. · Division of Cardiology, St. Lukes Roosevelt Hospital, New York, NY, USA. · Department of Cardiac Imaging (Division of Nuclear Medicine), The Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Cardiology, The Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA. · Department of Cardiac Imaging (Division of Nuclear Medicine), The Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Cardiology, The Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Department of Biomedical Sciences and Biomedical Imaging Research Institute, Cedars-Sinai Medical Center, CA, USA. · Department of Radiology and Medicine Weill Cornell Medical College, New York, NY, USA. · Emory Clinical Cardiovascular Research Institute (ECCRI), Emory University School of Medicine, Atlanta, GA, USA. ·Atherosclerosis · Pubmed #25461732.

ABSTRACT: OBJECTIVES: The predictive value of thoracic aortic calcium (TAC) scores for coronary artery calcium (CAC) conversion (CAC>0) has not been fully evaluated. METHODS: We studied 1648 asymptomatic subjects (mean age 52 ± 9 years, 54% male) with baseline CAC = 0 who underwent repeat CAC scanning 5 years later (range 3-14 years). TAC was assessed in the ascending and descending aorta. CAC and TAC were measured using Agatston scores. The cohort was categorized by baseline TAC scores: TAC = 0 (n = 1381 subjects), TAC 1-9 (n = 54), TAC 10-99 (n = 132) and TAC≥100 (n = 81). Logistic regression was used to examine the predictive value of baseline TAC scores for CAC>0 on repeat scans. RESULTS: On repeat scanning, 380 subjects (23%) developed CAC>0. The frequency of CAC>0 increased progressively across baseline TAC (TAC = 0, TAC 1-9, TAC 10-99 and TAC≥100) 22%, 26%, 26% and 37%, respectively (P for trend = 0.0025). Univariate analysis showed baseline TAC ≥100 was a significant predictor of CAC>0 in repeat scans, while either TAC 1-9 or TAC 10-99 were not, OR 2.10 [CI 1.32-3.36], P = 0.002; OR 1.25 [CI 0.67-2.33], P = 0.5; OR 1.24 [CI 0.82-1.87], P = 0.3, respectively. In multivariable analysis, TAC ≥100 OR 1.90 [CI 1.08-3.33], P = 0.026, was a significant predictor of CAC>0, along with age, male gender, diabetes, hypertension, hypercholesterolemia and time between scans. CONCLUSIONS: The likelihood of conversion to CAC>0 increases with increasing TAC scores. TAC ≥ 100 is an independent predictor of CAC conversion. Subjects with CAC = 0 and extensive TAC (TAC ≥ 100) may merit earlier repeat scanning than those with no TAC or lower TAC scores.

11 Article Marked acceleration of atherosclerosis after Lactobacillus casei-induced coronary arteritis in a mouse model of Kawasaki disease. 2012

Chen, Shuang / Lee, Youngho / Crother, Timothy R / Fishbein, Michael / Zhang, Wenxuan / Yilmaz, Atilla / Shimada, Kenichi / Schulte, Danica J / Lehman, Thomas J A / Shah, Prediman K / Arditi, Moshe. ·David Geffen School of Medicine at the University of California, Division of Pediatric Infectious Diseases and Immunology, Burns and Allen Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048, USA. ·Arterioscler Thromb Vasc Biol · Pubmed #22628430.

ABSTRACT: OBJECTIVE: The purpose of this study was to investigate whether Lactobacillus casei cell wall extract-induced Kawasaki disease (KD) accelerates atherosclerosis in hypercholesterolemic mice. Method and Results- Apolipoprotein E knockout or low-density lipoprotein receptor knockout mice were injected with Lactobacillus casei cell wall extract (KD mice) or PBS, fed high-fat diet for 8 weeks, and atherosclerotic lesions in aortic sinuses, arch (AC), and whole aorta were assessed. KD mice had larger, more complex aortic lesions with abundant collagen, and both extracellular and intracellular lipid and foam cells, compared with lesions in control mice despite similar cholesterol levels. Both apolipoprotein E knockout KD and low-density lipoprotein receptor knockout KD mice showed dramatic acceleration in atherosclerosis versus controls, with increases in en face aortic atherosclerosis and plaque size in both the aortic sinuses and AC plaques. Accelerated atherosclerosis was associated with increased circulating interleukin-12p40, interferon-γ, tumor necrosis factor-α, and increased macrophage, dendritic cell, and T-cell recruitment in lesions. Furthermore, daily injections of the interleukin-1Ra, which inhibits Lactobacillus casei cell wall extract-induced KD vasculitis, prevented the acceleration of atherosclerosis. CONCLUSIONS: Our results suggest an important pathophysiologic link between coronary arteritis/vasculitis in the KD mouse model and subsequent atherosclerotic acceleration, supporting the concept that a similar relation may also be present in KD patients. These results also suggest that KD in childhood may predispose to accelerated and early atherosclerosis as adults.

12 Article High levels of IgM against methylglyoxal-modified apolipoprotein B100 are associated with less coronary artery calcification in patients with type 2 diabetes. 2012

Engelbertsen, D / Anand, D V / Fredrikson, G N / Hopkins, D / Corder, R / Shah, P K / Lahiri, A / Nilsson, J / Bengtsson, E. ·Department of Clinical Sciences, Skåne University Hospital, Lund University, Malmö, Sweden. daniel.engelbertsen@med.lu.se ·J Intern Med · Pubmed #21668821.

ABSTRACT: OBJECTIVE:   Advanced glycation end products (AGE) have been implicated in diabetic vascular complications through activation of pro-inflammatory genes. AGE-modified proteins are also targeted by the immune system resulting in the generation of AGE-specific autoantibodies, but the association of these immune responses with diabetic vasculopathy remains to be fully elucidated. The aim of this study was to determine whether antibodies against apolipoprotein B100 modified by methylglyoxal (MGO-apoB100) are associated with coronary atherosclerosis in patients with type 2 diabetes. METHODS:   We measured antibodies against MGO-apoB100 in plasma from 497 type 2 diabetic patients without clinical signs of cardiovascular disease. Severity of coronary disease was assessed as coronary artery calcium (CAC) imaging. Immunoglobulin (Ig)M and IgG levels recognizing MGO-apoB100 were determined by enzyme-linked immunosorbent assay. RESULTS:   Anti-MGO-apoB100 IgM antibody levels were higher in subjects with a low to moderate CAC score (≤400 Agatston units) than in subjects with a high score (>400 Agatston units; 136.8±4.4 vs. 101.6± 7.4 arbitrary units (AU), P<0.0001) and in subjects demonstrating no progression of CAC during 30 months of follow-up (136.4±5.7 vs. 113.9 ± 6.2 AU in subjects with progression, P<0.0001). Subjects with a family history of premature myocardial infarction had lower levels of anti-MGO-apoB100 IgM. Female subjects had higher levels of anti-MGO-apoB100 antibodies and lower CAC than men. Accordingly, high levels of IgM against MGO-apoB100 are associated with less severe and a lower risk of progression of coronary disease in subjects with type 2 diabetes. CONCLUSIONS: Although conclusions regarding causal relationships based on epidemiological observations need to be made with caution, our findings suggest the possibility that anti-MGO-apoB100 IgM may be protective in diabetic vasculopathy.

13 Article Atherosclerosis: targeting endogenous apo A-I--a new approach for raising HDL. 2011

Shah, Prediman K. ·Division of Cardiology and Oppenheimer Atherosclerosis Research Center, Cedars Sinai Heart Institute, Suite 5531, Cedars Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. shahp@cshs.org ·Nat Rev Cardiol · Pubmed #21364534.

ABSTRACT: -- No abstract --