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Coronary Artery Disease: HELP
Articles by Prediman K. Shah
Based on 13 articles published since 2008
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Between 2008 and 2019, 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 Review Contemporary approach to the diagnosis and management of non-ST-segment elevation acute coronary syndromes. 2008

Boden, William E / Shah, Prediman K / Gupta, Vipul / Ohman, E Magnus. ·Division of Cardiology, Department of Medicine, Buffalo General Hospital and Kaleida Health, State University of New York (SUNY) at Buffalo School of Medicine and Biomedical Science, Buffalo, NY 14203, USA. ·Prog Cardiovasc Dis · Pubmed #18313479.

ABSTRACT: The management of patients with acute coronary syndromes (ACS) has evolved dramatically over the past decade and, in many respects, represents a rapidly moving target for the cardiologist and internist who seek to integrate these recent advances into contemporary clinical practice. Unstable angina and non-ST-segment elevation myocardial infarction (MI) comprise a growing percentage of patients with ACS and is emerging as a major public health problem worldwide, especially in Western countries, despite significant improvements and refinements in management over the past 20 years. Against this backdrop of a multitude of randomized, controlled clinical trials that have established the scientific foundation upon which evidence-based treatment strategies have emerged and become increasingly refined, the clinician is frequently confronted with panoply of choices that can create uncertainty or confusion regarding "optimal management". While the debate about the ideal approach to the management of non-ST-segment elevation (NSTE) ACS (i.e., routine "early invasive strategy" versus an "ischemia-guided", or "conservative", strategy) has been ongoing for over a decade, clinical trials results provide compelling evidence that intermediate- and high-risk ACS patients derived significant reductions in both morbidity and mortality with mechanical or surgical intervention, especially when revascularization is coupled with aggressive, multifaceted (anti-platelet, antithrombin, anti-ischemic and anti-atherogenic) medical therapy along with risk factor modification. For these reasons, it seems especially timely and appropriate to present a state-of-the-art paper that reviews the latest advances in the management of NSTE ACS, mindful of the fact that even this noble effort to synthesize and integrate a prodigious amount of scientific information and cardiovascular therapeutics is destined to evolve still further as our full-scale assault on optimizing clinical outcomes by harmonizing the advances in mechanical and pharmacologic interventions continues unabated.

8 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.

9 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.

10 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.

11 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.

12 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 --

13 Article The editor's roundtable: atherosclerosis regression. 2008

Friedewald, Vincent E / Ballantyne, Christie M / Nissen, Steven E / Shah, P K / Roberts, William C. ·Department of Internal Medicine, The University of Texas Medical School at Houston, Houston, TX, USA. vfriedew@nd.edu ·Am J Cardiol · Pubmed #18359316.

ABSTRACT: -- No abstract --