American Journal of Preventive Cardiology

2022

DOI: 10.1016/j.ajpc.2022.100335

|View full text |Cite

|

Sign up to set email alerts

|

Atherosclerotic cardiovascular disease risk assessment: An American Society for Preventive Cardiology clinical practice statement

¹

,

Matthew J. Budoff

²

,

Keith C. Ferdinand

³

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Introduction2

Epidemiologic Studies About Remnant Cholesterol Levels and A...1

Citation Types

Supporting

2

Mentioning

65

Contrasting

0

Year Published

2022

2022

2024

2024

Publication Types

Select...

Article8

Book2

Relationship

Self Cite1

Independent9

Authors

Journals

Cited by 120 publications

(67 citation statements)

References 237 publications

Supporting

2

Mentioning

65

Contrasting

0

Order By: Relevance

“…So far, epidemiological research has confirmed that triglycerides is an independent risk factor for atherosclerotic coronary heart disease ( 35 ). The relationship between triglycerides and coronary heart disease was statistically significant when the adjusted multivariate logistic regression models were performed on triglycerides and other factors ( 14 , 36 ).…”

Section: Epidemiologic Studies About Remnant Cholesterol Levels and A...mentioning

confidence: 99%

Remnant cholesterol and atherosclerotic cardiovascular disease: Metabolism, mechanism, evidence, and treatment

¹

,

²

,

³

et al. 2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

This review aimed to summarize the evidence of elevated remnant cholesterol and the risks of atherosclerotic cardiovascular disease (ASCVD) and to search for further guidance in clinical therapy. The lipids-lowering treatments such as statins and ezetimibe targeted on low-density lipoprotein cholesterol (LDL-C) have always been the first-line therapy for ASCVD. However, even after statins or new lipid-lowering drugs lowered LDL-C to recommended concentrations, and with other risk factors well-controlled, such as high blood pressure, the risks of developing ASCVD remained. Remnant cholesterol (RC) referred to the cholesterol contained in all remnant lipoprotein particles, which was the cholesterol in the hydrolyzed very-low-density lipoprotein and intermediate-density lipoprotein in the fasting state, and the cholesterol in the chylomicron remnants in the postprandial state. Evidence from in vitro and animal pathogenic mechanisms studies, epidemiology, and genetic studies all indicated that RC played an important role in predicting the incidence of ASCVD. As a new indicator to reflect atherosclerosis, especially when LDL-C has been controlled to a recommended level, RC was considered as a priority treatment target for people at high risk of ASCVD. The use of statins, fibrates, APOC3 inhibitors, PCSK9 inhibitors, and omega-3 fatty acids to reduce RC levels in the plasma may provide long-term benefits. However, the standardized detection of RC was still controversial, and more studies on appropriate treatments of elevated RC are urgently needed. These positive trials may benefit more patients at high ASCVD risks worldwide in the future.

“…So far, epidemiological research has confirmed that triglycerides is an independent risk factor for atherosclerotic coronary heart disease ( 35 ). The relationship between triglycerides and coronary heart disease was statistically significant when the adjusted multivariate logistic regression models were performed on triglycerides and other factors ( 14 , 36 ).…”

Section: Epidemiologic Studies About Remnant Cholesterol Levels and A...mentioning

confidence: 99%

Remnant cholesterol and atherosclerotic cardiovascular disease: Metabolism, mechanism, evidence, and treatment

¹

,

²

,

³

et al. 2022

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

This review aimed to summarize the evidence of elevated remnant cholesterol and the risks of atherosclerotic cardiovascular disease (ASCVD) and to search for further guidance in clinical therapy. The lipids-lowering treatments such as statins and ezetimibe targeted on low-density lipoprotein cholesterol (LDL-C) have always been the first-line therapy for ASCVD. However, even after statins or new lipid-lowering drugs lowered LDL-C to recommended concentrations, and with other risk factors well-controlled, such as high blood pressure, the risks of developing ASCVD remained. Remnant cholesterol (RC) referred to the cholesterol contained in all remnant lipoprotein particles, which was the cholesterol in the hydrolyzed very-low-density lipoprotein and intermediate-density lipoprotein in the fasting state, and the cholesterol in the chylomicron remnants in the postprandial state. Evidence from in vitro and animal pathogenic mechanisms studies, epidemiology, and genetic studies all indicated that RC played an important role in predicting the incidence of ASCVD. As a new indicator to reflect atherosclerosis, especially when LDL-C has been controlled to a recommended level, RC was considered as a priority treatment target for people at high risk of ASCVD. The use of statins, fibrates, APOC3 inhibitors, PCSK9 inhibitors, and omega-3 fatty acids to reduce RC levels in the plasma may provide long-term benefits. However, the standardized detection of RC was still controversial, and more studies on appropriate treatments of elevated RC are urgently needed. These positive trials may benefit more patients at high ASCVD risks worldwide in the future.

“…Cardiovascular diseases (CVDs) are a group of disorders of the heart and blood vessels [ 1 ]. They are a set of heterogeneous diseases whose underlying cause of development is most often atherosclerosis [ 2 ]. CVDs are chronic diseases that gradually evolve throughout life and remain asymptomatic for a long time [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

¹

,

²

,

³

et al. 2022

View full text Add to dashboard Cite

Cardiovascular diseases (CVDs) are disorders associated with the heart and circulatory system. Atherosclerosis is its major underlying cause. CVDs are chronic and can remain hidden for a long time. Moreover, CVDs are the leading cause of global morbidity and mortality, thus creating a major public health concern. This review summarizes the available information on the pathophysiological implications of CVDs, focusing on coronary artery disease along with atherosclerosis as its major cause and arterial hypertension. We discuss the endothelium dysfunction, inflammatory factors, and oxidation associated with atherosclerosis. Mechanisms such as dysfunction of the endothelium and inflammation, which have been identified as critical pathways for development of coronary artery disease, have become easier to diagnose in recent years. Relatively recently, evidence has been found indicating that interactions of the molecular and cellular elements such as matrix metalloproteinases, elements of the immune system, and oxidative stress are involved in the pathophysiology of arterial hypertension. Many studies have revealed several important inflammatory and genetic risk factors associated with CVDs. However, further investigation is crucial to improve our knowledge of CVDs progression and, more importantly, accelerate basic research to improve our understanding of the mechanism of pathophysiology.

“…Hypertension, a chronic condition of elevation in blood pressure (BP), is a well-known risk factor for the development of cardiovascular diseases (CVDs), including heart failure, coronary heart diseases, myocardial fibrosis, and infarction [ 1 ], atherosclerosis [ 1 , 2 ], stroke [ 1 , 3 ], and kidney failure [ 4 ]. The pathogenesis of hypertension is multifaceted, and one of the well-characterized causes is endothelial dysfunction resulting from nitric oxide (NO) deficiency [ 5 , 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Disparate Roles of Oxidative Stress in Rostral Ventrolateral Medulla in Age-Dependent Susceptibility to Hypertension Induced by Systemic l-NAME Treatment in Rats

¹

,

²

2022

View full text Add to dashboard Cite

This study aims to investigate whether tissue oxidative stress in the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons reside, plays an active role in age-dependent susceptibility to hypertension in response to nitric oxide (NO) deficiency induced by systemic L-NAME treatment, and to decipher the underlying molecular mechanisms. Systolic blood pressure (SBP) and heart rate (HR) in conscious rats were recorded, along with measurements of plasma and RVLM level of NO and reactive oxygen species (ROS), and expression of mRNA and protein involved in ROS production and clearance, in both young and adult rats subjected to intraperitoneal (i.p.) infusion of L-NAME. Pharmacological treatments were administered by oral gavage or intracisternal infusion. Gene silencing of target mRNA was made by bilateral microinjection into RVLM of lentivirus that encodes a short hairpin RNA (shRNA) to knock down gene expression of NADPH oxidase activator 1 (Noxa1). We found that i.p. infusion of L-NAME resulted in increases in SBP, sympathetic neurogenic vasomotor activity, and plasma norepinephrine levels in an age-dependent manner. Systemic L-NAME also evoked oxidative stress in RVLM of adult, but not young rats, accompanied by augmented enzyme activity of NADPH oxidase and reduced mitochondrial electron transport enzyme activities. Treatment with L-arginine via oral gavage or infusion into the cistern magna (i.c.), but not i.c. tempol or mitoQ10, significantly offset the L-NAME-induced hypertension in young rats. On the other hand, all treatments appreciably reduced L-NAME-induced hypertension in adult rats. The mRNA microarray analysis revealed that four genes involved in ROS production and clearance were differentially expressed in RVLM in an age-related manner. Of them, Noxa1, and GPx2 were upregulated and Duox2 and Ucp3 were downregulated. Systemic L-NAME treatment caused greater upregulation of Noxa1, but not Ucp3, mRNA expression in RVLM of adult rats. Gene silencing of Noxa1 in RVLM effectively alleviated oxidative stress and protected adult rats against L-NAME-induced hypertension. These data together suggest that hypertension induced by systemic L-NAME treatment in young rats is mediated primarily by NO deficiency that occurs both in vascular smooth muscle cells and RVLM. On the other hand, enhanced augmentation of oxidative stress in RVLM may contribute to the heightened susceptibility of adult rats to hypertension induced by systemic L-NAME treatment.

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Product

Browser Extension Assistant by scite Citation Statement Search Reference Check Visualizations Dashboards Explore Journals Explore Organizations Explore Funders Embedding Badge Embedding Citation Search Pricing

Resources

Blog Help & FAQ Accessibility Statement API Terms For Universities & Governments For Researchers For Publishers For Corporate, Pharma & Enterprise Author Marketing Become an Affiliate Get an organization trial or quote scite Data & Services

About

News & Press Careers Read our Paper Coverage

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Copyright © 2024 scite LLC. All rights reserved.

Made with 💙 for researchers

Part of the Research Solutions Family.