Showing 6 ideas for tag "atherosclerosis"

Goal 2: Reduce Human Disease

What pathobiology underlies the interaction of the diabetogenic hormone amylin with vascular media ?

Amylin is synthesized and co-secreted with insulin by pancreatic beta-cells, plays a complex role in peripheral energy homeostasis, and shows also a high propensity to oligomerize when overexpressed (hyperamylinemia). Accumulation of oligomerized amylin is a pathological hallmark of the islet in diabetic patients and induces oxidative stress, inflammation and apoptosis. However, recent studies found significant deposits... more »

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Goal 2: Reduce Human Disease

Translational and basic research on high triglycerides as an additional risk for cardiovascular disease.

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Previous studies have focused on high cholesterol as a risk factor for cardiovascular disease (CVD). Recent epidemiologic and genetic studies with apoCIII mutation, for example, have identified significant contribution of high triglycerides (TGs) to the development of atherosclerotic CVD. In particular, the epidemics of obesity, even from young age, in the US and worldwide have caused significant increases in the prevalence of hypertriglyceridemia, which has become a serious health problem. However, how hypertriglyceridemia increases risk for atherosclerotic CVD remains largely unknown. Further translational and basic studies would be needed to examine how TG-rich lipoproteins and cholesterol-rich lipoproteins cooperate to increase the risk for CVD. Basic research would need to be conducted at integrative, cellular and molecular levels including examining how TGs are metabolized and how TG-rich lipoproteins, along with cholesterol-rich lipoproteins, cause atherosclerosis. These studies would guide clinical approach on TG- versus cholesterol-lowering therapy for prevention and treatment of atherosclerotic CVD.

Feasibility and challenges of addressing this CQ or CC

The challenges include combining large clinical studies and basic research. Clinical studies includes confirming high TGs as an independent risk for atherosclerotic CVD, developing novel TG-lowering therapy and examining whether these novel TG-lowering therapy, with apoCIII as a target for example, would be beneficial in prevention and treatment of CVD. It is also important to examine effects of novel TG-lowering therapy on adiposity, adipose tissue function and risk of diabetes. Basic science needs to elucidate how TGs are metabolized in vivo, causing hypertriglyceridemia, and how hypertriglyceridemia increases risk for atherosclerotic CVD, and identify novel pathways for these pathophysiological processes, which would provide novel strategies for development of new therapy for CVD. Collaborative approach with great financial support will make all these feasible.

Name of idea submitter and other team members who worked on this idea Huaizhu Wu, MD

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Goal 2: Reduce Human Disease

More funding for Kawasaki Disease Vasculitis

Kawasaki Disease is the most common cause of acquired heart disease among children and we just started to understand that Kawasaki Disease 9 unrecognized during childhood) maybe responsible for a large number of adult atherosclerotic diseases and excellent animal models for this vasculitis exist and more funding should be allocated for this disease. We are now starting to understand that Kawasaki Disease is NOT a self... more »

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Goal 2: Reduce Human Disease

Predicting and monitoring atherosclerosis progression and vulnerable plaque

How to develop novel methods for predicting and monitoring atherosclerosis progression and vulnerable plaque including biomarkers and imaging?

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Name of idea submitter and other team members who worked on this idea Society for Vascular Surgery

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Goal 2: Reduce Human Disease

What is the Relationship Between CVD and Dementia in the Elderly?

The successes of preventing and treating CHD, CVD has resulted in a substantial increase in life expectancy, a very important success story, but unfortunately it has led to a growing population of elderly 80+ years of age.

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Their high prevalence of congestive heart failure (CHF), atrial fibrillation (Afib), stroke, peripheral vascular disease, dementia, frailty, and disability is clearly going to lead to the public health tsunami of the 21st century and bankrupt the health systems. Further studies are badly needed to determine the interrelationship between CVD, dementia, disability, and whether prevention of CVD beginning early in life, middle ages, or even at older ages can impact on successful aging with reduced risks of dementia and disability.

Feasibility and challenges of addressing this CQ or CC

Older individuals with 0 coronary artery calcium (CAC) have extremely low risk of subsequent clinical CHD, CVD, and total mortality even at older ages. Whether these individuals with low risk, e.g. very low CAC, have less extensive brain abnormalities associated with increased risk of dementia needs to be evaluated.

The NHLBI should establish a registry of individuals who have had very low CAC scores at older ages, determine the relationship between these very low CAC scores and risk factors, genetics, and then consider trials to prevent CVD, CHD among older individuals 80+ with relatively low levels of CAC, with dementia, stroke, CHF, Afib, as primary endpoints. The NHLBI should also consider trials in middle-aged individuals to prevent the development and progression of coronary atherosclerosis, e.g. maintenance of 0 CAC. The NHLBI, in collaboration with other institutes at NIH, should evaluate the interrelationship between coronary artery atherosclerosis, e.g. CAC, and other measures of atherosclerosis, other manifestations of CVD, such as CHF, Afib, and brain changes and the development of dementia and Alzheimer’s disease.

Name of idea submitter and other team members who worked on this idea Lewis H. Kuller, MD, DrPH

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Goal 2: Reduce Human Disease

Does lowering circulating lipoprotein(a) levels influence cardiovascular outcomes?

A comprehensive research strategy and plan is needed to determine the most efficient, safe, cost-effective and widely applicable strategy to decrease circulating levels of lipoprotein(a) and to determine whether lowering circulating lipoprotein(a) levels will reduce the risk of developing cardiovascular disease such as a heart attack or a stroke as well as the progression of atherosclerosis or aortic stenosis.

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Approximately 20% of the population are characterized by elevated circulating levels of lipoprotein(a), regardless of age, gender or blood cholesterol levels. Estimates suggest that up to 90% of the variation in plasma lipoprotein(a) levels could be due to genetic factors, which makes lipoprotein(a) the most prevalent inherited risk factor for cardiovascular diseases (CVD). Large-scale genetic studies have shown that Lipoprotein(a) was the strongest genetic determinant of CVD such as atherosclerosis and aortic stenosis. Lipoprotein(a) is one of the strongest predictors of residual CVD risk and has been shown to improve CVD risk prediction in several population-based studies. Lipoprotein(a) is also one of the strongest known risk factors for spontaneous ischemic stroke in childhood.
A comprehensive research strategy aiming at identifying, evaluating interaction with other risk factors, treating and educating patients with elevated lipoprotein(a) levels would result in substantial reductions of health care costs in the US and around the globe by reducing the burden of CVD while simultaneously improving the quality of life of these patients.

Feasibility and challenges of addressing this CQ or CC

The list of pharmaceutical agents that reduce lipoprotein(a) levels is steadily increasing. There are approximately half a dozen strategies that have been shown to significantly and safely lower lipoprotein(a) levels. One of the challenges of this research strategy will be to determine which of these strategies represent the most efficient, safe, cost-effective and widely applicable approach to lower lipoprotein(a) levels and CVD outcomes.
Increasing awareness on lipoprotein(a) and CVD will also be of utmost importance for this effort as relatively few physicians perform lipoprotein(a) testing and even fewer patients are aware of their lipoprotein(a) level. The first sign of high lipoprotein(a) is often a heart attack or stroke. Our challenge will be to identify patients with high lipoprotein(a) that could be enrolled in trials of risk characterization and lipoprotein(a)-lowering.

Name of idea submitter and other team members who worked on this idea Sandra Revill Tremulis on behalf of the Lipoprotein(a) Foundation Scientific Advisory Board

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