Slide Library

Managing Lipids in Diabetes - Landmark Trials of Intensive Diabetes Control and Cardiovascular Complications

What impact does intensive blood glucose control have on CV complications in patients with diabetes? What are the major findings of CV outcome trials conducted the past 10 years? Does intensive glucose control improve CV mortality? What are important considerations for future studies?
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Managing Lipids in Diabetes - Cardiovascular Outcomes Trials in Type 2 Diabetes

What are the main objectives of the cardiovascular outcomes trials (CVOT) for type 2 diabetes (T2D) therapeutics? Over the past 7 years, what have the outcomes of major CVOTs for T2D therapeutics shown? Which drug classes have demonstrated the greatest cardiovascular benefits? How have diabetes guidelines changed in response to results of CVOT trials?
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Risk Assessment & Goals - Assessing CVD Risk: Risk Calculators

How is ASCVD risk assessed? What are the benefits and disadvantages of the various available risk assessment tools? Is metabolic syndrome a stronger predictor of CV risk compared to CV risk scoring tools? How do emerging risk markers further refine risk stratification?
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Risk Assessment & Goals - The Cholesterol Hypothesis to the Cholesterol Principle: Genetic, Epidemiologic, and Clinical Trials Proving Causality

The Cholesterol Hypothesis, also known as the Lipid Hypothesis, postulates a direct link between blood cholesterol levels and CHD. Studies show a higher and earlier occurrence of heart disease in patients with higher blood lipid levels. Strategies to decrease plasma lipid levels (primarily LDL - C) reduces CHD risk at the patient and population level. Although other CHD risk factors exist, the causal role of lipid accumulation in CHD pathogenesis has been shown in clinical, epidemiologic, and genetic analyses. Based on the strength of available evidence, is it time to rename the “Cholesterol Hypothesis” the “Cholesterol Principle”?
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Risk Assessment & Goals - Triglyceride-Rich Lipoproteins

What are the types and key features of triglyceride - rich lipoproteins (T G RLs)? What are the endogenous and exogenous metabolic pathways of T G RLs ? What is the role of polymorphisms in metabolic abnormalities of triglycerides? What role do T G RLs play in atherosclerotic cardiovascular disease (ASCVD)?
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Treatment Strategies - Niacin Nicotinic Acid (Vitamin B3)

What is nico7nic acid (niacin)? What are the recognized side effects of niacin? What are the key results from clinical and imaging trials of niacin treatment? How did results from “historical” trials differ from results of the more “recent” AIM - HIGH and HPS2 - THRIVE RCTs, and how did trial designs differ?
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Treatment Strategies - Statins

What is the role of statin therapy in the management of dyslipidemia and prevention of CVD? What are starting statin doses, dosage ranges, metabolic effects, and main considerations? How should statin treatment be monitored? What is the major evidence supporting the use of statin therapy?
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Treatment Strategies - Merits of Targeting LDL - C, Triglycerides, HDL - C, and Non - HDL - C, and Addressing Residual Risk

What risk factors contribute to a patient's total risk profile for cardiometabolic disease, including residual CAD risk? How does targeting HDL - C vs HDL - P affect risk? What are the merits of targeting (reducing) TG and how does the setting of high cholesterol contribute to risk associated with high TGs? What are the benefits of lowering LDL - C, non - HDL - C, Apo B, and LDL - P? How low should LDL - C lowering go?
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Treatment Strategies - Proprotein Convertase Sub1lisin/ Kexin Type 9 (PCSK9) Inhibitors

What are proprotein convertase subtilisin/ kexin type 9 ( PCSK9) inhibitors and how do they work? Which patients are candidates for PCSK9 inhibitor therapy? What is the expected response to PCSK9 inhibitor therapy?
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Treatment Strategies - Novel New Therapeutic Classes for Atherosclerotic Cardiovascular Disease

What have recent studies shown regarding residual CV risk in patients on statins? What new agents are available to address residual risk? What are the mechanisms of action of these therapeutics, and what patient populations do they benefit? What are current AACE recommendations for the use of novel new therapeutic agents for ASCVD?
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Treatment Strategies - Assessment and Treatment of Hypertriglyceridemia

What is the risk burden of hypertriglyceridemia? What is the clinical and gene7c evidence for the associa7on between elevated TG and atherosclerosis? What are the evidence - based guideline recommenda7ons for managing pa7ents with hypertriglyceridemia? What TG - lowering agents are available, and what are their an7 - atherosclero7c and an7 - inflammatory proper7es?
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Treatment Strategies - Dyslipidemia Management

What are the causes of dyslipidemia? What are current lipid treatment goals? What treatments are available for dyslipidemia? How should treatment be monitored?
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Treatment Strategies - Fibrates

What is the role of fibrates in the treatment of dyslipidemia? What key studies have demonstrated significant clinical benefit with combination therapy (statins + fibrates)? What are the current AACE treatment guidelines regarding the use of fibrates for dyslipidemia management? What specific populations benefit from fibrate therapy?
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Treatment Strategies - Omega - 3 Fatty Acids

What are omega - 3 fatty acids/fish oil and how do they fit into treatment for dyslipidemia? What are the recommendations and considerations for treatment with omega - 3 fatty acids/fish oil?
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Treatment Strategies - Dietary Strategies for Improving Cardiovascular Health

What dietary factors increase the risk of CVD? What is the place of nutrition in reducing the risk of CVD and improving cardiovascular health in patients with dyslipidemia? How do different nutrients contribute to improving CVD health?
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ACSVD Risk in Special Situations - Familial Chylomicronemia Syndrome (FCS)

What is familial chylomicronemia syndrome (FCS) and how does it differ from other types of severe HTG? What is the pathophysiology of severe HTG and FCS? What are the adverse consequences of severe HTG (with or without FCS) and what is their pathophysiology? How should FCS be diagnosed? How should FCS be management?
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