This document summarizes clinical guidelines for cholesterol management and cardiovascular risk reduction. It compares the 2013 ACC/AHA guidelines to previous NCEP ATP III guidelines. The new guidelines have a focus on reducing atherosclerotic cardiovascular disease risk rather than just coronary heart disease risk. They recommend high-intensity statin therapy for more patient groups based on revised risk assessment categories and calculators. Key changes include expanding statin benefit to those with diabetes or a 7.5% or higher 10-year risk without cardiovascular disease. Management of high triglycerides is also discussed.
This document provides guidelines for the assessment and management of dyslipidemia from several major organizations. It discusses risk assessment tools for cardiovascular disease from ATP III, ADA, ACC/AHA, and QRISK2. It also compares statin intensity categories between NICE and ACC/AHA guidelines. The document recommends lifestyle modification as first-line treatment and the use of high-intensity statins for primary and secondary prevention of CVD according to the guidelines of NICE, ADA, and ACC/AHA.
The document discusses lipid abnormalities and cardiovascular risk in patients with insulin resistance and diabetes. It notes that lipid abnormalities affect all lipid fractions, characterized by elevated triglycerides, remnant lipoproteins, small dense LDL, and low HDL. Lifestyle modifications and medical therapies can help treat diabetic dyslipidemia and reduce cardiovascular risk. The guidelines recommend statin therapy along with lifestyle changes to lower LDL and reduce risk, and address other lipid abnormalities as needed.
This document provides guidelines and recommendations for lipid management:
1. It summarizes the 2013 ACC/AHA guidelines and 2016 ACC expert consensus, focusing on proven therapy rather than arbitrary lipid targets. Lifestyle changes like diet and exercise are encouraged for all.
2. Statins are recommended for four major groups to reduce ASCVD risk. High, moderate, and low intensity statin therapies are defined based on average LDL-C reduction.
3. For patients who are truly statin intolerant or require additional lowering, the document provides guidance on use of non-statin therapies like ezetimibe, basing selection on risk level and comorbidities.
This document provides guidelines for the management of dyslipidemia from the European Society of Cardiology in 2016. It discusses lipid profiling, total cardiovascular risk assessment, treatment strategies, lifestyle modifications, treatment targets, and choice of treatment. Lipid profiling is recommended for those with cardiovascular disease, at increased risk, or for risk stratification. LDL-C is the primary treatment target, while non-HDL-C and apoB are secondary targets. Lifestyle changes and statin therapy are first-line treatment, with fibrates, nicotinic acid or PCSK9 inhibitors as options for additional lowering of lipids. Guidelines for treatment targets and special populations are also covered.
This document provides an overview of dyslipidemia including the physiology of lipid metabolism, the role of lipoproteins in atherosclerosis, screening and treatment approaches. It covers topics such as the exogenous and endogenous pathways of lipid metabolism, key enzymes involved, how lipids contribute to atherosclerosis, diagnostic evaluation, and management with an emphasis on statin therapy and other lipid-lowering drug classes and their mechanisms of action and side effects.
This document provides an overview of the management of dyslipidemia. It discusses lipoprotein classification and composition. It also outlines the non-pharmacological and pharmacological treatment approaches for different dyslipidemia scenarios, including various drug classes like statins, PCSK9 inhibitors, fibrates and their effects. It discusses treatment approaches for different patient groups such as those with cardiovascular disease, diabetes, chronic kidney disease, inflammatory conditions and others. The guidelines for screening and management of dyslipidemia in various clinical situations are summarized.
- The patient is a 50-year-old male smoker with hypertension for 6 years. His lipid profile shows a total cholesterol of 210 mg/dL, triglycerides of 180 mg/dL, LDL of 119 mg/dL, and HDL of 30 mg/dL.
- According to guidelines, he is at high cardiovascular risk due to smoking, hypertension, and lipid levels. Egypt is also considered a very high risk country.
- The appropriate measures for this high risk patient include lifestyle modifications plus high-intensity statin therapy, with an LDL cholesterol goal of less than 70 mg/dL. Monitoring is also needed.
This document provides guidelines for the assessment and management of dyslipidemia from several major organizations. It discusses risk assessment tools for cardiovascular disease from ATP III, ADA, ACC/AHA, and QRISK2. It also compares statin intensity categories between NICE and ACC/AHA guidelines. The document recommends lifestyle modification as first-line treatment and the use of high-intensity statins for primary and secondary prevention of CVD according to the guidelines of NICE, ADA, and ACC/AHA.
The document discusses lipid abnormalities and cardiovascular risk in patients with insulin resistance and diabetes. It notes that lipid abnormalities affect all lipid fractions, characterized by elevated triglycerides, remnant lipoproteins, small dense LDL, and low HDL. Lifestyle modifications and medical therapies can help treat diabetic dyslipidemia and reduce cardiovascular risk. The guidelines recommend statin therapy along with lifestyle changes to lower LDL and reduce risk, and address other lipid abnormalities as needed.
This document provides guidelines and recommendations for lipid management:
1. It summarizes the 2013 ACC/AHA guidelines and 2016 ACC expert consensus, focusing on proven therapy rather than arbitrary lipid targets. Lifestyle changes like diet and exercise are encouraged for all.
2. Statins are recommended for four major groups to reduce ASCVD risk. High, moderate, and low intensity statin therapies are defined based on average LDL-C reduction.
3. For patients who are truly statin intolerant or require additional lowering, the document provides guidance on use of non-statin therapies like ezetimibe, basing selection on risk level and comorbidities.
This document provides guidelines for the management of dyslipidemia from the European Society of Cardiology in 2016. It discusses lipid profiling, total cardiovascular risk assessment, treatment strategies, lifestyle modifications, treatment targets, and choice of treatment. Lipid profiling is recommended for those with cardiovascular disease, at increased risk, or for risk stratification. LDL-C is the primary treatment target, while non-HDL-C and apoB are secondary targets. Lifestyle changes and statin therapy are first-line treatment, with fibrates, nicotinic acid or PCSK9 inhibitors as options for additional lowering of lipids. Guidelines for treatment targets and special populations are also covered.
This document provides an overview of dyslipidemia including the physiology of lipid metabolism, the role of lipoproteins in atherosclerosis, screening and treatment approaches. It covers topics such as the exogenous and endogenous pathways of lipid metabolism, key enzymes involved, how lipids contribute to atherosclerosis, diagnostic evaluation, and management with an emphasis on statin therapy and other lipid-lowering drug classes and their mechanisms of action and side effects.
This document provides an overview of the management of dyslipidemia. It discusses lipoprotein classification and composition. It also outlines the non-pharmacological and pharmacological treatment approaches for different dyslipidemia scenarios, including various drug classes like statins, PCSK9 inhibitors, fibrates and their effects. It discusses treatment approaches for different patient groups such as those with cardiovascular disease, diabetes, chronic kidney disease, inflammatory conditions and others. The guidelines for screening and management of dyslipidemia in various clinical situations are summarized.
- The patient is a 50-year-old male smoker with hypertension for 6 years. His lipid profile shows a total cholesterol of 210 mg/dL, triglycerides of 180 mg/dL, LDL of 119 mg/dL, and HDL of 30 mg/dL.
- According to guidelines, he is at high cardiovascular risk due to smoking, hypertension, and lipid levels. Egypt is also considered a very high risk country.
- The appropriate measures for this high risk patient include lifestyle modifications plus high-intensity statin therapy, with an LDL cholesterol goal of less than 70 mg/dL. Monitoring is also needed.
This document discusses guidelines for managing dyslipidemia with statins. It identifies 4 main groups that benefit from statin treatment based on their ASCVD risk: 1) those with clinical ASCVD, 2) those with LDL-C >190 mg/dL, 3) those with diabetes aged 40-75 with LDL-C 70-189 mg/dL, and 4) those aged 40-75 without clinical ASCVD or diabetes but with LDL-C 70-189 mg/dL and 10-year ASCVD risk >7.5%. The document reviews evidence that moderate- and high-intensity statin therapy lowers ASCVD risk across all baseline LDL-C levels above 70 mg/dL. It provides guidance on
This document discusses dyslipidemia and cholesterol metabolism. It defines dyslipidemia as abnormal lipoprotein metabolism characterized by elevated total cholesterol, LDL, triglycerides, and decreased HDL. Primary dyslipidemias are caused by genetic mutations affecting lipid production and clearance. Secondary dyslipidemias are more common and caused by lifestyle and medical factors like diabetes or hypothyroidism. The document outlines the different lipoproteins, cholesterol types, their roles in atherosclerosis, and recommendations for treatment and lipid goals from ATP III guidelines based on a patient's risk factors.
The document discusses treatment of hypertensive patients who also have dyslipidemia. It describes a case study of a 57-year-old man with prior myocardial infarction, uncontrolled hypertension, and elevated LDL cholesterol. Clinical trials show that intensive statin therapy to achieve lower LDL levels reduces cardiovascular risks more than moderate statin therapy. The Heart Protection Study also found that simvastatin reduced cardiovascular events in high-risk patients, regardless of baseline LDL level.
"48 SLIDES???!!", my friends shouted.
A boring "48 slides" is depend on how you arrange it. And this is not the one for sure.
I always love to prepare a short and sweet presentation. Or maybe long but sweet presentation? Oh yeah! Enjoy!
#SLIDESKILLSvsSLIDEKILLS
The document discusses guidelines for managing dyslipidemia, including interpreting lipid profiles and determining when to treat patients with high LDL or low HDL levels. It recommends treating individuals with clinical atherosclerotic cardiovascular disease, primary LDL elevations over 190 mg/dL, diabetes with LDL between 70-189 mg/dL, or without diabetes or clinical ASCVD but with a 10-year risk over 7.5% and LDL between 70-189 mg/dL. Clinical atherosclerotic cardiovascular disease is defined as conditions like heart attacks, angina, stroke, and peripheral arterial disease presumed to be from atherosclerosis. The document emphasizes determining when treatment is necessary based on a patient's lipid levels and risk factors.
Dyslipidemia, or abnormal lipid levels in the blood, increases the risk of atherosclerosis and cardiovascular disease. The document discusses the definition and causes of dyslipidemia as well as screening recommendations. It also summarizes the roles of different lipids like LDL, HDL, and triglycerides in atherosclerosis. The treatment approaches for different lipid abnormalities are outlined, including lifestyle modifications and medications like statins, fibrates, bile acid sequestrants, nicotinic acid, and ezetimibe.
This document summarizes guidelines for managing diabetes in cardiac patients from the American Diabetes Association in 2011. It discusses studies that show intensive glucose control reduces cardiovascular outcomes for type 2 diabetes patients. However, the ACCORD trial found intensive control increased mortality, likely due to hypoglycemia. The ADA evidence grading system and criteria for diagnosing diabetes are also presented.
This patient presents with multiple metabolic risk factors including obesity, elevated triglycerides and fasting blood glucose, and a family history of diabetes. While she does not meet the criteria for metabolic syndrome, her 10-year risk of heart disease is elevated. Her LDL cholesterol goal according to NCEP guidelines is less than 160 mg/dL. Fasting glucose would be most influential in determining her treatment plan given her risk factors.
Dyslipidemia
Disorder of Lipid & Lipoprotein Metabolism
A common form of Dyslipidemia is characterized
by three lipid abnormalities:
Elevated triglycerides,
Elevated LDL and
Reduced HDL cholesterol.
Important Modifiable Risk Factor for CAD
This document outlines guidelines for screening and treating dyslipidemia. It discusses lipid handling in the body and pathophysiology of atherosclerosis. Current drug treatments include statins as first-line therapy, with bile acid sequestrants, nicotinic acid, fibrates, ezetimibe, and omega-3 fatty acids as alternatives. Newer drugs that inhibit PCSK9 are also mentioned. Treatment goals depend on risk level, with lifestyle changes recommended initially before adding drug therapy for higher risk patients.
Dyslipidemia management an evidence based approachDr Vivek Baliga
In this presentation by Dr Vivek Baliga, he discusses the different available statins and how you can choose the right one in different clinical situations. See articles from Dr Baliga on http://drvivekbaliga.net
This document discusses metabolic syndrome, which is a combination of medical disorders that increase the risk of cardiovascular disease and diabetes when occurring together. It affects about 20% of the Malaysian population. The core components include hypertension, high triglycerides, low HDL cholesterol, obesity, and impaired glucose tolerance. There are different criteria for diagnosing metabolic syndrome, but central to all definitions is insulin resistance. If left untreated, metabolic syndrome can increase the risk of serious health conditions such as heart disease, stroke, and type 2 diabetes.
Dyslipidemia refers to abnormalities in lipoprotein metabolism that result in high total cholesterol, high LDL cholesterol, low HDL cholesterol, and high triglycerides. The prevalence of dyslipidemia varies but is estimated to affect over 100 million Americans. Dyslipidemia is caused by both genetic factors like familial hypercholesterolemia as well as secondary factors such as diabetes, hypothyroidism, and certain medications. It is a major risk factor for cardiovascular disease.
This document provides an overview of diabetic dyslipidemia and lipid management recommendations for patients with diabetes. It discusses that excess fat contributes to atherosclerosis and mortality in diabetes. It outlines traditional and non-traditional risk factors for cardiovascular disease. The spectrum of diabetic dyslipidemia includes quantitative changes like high triglycerides and qualitative changes in lipoprotein composition. Lifestyle modifications and statin therapy are recommended to improve lipid profiles and reduce cardiovascular risk according to guidelines. The appropriate screening, interpretation of results, and intensity of statin therapy depends on individual patient risk factors and characteristics.
The document provides guidelines for cholesterol management and cardiovascular disease (CVD) risk assessment. It discusses guidelines for measuring cholesterol and lipid levels, calculating LDL and VLDL values, and assessing CVD risk. It recommends starting moderate- or high-intensity statin therapy for most adults aged 40-75 years with diabetes or LDL ≥70 mg/dL. For those without diabetes but with a CVD risk of 7.5% or higher, it recommends discussing statin therapy. The guidelines also provide recommendations for managing statin side effects, evaluating risk factors, and refining risk assessment using coronary artery calcium scoring. The main messages are to emphasize lifestyle changes, use high-intensity statins for high-risk patients, and consider patient risk
Diabetes and heart two sides of the same coinSunil Wadhwa
This ppt presented in a CME of doctors in March 2017 discusses-if all Diabetics should be treated aggressively for prevention of coronary artery disease & SHOULD IT BE PRESUMED AS IF THEY ARE ALREADY PATIENTS OF CAD?
This presentation is updated till March 2017
This document discusses cardiovascular disease risk factors and prevention strategies. It covers primary and secondary prevention. Key modifiable risk factors discussed include smoking, hypertension, hyperlipidemia, diabetes, obesity, physical inactivity, and diet. Prevention strategies focus on lifestyle modifications, risk factor control through medications if needed, and cardiac rehabilitation. Population-level interventions to reduce salt and saturated fat intake are also recommended.
1) The patient has a 10.8% 10-year ASCVD risk, placing him in the intermediate risk category.
2) For patients in this category, guidelines recommend evaluating additional risk enhancers such as family history of premature CVD, metabolic syndrome, inflammation, and coronary artery calcium score.
3) Based on the assessment of risk enhancers, the guidelines recommend either moderate or high-intensity statin therapy.
Ponencia realizada por el Prof. Alberto Zambon en la segunda sesión de CardioVascular Virtual Topic 2022, titulada Residual cardiovascular risk. What is the role of icosapent ethyl?
The document discusses guidelines for managing dyslipidemia and cardiovascular disease risk, including:
1) It provides risk levels (very high, high, moderate, low) based on calculated cardiovascular risk and clinical factors and recommends LDL-C treatment targets for each level.
2) It discusses statin treatment for different risk levels, recommending the highest tolerated dose to reach LDL-C targets.
3) It summarizes trials comparing different statins and their average LDL-C reduction, finding some are more effective than others at reducing LDL-C.
This document discusses guidelines for managing dyslipidemia with statins. It identifies 4 main groups that benefit from statin treatment based on their ASCVD risk: 1) those with clinical ASCVD, 2) those with LDL-C >190 mg/dL, 3) those with diabetes aged 40-75 with LDL-C 70-189 mg/dL, and 4) those aged 40-75 without clinical ASCVD or diabetes but with LDL-C 70-189 mg/dL and 10-year ASCVD risk >7.5%. The document reviews evidence that moderate- and high-intensity statin therapy lowers ASCVD risk across all baseline LDL-C levels above 70 mg/dL. It provides guidance on
This document discusses dyslipidemia and cholesterol metabolism. It defines dyslipidemia as abnormal lipoprotein metabolism characterized by elevated total cholesterol, LDL, triglycerides, and decreased HDL. Primary dyslipidemias are caused by genetic mutations affecting lipid production and clearance. Secondary dyslipidemias are more common and caused by lifestyle and medical factors like diabetes or hypothyroidism. The document outlines the different lipoproteins, cholesterol types, their roles in atherosclerosis, and recommendations for treatment and lipid goals from ATP III guidelines based on a patient's risk factors.
The document discusses treatment of hypertensive patients who also have dyslipidemia. It describes a case study of a 57-year-old man with prior myocardial infarction, uncontrolled hypertension, and elevated LDL cholesterol. Clinical trials show that intensive statin therapy to achieve lower LDL levels reduces cardiovascular risks more than moderate statin therapy. The Heart Protection Study also found that simvastatin reduced cardiovascular events in high-risk patients, regardless of baseline LDL level.
"48 SLIDES???!!", my friends shouted.
A boring "48 slides" is depend on how you arrange it. And this is not the one for sure.
I always love to prepare a short and sweet presentation. Or maybe long but sweet presentation? Oh yeah! Enjoy!
#SLIDESKILLSvsSLIDEKILLS
The document discusses guidelines for managing dyslipidemia, including interpreting lipid profiles and determining when to treat patients with high LDL or low HDL levels. It recommends treating individuals with clinical atherosclerotic cardiovascular disease, primary LDL elevations over 190 mg/dL, diabetes with LDL between 70-189 mg/dL, or without diabetes or clinical ASCVD but with a 10-year risk over 7.5% and LDL between 70-189 mg/dL. Clinical atherosclerotic cardiovascular disease is defined as conditions like heart attacks, angina, stroke, and peripheral arterial disease presumed to be from atherosclerosis. The document emphasizes determining when treatment is necessary based on a patient's lipid levels and risk factors.
Dyslipidemia, or abnormal lipid levels in the blood, increases the risk of atherosclerosis and cardiovascular disease. The document discusses the definition and causes of dyslipidemia as well as screening recommendations. It also summarizes the roles of different lipids like LDL, HDL, and triglycerides in atherosclerosis. The treatment approaches for different lipid abnormalities are outlined, including lifestyle modifications and medications like statins, fibrates, bile acid sequestrants, nicotinic acid, and ezetimibe.
This document summarizes guidelines for managing diabetes in cardiac patients from the American Diabetes Association in 2011. It discusses studies that show intensive glucose control reduces cardiovascular outcomes for type 2 diabetes patients. However, the ACCORD trial found intensive control increased mortality, likely due to hypoglycemia. The ADA evidence grading system and criteria for diagnosing diabetes are also presented.
This patient presents with multiple metabolic risk factors including obesity, elevated triglycerides and fasting blood glucose, and a family history of diabetes. While she does not meet the criteria for metabolic syndrome, her 10-year risk of heart disease is elevated. Her LDL cholesterol goal according to NCEP guidelines is less than 160 mg/dL. Fasting glucose would be most influential in determining her treatment plan given her risk factors.
Dyslipidemia
Disorder of Lipid & Lipoprotein Metabolism
A common form of Dyslipidemia is characterized
by three lipid abnormalities:
Elevated triglycerides,
Elevated LDL and
Reduced HDL cholesterol.
Important Modifiable Risk Factor for CAD
This document outlines guidelines for screening and treating dyslipidemia. It discusses lipid handling in the body and pathophysiology of atherosclerosis. Current drug treatments include statins as first-line therapy, with bile acid sequestrants, nicotinic acid, fibrates, ezetimibe, and omega-3 fatty acids as alternatives. Newer drugs that inhibit PCSK9 are also mentioned. Treatment goals depend on risk level, with lifestyle changes recommended initially before adding drug therapy for higher risk patients.
Dyslipidemia management an evidence based approachDr Vivek Baliga
In this presentation by Dr Vivek Baliga, he discusses the different available statins and how you can choose the right one in different clinical situations. See articles from Dr Baliga on http://drvivekbaliga.net
This document discusses metabolic syndrome, which is a combination of medical disorders that increase the risk of cardiovascular disease and diabetes when occurring together. It affects about 20% of the Malaysian population. The core components include hypertension, high triglycerides, low HDL cholesterol, obesity, and impaired glucose tolerance. There are different criteria for diagnosing metabolic syndrome, but central to all definitions is insulin resistance. If left untreated, metabolic syndrome can increase the risk of serious health conditions such as heart disease, stroke, and type 2 diabetes.
Dyslipidemia refers to abnormalities in lipoprotein metabolism that result in high total cholesterol, high LDL cholesterol, low HDL cholesterol, and high triglycerides. The prevalence of dyslipidemia varies but is estimated to affect over 100 million Americans. Dyslipidemia is caused by both genetic factors like familial hypercholesterolemia as well as secondary factors such as diabetes, hypothyroidism, and certain medications. It is a major risk factor for cardiovascular disease.
This document provides an overview of diabetic dyslipidemia and lipid management recommendations for patients with diabetes. It discusses that excess fat contributes to atherosclerosis and mortality in diabetes. It outlines traditional and non-traditional risk factors for cardiovascular disease. The spectrum of diabetic dyslipidemia includes quantitative changes like high triglycerides and qualitative changes in lipoprotein composition. Lifestyle modifications and statin therapy are recommended to improve lipid profiles and reduce cardiovascular risk according to guidelines. The appropriate screening, interpretation of results, and intensity of statin therapy depends on individual patient risk factors and characteristics.
The document provides guidelines for cholesterol management and cardiovascular disease (CVD) risk assessment. It discusses guidelines for measuring cholesterol and lipid levels, calculating LDL and VLDL values, and assessing CVD risk. It recommends starting moderate- or high-intensity statin therapy for most adults aged 40-75 years with diabetes or LDL ≥70 mg/dL. For those without diabetes but with a CVD risk of 7.5% or higher, it recommends discussing statin therapy. The guidelines also provide recommendations for managing statin side effects, evaluating risk factors, and refining risk assessment using coronary artery calcium scoring. The main messages are to emphasize lifestyle changes, use high-intensity statins for high-risk patients, and consider patient risk
Diabetes and heart two sides of the same coinSunil Wadhwa
This ppt presented in a CME of doctors in March 2017 discusses-if all Diabetics should be treated aggressively for prevention of coronary artery disease & SHOULD IT BE PRESUMED AS IF THEY ARE ALREADY PATIENTS OF CAD?
This presentation is updated till March 2017
This document discusses cardiovascular disease risk factors and prevention strategies. It covers primary and secondary prevention. Key modifiable risk factors discussed include smoking, hypertension, hyperlipidemia, diabetes, obesity, physical inactivity, and diet. Prevention strategies focus on lifestyle modifications, risk factor control through medications if needed, and cardiac rehabilitation. Population-level interventions to reduce salt and saturated fat intake are also recommended.
1) The patient has a 10.8% 10-year ASCVD risk, placing him in the intermediate risk category.
2) For patients in this category, guidelines recommend evaluating additional risk enhancers such as family history of premature CVD, metabolic syndrome, inflammation, and coronary artery calcium score.
3) Based on the assessment of risk enhancers, the guidelines recommend either moderate or high-intensity statin therapy.
Ponencia realizada por el Prof. Alberto Zambon en la segunda sesión de CardioVascular Virtual Topic 2022, titulada Residual cardiovascular risk. What is the role of icosapent ethyl?
The document discusses guidelines for managing dyslipidemia and cardiovascular disease risk, including:
1) It provides risk levels (very high, high, moderate, low) based on calculated cardiovascular risk and clinical factors and recommends LDL-C treatment targets for each level.
2) It discusses statin treatment for different risk levels, recommending the highest tolerated dose to reach LDL-C targets.
3) It summarizes trials comparing different statins and their average LDL-C reduction, finding some are more effective than others at reducing LDL-C.
This is a case of a 74-year-old woman with a history of myocardial infarction who presents for routine follow-up. Her current medications include a statin but her lipid levels are not at goal. The guidelines recommend an LDL goal of <55 mg/dL and at least a 50% reduction for very high risk patients like her. After increasing her statin and adding ezetimibe, her LDL decreased to 53 mg/dL but she had a transient ischemic attack. Additional treatment options to further lower her risk should be considered.
1. The document provides guidelines for assessing and treating high blood cholesterol according to a patient's risk level. It outlines 5 steps to determine a patient's risk category and appropriate cholesterol goals and treatment.
2. Risk is determined based on LDL cholesterol levels, presence of cardiovascular disease or risk equivalents, additional risk factors, and 10-year heart disease risk scores.
3. Based on risk category, LDL cholesterol goals and thresholds for lifestyle changes and drug therapy are established. Lifestyle modification and drug therapy options to lower cholesterol and treat related conditions are also described.
This document summarizes the key guidelines from the Adult Treatment Panel III (ATP III) on cholesterol treatment and prevention. The guidelines focus on multiple risk factors like diabetes, which is considered a cardiovascular disease risk equivalent. It modifies lipid classification cut-offs and recommends a complete lipoprotein profile for screening. It provides LDL cholesterol goals and criteria for lifestyle changes or drug therapy based on a patient's risk category of having cardiovascular disease, multiple risk factors, or 0-1 risk factor. The metabolic syndrome is highlighted as a secondary target of therapy beyond LDL lowering. Case examples are given to demonstrate how the guidelines would be applied.
2013 ACC/AHA guidelines for blood cholesterol managementPraveen Nagula
The 2013 ACC/AHA blood cholesterol treatment guidelines focus on reducing atherosclerotic cardiovascular disease (ASCVD) risk through statin therapy rather than targeting specific LDL-C levels. The guidelines are based on evidence from randomized controlled trials showing consistent ASCVD risk reduction from high- and moderate-intensity statin regimens. They recommend a patient-centered approach and starting statins based on estimated 10-year ASCVD risk rather than using non-HDL or other targets. While lifestyle changes remain important, the guidelines emphasize intensity of statin therapy over addition of nonstatin drugs or targeting specific lipid levels.
The document summarizes the 2013 ACC/AHA blood cholesterol treatment guidelines. The guidelines aim to reduce atherosclerotic cardiovascular disease risk based on evidence from statin randomized controlled trials. The guidelines recommend a patient-centered approach and emphasize that high- and moderate-intensity statin therapy provides the greatest reduction in risk across all baseline LDL-C levels. Primary prevention recommendations are based on estimated 10-year cardiovascular risk. The guidelines do not recommend targeting specific LDL-C levels but rather emphasize intensity of statin therapy.
The American Heart Association and American College of Cardiology, in partnership with the National Heart, Lung and Blood Institute, have released new joint guidelines on cardiovascular disease prevention focusing on hyperlipidemia, hypertension, cardiovascular risk assessment, lifestyle interventions, and obesity. The guidelines provide recommendations on screening and treating dyslipidemia and cardiovascular risk through lifestyle modifications like diet, exercise, weight loss and smoking cessation as well as pharmacological interventions including statin therapy. The guidelines stratify treatment approaches based on levels of cardiovascular risk and recommend high or moderate intensity statins for primary and secondary prevention.
This document discusses diabetic dyslipidemia and lipid management for patients with diabetes. It begins by outlining the pathophysiology of lipid abnormalities in type 2 diabetes, noting insulin resistance leads to increased free fatty acids and triglycerides. It then discusses dyslipidemia as a major risk factor for cardiovascular disease in diabetes. The document reviews the 2013 ADA standards for lipid screening and treatment, including lifestyle modifications and statin therapy goals. It concludes by discussing various antilipidemic drug classes and their effects on lowering LDL, HDL, and triglycerides.
This document discusses guidelines for managing dyslipidemia from several organizations. It summarizes that the ATP III guidelines from 2001 focused on multiple risk factors and modified lipid classifications. It describes risk stratification groups from different guidelines and LDL and non-HDL cholesterol goals. It also discusses management of elevated triglycerides, the metabolic syndrome, and medications and lifestyle changes used to treat dyslipidemia.
Diabetic patients are at high risk for cardiovascular disease due to dyslipidemia and should be treated aggressively to target lipid levels. Lifestyle modifications such as diet, exercise, and weight management are first-line treatment along with statin therapy. Statins should be prescribed to diabetic patients over age 40 with one or more other cardiovascular risk factors, or to those of any age with existing cardiovascular disease, to reduce LDL cholesterol. The main treatment goals are lowering LDL cholesterol to less than 100 mg/dL for patients without cardiovascular disease and less than 70 mg/dL for those with cardiovascular disease.
The document discusses lipid analysis and cardiovascular risk assessment. It recommends using non-fasting lipid samples for general risk screening as they seem to have similar prognostic value as fasting samples. It also recommends using non-HDL cholesterol as a primary treatment target along with LDL cholesterol, as non-HDL cholesterol does not require fasting and accounts for both LDL and triglyceride levels. The document provides guidelines on lipid analysis, risk stratification, and lipid-lowering treatment goals and strategies based on various risk factors.
the aim of sharing this material to help students and provide delayed information regarding topic.You all are most welcome for you suggestion to make i more easy, graspable and attractive.(easy to learn in creative way)
Dyslipidemia guideline review : the transatlantic differencesAshraf Reda
This document summarizes guidelines from various medical organizations for treating dyslipidemia and reducing cardiovascular risk. It outlines LDL-C and non-HDL-C goals for high-risk patients, including those with diabetes or cardiovascular disease. Guidelines from the ADA/ACC, ESC/EAS, and American Diabetes Association are presented, focusing on statin therapy and alternative lipid-lowering agents. The document also discusses evaluating cardiovascular risk using methods like SCORE, targeting atherogenic lipoproteins, managing high triglycerides, addressing genetic dyslipidemias, and improving adherence to treatment.
- Studies have shown that lowering LDL cholesterol through statin therapy such as atorvastatin provides significant cardiovascular benefits in both primary and secondary prevention. Atorvastatin in particular has been shown in clinical trials to reduce cardiovascular events and mortality when used for acute coronary syndromes, stable coronary heart disease, and among those at high risk of cardiovascular disease. Atorvastatin may be a good choice of statin due to its proven efficacy in improving cardiovascular outcomes.
1) While statins are effective at lowering LDL-C and reducing cardiovascular risk, a substantial residual risk remains. Non-HDL cholesterol provides a better assessment of this residual risk as it includes all atherogenic lipoproteins.
2) Guidelines now recommend treating to targets of both LDL-C and non-HDL-C levels in order to lower cardiovascular risk. Triglyceride levels of 200 mg/dL or higher also indicate increased risk.
3) Recent studies show that triglyceride-rich lipoproteins and small, dense LDL particles are strongly associated with risk of myocardial infarction and peripheral artery disease, highlighting the importance of addressing these lipids.
1. The new guidelines recommend initiating moderate or high-intensity statin therapy for patients in four categories based on their cardiovascular risk, rather than targeting a specific LDL-C level.
2. The four categories are: individuals with clinical atherosclerotic cardiovascular disease, LDL-C over 190 mg/dL, diabetes between ages 40-75 with LDL-C 70-189 mg/dL, and 10-year risk over 7.5% for ages 40-75 with LDL-C 70-189 mg/dL.
3. Lipids should be measured during follow-ups to assess adherence, not to achieve a specific target level.
This document provides an overview of the approach to evaluating and diagnosing wide complex tachycardias. It begins with definitions of terms like wide complex tachycardia, ventricular tachycardia, and supraventricular tachycardia. It then discusses the importance of making an accurate diagnosis to avoid inappropriate treatment. Various ECG criteria are presented to help distinguish ventricular from supraventricular rhythms based on features like AV dissociation, QRS morphology, axis, and precordial patterns. Specific criteria for right bundle branch block and left bundle branch block morphologies are also outlined. The document emphasizes taking a stepwise approach and considering clinical history in narrowing the differential diagnosis of wide complex tachycardias.
Ms. Lamia, a 10-year old female from Potuakhali, Barisal, presented with breathlessness for 2-3 weeks and bluish discoloration of her skin since childhood, which worsens with exertion. Examination found central cyanosis, clubbing, and a grade 3/6 ejection systolic murmur, suggesting congenital cyanotic heart disease, most likely Tetralogy of Fallot. Medical management and potential surgical options were discussed.
Echo assessment of Aortic valve disease, Dr Ferdous assistant registrar, Card...Nizam Uddin
This document discusses the echocardiographic evaluation of aortic stenosis. It begins by describing normal aortic valve anatomy and various views used to visualize the aortic valve via 2D echocardiography. It then discusses the classification and causes of aortic stenosis, including calcific, rheumatic, and bicuspid aortic valve stenosis. Evaluation techniques covered include determining aortic valve area using the continuity equation and measuring transaortic jet velocity via continuous-wave Doppler. The document concludes by outlining the anatomical assessment of the aortic valve, methods for determining stenosis severity, and hemodynamic progression of untreated aortic stenosis over time.
This document discusses the limitations and techniques for assessing right ventricular (RV) function using echocardiography. It is difficult to accurately evaluate RV volume, delineate borders, and image the entire RV using echocardiography due to its complex crescent shape. However, the document recommends using RV fractional area change, tricuspid annular plane systolic excursion, tissue Doppler S' velocity, and Tei index to quantitatively assess RV systolic function as they are reproducible methods. RV dimensions, wall thickness, and outflow tract size can also provide information on RV size and function. Assessment of RV diastolic function includes parameters like E/A ratio, E/E' ratio, and deceleration time.
This document discusses the investigation and management of atrial septal defects (ASD). Key points include:
ECG, echocardiography, chest x-ray and cardiac catheterization are used to diagnose ASD. Echocardiography can image the interatrial septum from various views and detect flow between the atria with color Doppler. ASDs are often asymptomatic but can cause complications like pulmonary hypertension. Small and moderate ASDs may be treated with percutaneous device closure while larger defects or those with complications may require surgical repair via patch. The take home message is that small ASDs can often be asymptomatic for life while larger defects cause issues in adulthood, and definitive treatment is via device
The document provides an overview of basic pacing concepts including:
- Types of pacemakers such as single chamber, dual chamber, and triple chamber systems.
- Components of a pacemaker system including the pulse generator, leads, and electrical concepts such as voltage, current, and impedance.
- Factors that can affect pacing thresholds and how to test the pacemaker circuit including identifying high and low impedance conditions.
This document discusses pregnancy and valvular heart disease. It notes that pregnancy places significant strain on the heart and can negatively impact both mother and fetus if the mother has an existing heart condition. It provides details on common valvular heart conditions like mitral stenosis, aortic stenosis, and mechanical heart valves. It discusses physiological changes during pregnancy, risks associated with different conditions, management approaches including medical therapy and delivery planning, and important considerations for monitoring and treatment. The goal is to carefully manage high-risk pregnancies involving heart conditions to optimize outcomes for both mother and baby.
This document discusses pulmonary stenosis, including its investigation and management. Some key points:
- ECG and echocardiography are recommended for initial evaluation and follow-up every 5-10 years. Cardiac catheterization is recommended if Doppler peak jet velocity is over 3m/s.
- Balloon valvuloplasty is recommended for symptomatic patients with gradients over 30mmHg or asymptomatic patients over 40mmHg. It produces excellent short and long-term results.
- Follow-up depends on severity but is usually visits at 6-12 months, 5 years, and every 10 years post-procedure. Pregnancy is generally tolerated for asymptomatic patients but activity should be limited in second half.
This document contains a medical case report for a 40-year-old male electrician named Rubel who was admitted to the hospital for shortness of breath and easy fatigability for the past two months. Upon examination, a murmur was detected consistent with mitral stenosis. Further tests revealed the patient has chronic rheumatic heart disease with moderate mitral stenosis and pulmonary hypertension. He was started on medication and may require a mitral valve procedure or surgery going forward.
A 40-year-old woman presented with recurrent palpitations and breathlessness since childhood. She reports palpitations that worsen with exertion and swelling of her body. On examination, she has clubbing and a thrill present in her pulmonary and tricuspid areas. Her past medical history is notable for multiple visits to local doctors for breathlessness where she was told of an abnormal heart condition.
A 55-year-old female presented with complaints of breathlessness, cough, palpitations and weakness for several months. Examination findings included elevated heart rate, elevated jugular venous pressure, ejection systolic murmur, and basal crepitations. ECG and echocardiogram revealed atrial septal defect with pulmonary hypertension. She was diagnosed with atrial septal defect with congestive cardiac failure and moderate pulmonary hypertension. She was started on medical management including diuretics, ACE inhibitors and digoxin. Surgical or device closure of the defect was recommended.
This document summarizes the 2016 European Society of Cardiology guidelines for the management of atrial fibrillation. It begins with an introduction stating that AF remains a major cause of stroke, heart failure, and other cardiovascular issues worldwide. It also notes that the number of AF patients is predicted to rise significantly. The document then discusses common problems seen with AF patients in critical care and outpatient settings. It lists "do nots" in AF management, such as not using antiplatelet therapy alone for stroke prevention. It provides recommendations on rate control, rhythm control, anticoagulation for stroke prevention, and managing bleeding. It asks about determining the CHA2DS2-VASC score for a hypothetical patient case and discusses
This document provides information on acute rheumatic fever (ARF), including its definition, incidence, pathophysiology, diagnosis, management, and secondary prevention. ARF is an autoimmune response to Group A streptococcal infection that causes inflammation of the heart, joints, brain and skin. It predominantly affects school-aged children and those in low socioeconomic conditions. Accurate diagnosis is important to avoid over- or under-treatment. Management involves treating streptococcal infections, suppressing inflammation, and long-term antibiotic prophylaxis to prevent recurrence.
The document provides guidelines for perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery. It was developed by an expert panel representing multiple medical societies. The guidelines include recommendations on preoperative risk assessment, management of valvular heart disease and pulmonary hypertension, use of cardiovascular implantable electronic devices, and approaches to predicting and reducing perioperative cardiac risk. A stepwise approach to preoperative cardiac assessment and management is presented based on urgency of surgery and estimated risk of major adverse cardiac events.
Heart failure is a clinical syndrome characterized by symptoms such as breathlessness and fatigue caused by structural or functional abnormalities of the heart. It is a leading cause of hospitalization in people over 65. Up to 50% of heart failure patients die within 5 years of diagnosis.
The document discusses classifications of heart failure based on ejection fraction and functional capacity. It provides guidelines on the management of acute heart failure, including treatments to reduce congestion and increase perfusion. Chronic heart failure treatment focuses on reducing mortality and hospitalizations through optimized medical therapy including ACE inhibitors, beta-blockers, MRAs, and newer drugs like sacubitril/valsartan. Device therapies like ICDs and CRT are recommended for
This document discusses drugs used to treat heart failure. It defines heart failure and provides global statistics on prevalence. The goals of pharmacotherapy are to relieve symptoms, improve cardiac function, prevent disease progression and prolong survival. Drugs discussed include ACE inhibitors, ARBs, beta-blockers, aldosterone antagonists, ARNIs, diuretics, digoxin, ivabradine, and omega-3 fatty acids. Recommendations are provided on use of these drugs for heart failure with reduced ejection fraction based on guidelines. The document also briefly discusses treatment of heart failure with preserved ejection fraction.
Tetralogy of Fallot long case discussionNizam Uddin
Ms. Lamia, a 10-year old girl from Potuakhali, Barisal, presented with breathlessness for 2-3 weeks and bluish discoloration of her skin since childhood. Examination found central cyanosis, clubbing, and a grade 3/6 ejection systolic murmur, suggesting congenital cyanotic heart disease, most likely Tetralogy of Fallot. Medical management and potential surgical options were discussed.
This document provides an overview of aortic dissection, including:
- King George II's death in 1760 which was one of the first documented cases.
- The first successful surgical repair was performed by DeBakey in 1955.
- It involves a tear in the inner layer of the aorta that allows blood to enter and force open the middle layer.
- Presentation includes sudden, severe chest pain that may radiate to the back. Early mortality can be as high as 5% per hour without treatment.
- Risk factors include hypertension, connective tissue disorders like Marfan syndrome, and aortic abnormalities.
- Diagnosis involves features like widened mediastinum on C
Restrictive cardiomyopathy is characterized by stiff ventricles that do not fill properly, though systolic function is usually preserved initially. It can be caused by infiltrative diseases, fibrosis, or other processes that restrict ventricular filling. On echocardiogram, restrictive cardiomyopathy shows impaired ventricular filling and enlarged atria, while cardiac catheterization reveals elevated diastolic pressures and a distinctive "square root sign" pressure tracing. Treatment focuses on managing symptoms and underlying causes if identifiable, though prognosis is often poor without transplantation.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
3. ATP III Classification of Cholesterol
Concentrations
Lipoprotein Concentration (mg/dL) Interpretation
TC < 200
200-239
≥240
Desirable
Borderline high
High
LDL-c <100
100-129
130-159
160-189
≥190
Optimal
Near/above optimal
Borderline high
High
Very high
HDL-c <40
≥60
Low
High
TG <150
150-199
200-499
≥500
Normal
Borderline high
High
Very high
4. ATP III Treatment Targets
Exception: TG lowering is an immediate target if ≥ 500
mg/dL
Primary Target:
LDL-c
Secondary Target:
Non-HDL-c
(Once LDL goal met and if TG ≥200)
5. NCEP ATP III: Determining
LDL-c Goals
Yes No
Yes No
Presence of ASVD, DM
High-Risk:
<100mg/dL,
optional <70mg/dL
≥2 major CV risk factors*
10-year CHD risk: FRS
>20% 10-20% <10%
High-Risk:
<100mg/dL
Mod-high Risk:
<130mg/dL,
optional
<100mg/dL
Moderate risk
<130mg/dL
Lower risk
<160mg/dL
6. Targets for Therapy after LDL-C Goal in Patients
with TG 200 mg/dL
Patient Category
LDL-C target
(mg/dL)
Non-HDL-C
target (mg/dL)
CHD or CHD risk
equivalent
<100 <130
No CHD, 2+ RF <130 <160
No CHD, <2 RF <160 <190
10. Individuals with
clinical Atherosclerotic
Cardiovascular Disease (ASCVD)
Individuals ≥ 21 years of age
with primary LDL-C ≥ 190 mg/dl
Individuals of
40-75 years of age with Diabetes
Individuals of 40-75 years of age with
10-year ASCVD risk ≥ 7.5% or higher
Even if they have LDL-C 70-189 mg/dl without ASCVD or Diabetes
12. NCEP ATP III vs ACC/AHA
NCEP ATP III AHA/ACC – ATP IV
Year 2001 (updated in 2004) 2013
Focus Reducing CHD risk Reducing risk of
atherosclerotic CV disease
(ASCVD) – includes CHD +
TIA/stroke, PAD or
revascularisation
Risk
assessment
Framingham 10 yr risk score
(CHD death + non fatal MI
Pooled cohort equations*
(fatal & nonfatal CHD +
fatal & nonfatal stroke
*Developed by the Risk Assessment Work Group to estimate the 10-year ASCVD risk
(defined as first-occurrence nonfatal and fatal MI and nonfatal and fatal stroke) for the
identification of candidates for statin therapy
13. NCEP ATP III vs ACC/AHA
NCEP ATP III AHA/ACC – ATP IV
Risk
Categories
3 main risk categories:
CHD / CHD risk equivalent (DM,
Clinical CHD, symptomatic CAD,
PAD)
2+ risk factors & 10-yr risk ≤ 20%
0-1 risk factors & 10-yr risk <10%
4 statin benefit groups:
Clinical ASCVD
Primary LDL-C elevations ≥190
mg/dl
DM without clinical ASCVD
No DM/CVD with 10-yr ASCVD
risk ≥7.5%
Rx targets LDL-C primary target
<100mg/dl
<130mg/dl (<100 if risk 10-20%)
<160mg/dl
(in the order of categories
mentioned above)
Intensity of statin therapy
High intensity statin therapy
(LDL-C reduction ≥50%)
recommended for most
patients in 4 statin benefit
groups
Rx
recommen
dations
Statin (or bile acid sequestrants or
nicotinic acid) to achieve LDL-C
goal
Maximally tolerated statin
first-line to reduce risk of
ASCVD events
19. Drug Therapy
Nicotinic Acid
• Major actions
Lowers LDL-C 5–25%
Lowers TG 20–50%
Raises HDL-C 15–35%
• Side effects: flushing, hyperglycemia,
hyperuricemia, upper GI distress, hepatotoxicity
• Contraindications: liver disease, severe gout,
peptic ulcer
20.
21. High Triglycerides
(200–499 mg/dL) ?
• Primary goal: achieve LDL-C goal
• First-line therapy for high triglycerides: weight reduction and
increased physical activity
• Second-line therapy: drugs to achieve non-HDL-C goal
– Statins: lowers both LDL-C and VLDL-C
– Fibrates: lowers VLDL-triglycerides and VLDL-C
– Nicotinic acid: lowers VLDL-triglycerides and VLDL-C
(500 mg/dL) ?
Drug therapy for lowering non-HDL-C
– High doses of statins (lower both LDL-C and VLDL-C)
– Moderate doses of statins and triglyceride-lowering drug (fibrate or
nicotinic acid):
• Caution: increased frequency of myopathy with statins + fibrates
25. Take home massage
• ASCVD risk reduction is the main goal by reducing LDL as
much as possible at tolerated doses.
• High intensity statin therapy (LDL-C reduction ≥50%)
recommended for most patients in 4 statin benefit groups
Clinical ASCVD
Primary LDL-C elevations ≥190 mg/dl
DM without clinical ASCVD
No DM/CVD with 10-yr ASCVD risk ≥7.5%
• Pharmacological management is required if isolated TG
500 mg/dL and after LDL-C goal in patients with TG 200
mg/dL
• Guidelines are not a replacement for clinical judgment
26. Hypertension
… the most prevalent modifiable risk factor for
cardiovascular and renal disease worldwide
Editor's Notes
Treatment was stopped after a median follow-up of 3.3 years. By that time, 100 primary events had occurred in the atorvastatin group compared with 154 events in the placebo group (hazard ratio 0.64 [95% CI 0.50-0.83], p=0.0005). This benefit emerged in the first year of follow-up. There was no significant heterogeneity among prespecified subgroups. Fatal and non-fatal stroke (89 atorvastatin vs 121 placebo, 0.73 [0.56-0.96], p=0.024), total cardiovascular events (389 vs 486, 0.79 [0.69-0.90], p=0.0005), and total coronary events (178 vs 247, 0.71 [0.59-0.86], p=0.0005) were also significantly lowered. There were 185 deaths in the atorvastatin group and 212 in the placebo group (0.87 [0.71-1.06], p=0.16). Atorvastatin lowered total serum cholesterol by about 1.3 mmol/L compared with placebo at 12 months, and by 1.1 mmol/L after 3 years of follow-up
The trial was stopped after a median follow-up of 1.9 years (maximum, 5.0). Rosuvastatin reduced LDL cholesterol levels by 50% and high-sensitivity C-reactive protein levels by 37%. The rates of the primary end point were 0.77 and 1.36 per 100 person-years of follow-up in the rosuvastatin and placebo groups, respectively (hazard ratio for rosuvastatin, 0.56; 95% confidence interval [CI], 0.46 to 0.69; P<0.00001), with corresponding rates of 0.17 and 0.37 for myocardial infarction (hazard ratio, 0.46; 95% CI, 0.30 to 0.70; P=0.0002), 0.18 and 0.34 for stroke (hazard ratio, 0.52; 95% CI, 0.34 to 0.79; P=0.002), 0.41 and 0.77 for revascularization or unstable angina (hazard ratio, 0.53; 95% CI, 0.40 to 0.70; P<0.00001), 0.45 and 0.85 for the combined end point of myocardial infarction, stroke, or death from cardiovascular causes (hazard ratio, 0.53; 95% CI, 0.40 to 0.69; P<0.00001), and 1.00 and 1.25 for death from any cause (hazard ratio, 0.80; 95% CI, 0.67 to 0.97; P=0.02). Consistent effects were observed in all subgroups evaluated. The rosuvastatin group did not have a significant increase in myopathy or cancer but did have a higher incidence of physician-reported diabetes
The relative risk of death in the simvastatin group was 0.70 (95% CI 0.58-0.85, p = 0.0003). The 6-year probabilities of survival in the placebo and simvastatin groups were 87.6% and 91.3%, respectively. There were 189 coronary deaths in the placebo group and 111 in the simvastatin group (relative risk 0.58, 95% CI 0.46-0.73), while noncardiovascular causes accounted for 49 and 46 deaths, respectively. 622 patients (28%) in the placebo group and 431 (19%) in the simvastatin group had one or more major coronary events. The relative risk was 0.66 (95% CI 0.59-0.75, p<0.00001), and the respective probabilities of escaping such events were 70.5% and 79.6%. This risk was also significantly reduced in subgroups consisting of women and patients of both sexes aged 60 or more. Other benefits of treatment included a 37% reduction (p<0.00001) in the risk of undergoing myocardial revascularisation procedures
The median LDL cholesterol level achieved during treatment was 95 mg per deciliter (2.46 mmol per liter) in the standard-dose pravastatin group and 62 mg per deciliter (1.60 mmol per liter) in the high-dose atorvastatin group (P<0.001). Kaplan-Meier estimates of the rates of the primary end point at two years were 26.3 percent in the pravastatin group and 22.4 percent in the atorvastatin group, reflecting a 16 percent reduction in the hazard ratio in favor of atorvastatin (P=0.005; 95 percent confidence interval, 5 to 26 percent). The study did not meet the prespecified criterion for equivalence but did identify the superiority of the more intensive regimen
Vital status was confirmed on all but 22 patients. Averaged over the 5 years' study duration, similar proportions in each group discontinued study medication (10% placebo vs 11% fenofibrate) and more patients allocated placebo (17%) than fenofibrate (8%; p<0.0001) commenced other lipid treatments, predominantly statins. 5.9% (n=288) of patients on placebo and 5.2% (n=256) of those on fenofibrate had a coronary event (relative reduction of 11%; hazard ratio [HR]0.89, 95% CI 0.75-1.05; p=0.16). This finding corresponds to a significant 24% reduction in non-fatal myocardial infarction (0.76, 0.62-0.94; p=0.010) and a non-significant increase in coronary heart disease mortality (1.19, 0.90-1.57; p=0.22). Total cardiovascular disease events were significantly reduced from 13.9% to 12.5% (0.89, 0.80-0.99; p=0.035). This finding included a 21% reduction in coronary revascularisation (0.79, 0.68-0.93; p=0.003). Total mortality was 6.6% in the placebo group and 7.3% in the fenofibrate group (p=0.18). Fenofibrate was associated with less albuminuria progression (p=0.002), and less retinopathy needing laser treatment (5.2%vs 3.6%, p=0.0003). There was a slight increase in pancreatitis (0.5%vs 0.8%, p=0.031) and pulmonary embolism (0.7%vs 1.1%, p=0.022), but no other significant adverse effects.
The annual rate of the primary outcome was 2.2% in the fenofibrate group and 2.4% in the placebo group (hazard ratio in the fenofibrate group, 0.92; 95% confidence interval [CI], 0.79 to 1.08; P=0.32). There were also no significant differences between the two study groups with respect to any secondary outcome. Annual rates of death were 1.5% in the fenofibrate group and 1.6% in the placebo group (hazard ratio, 0.91; 95% CI, 0.75 to 1.10; P=0.33). Prespecified subgroup analyses suggested heterogeneity in treatment effect according to sex, with a benefit for men and possible harm for women (P=0.01 for interaction), and a possible interaction according to lipid subgroup, with a possible benefit for patients with both a high baseline triglyceride level and a low baseline level of high-density lipoprotein cholesterol (P=0.057 for interaction
At 2 years, niacin therapy had significantly increased the median HDL cholesterol level from 35 mg per deciliter (0.91 mmol per liter) to 42 mg per deciliter (1.08 mmol per liter), lowered the triglyceride level from 164 mg per deciliter (1.85 mmol per liter) to 122 mg per deciliter (1.38 mmol per liter), and lowered the LDL cholesterol level from 74 mg per deciliter (1.91 mmol per liter) to 62 mg per deciliter (1.60 mmol per liter). The primary end point occurred in 282 patients in the niacin group (16.4%) and in 274 patients in the placebo group (16.2%) (hazard ratio, 1.02; 95% confidence interval, 0.87 to 1.21; P=0.79 by the log-rank test).
Laropirant – prostaglandin receptor antagonist
During a median follow-up period of 3.9 years, participants who were assigned to extended-release niacin-laropiprant had an LDL cholesterol level that was an average of 10 mg per deciliter (0.25 mmol per liter as measured in the central laboratory) lower and an HDL cholesterol level that was an average of 6 mg per deciliter (0.16 mmol per liter) higher than the levels in those assigned to placebo. Assignment to niacin-laropiprant, as compared with assignment to placebo, had no significant effect on the incidence of major vascular events (13.2% and 13.7% of participants with an event, respectively; rate ratio, 0.96; 95% confidence interval [CI], 0.90 to 1.03; P=0.29). Niacin-laropiprant was associated with an increased incidence of disturbances in diabetes control that were considered to be serious (absolute excess as compared with placebo, 3.7 percentage points; P<0.001) and with an increased incidence of diabetes diagnoses (absolute excess, 1.3 percentage points; P<0.001), as well as increases in serious adverse events associated with the gastrointestinal system (absolute excess, 1.0 percentage point; P<0.001), musculoskeletal system (absolute excess, 0.7 percentage points; P<0.001), skin (absolute excess, 0.3 percentage points; P=0.003), and unexpectedly, infection (absolute excess, 1.4 percentage points; P<0.001) and bleeding (absolute excess, 0.7 percentage points; P<0.001).
The median time-weighted average LDL cholesterol level during the study was 53.7 mg per deciliter (1.4 mmol per liter) in the simvastatin-ezetimibe group, as compared with 69.5 mg per deciliter (1.8 mmol per liter) in the simvastatin-monotherapy group (P<0.001). The Kaplan-Meier event rate for the primary end point at 7 years was 32.7% in the simvastatin-ezetimibe group, as compared with 34.7% in the simvastatin-monotherapy group (absolute risk difference, 2.0 percentage points; hazard ratio, 0.936; 95% confidence interval, 0.89 to 0.99; P=0.016). Rates of prespecified muscle, gallbladder, and hepatic adverse effects and cancer were similar in the two groups
No anticipated major changes here:
ATP II HDL low was < 35, ATP III < 40, goal was set to be the same for both men and women because of the view that a given level of HDL would impart the same risk for both genders (no sources sited)
These are classification of parameters, not goals. LDL goal and treatment is individualized based on risk.
Treatment targets are our primary focus to reduce CV risk and reduce CHD event. Expected to be an area of change..
If fasting TG > 500, then TG are primary target because of the risk of pancreatitis.
In all other patients, LDL-c is primary target for initiating and titrating therapy.
Non-HDL is identified as a secondary target in patients with fasting TG > 200. Many trials have demonstrated non-HDL levels are a better predictor of CVD risk than is LDLc. LDL underestimates the burden of atherogenic, cholesterol-carrying lipoproteins
Some experts are expecting more emphasis on non-HDL as a target in ATP IV. Some have gone as far to say it may become a co-target with LDL-c. It is an easy number available with current testing practices.
A recent meta-analysis published in JAMA March 2012 (8 trials, over 60,000 patients) evaluated the strengths of associations between LDL-c, non-HDL-c and apo B with CV risk in patients receiving statins. Although LDL-c, non-HDL-c and apo B levels were each strongly associated with risk of major CV events, the strength of association of future major CV events was higher for non-HDL-c than with LDL-c and apo B. Non-HDL may be proving to be a better surrogate marker for CHD risk and risk reduction. Guidelines are anticipated to reflect this information.
Based on recent trial data and Canadian and European guidelines: it is anticipated that HDL and TG as treatment targets will be deemphasized. But are indicators of metabolic syndrome/IR and other risk factors to modify.
No specific goal for raising HDL because of lack of evidence for benefit
Current : how we assign an individual LDL goal based on risk – stratified based on level of risk
ASVD:
CHD: (MI), angina, coronary artery procedures (angioplasty, bypass)
CHD risk equivalents:
Non-coronary forms of ASVD
Peripheral arterial disease (PAD), abdominal aortic aneurysm (AAA), carotid artery disease, renal artery stenosis
Diabetes (most pts have high risk of CHD events)
Framingham Risk Score > 20%= high risk of CHD event in next 10 year.
Targets for therapy after LDL-C goal in patients with TG 200 mg/dL
Epidemiologic and clinical studies have demonstrated that high blood triglyceride level is an independent risk factor for CHD and that CHD risk is amplified in patients who have elevations in both LDL-C and triglyceride levels. An elevated triglyceride level probably does not contribute to atherogenesis per se but most likely signals the presence of a constellation of lipid abnormalities that increase atherogenic risk, including increased levels of cholesterol-carrying remnant particles, low HDL-C levels, increased numbers of particles, and increased levels of small dense LDL. Patients with these abnormalities often have multiple other CHD risk factors, including central obesity, impaired glucose tolerance, and hypertension.
To address these issues and to enhance the potential for CHD risk reduction, ATP III recommends that secondary treatment targets, defined by non-HDL-C (total cholesterol – HDL-C), be established for those who have a triglyceride level 200 mg/dL, after the LDL-C goal has been achieved. Non-HDL-C goals may be achieved by intensifying lifestyle modification, accentuating LDL-C–lowering therapy, or adding a triglyceride-lowering drug to the LDL-C–lowering regimen. Time and additional clinical trials will establish the utility of these various approaches.
Reference:
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA 2001;285:2486-2497.
*Percent reduction in LDL-C can be used as an indication of response and adherence to therapy, but is not in itself a treatment goal. †The Pooled Cohort Equations can be used to estimate 10-year ASCVD risk in individuals With and without diabetes. The estimator within this application should be used to inform decision making in primary prevention patients Not on a statin.
‡Consider moderate-intensity statin as more appropriate in low-risk individuals.
§For those in whom a risk assessment is uncertain, consider factors such as primary LDL-C =160 mg/dL or other evidence of genetic hyperlipidemias, family history of premature ASCVD with onset <55 years of age in a first-degree male relative or <65 years of age in a first-degree female relative, hs-CRP =2 mg/L, CAC score =300 Agatston units, or =75th percentile for age, sex, and ethnicity (for additional information, see http://www.mesa-nhlbi. org/CACReference.aspx), ABI <0.9, or lifetime risk of ASCVD. Additional factors that may aid in individual risk assessment may be identified in the future.
‖Potential ASCVD risk-reduction benefits. The absolute reduction in ASCVD events from moderate- or high-intensity Statin therapy can be approximated by multiplying the estimated 10-year ASCVD risk by the anticipated relative-risk reduction from the Intensity of statin initiated (~30% for moderate-intensity statin or ~45% for high-intensity statin therapy). The net ASCVD risk-reduction benefit is estimated from the number of potential ASCVD events prevented with a statin, compared to the number of potential excess adverse effects.
¶Potential adverse effects. The excess risk of diabetes is the main consideration in ~0.1 excess cases per 100 individuals treated with a moderate-intensity statin for 1 year and ~0.3 excess cases per 100 individuals treated with a high-intensity statin for 1 year. In RCTs, both statin-treated and placebo-treated participants experienced the same rate of muscle symptoms. The actual rate of statin-related muscle symptoms in the clinical population is unclear. Muscle symptoms attributed to statin therapy should be evaluated (see Table 8, Safety Recommendation 8).
ABI indicates ankle-brachial index; ASCVD, atherosclerotic cardiovascular disease; CAC, coronary artery calcium; hs-CRP, high-sensitivity C-reactive protein; LDL-C, low-density lipoprotein cholesterol; MI, myocardial infarction; and RCT, randomized controlled trial.)
This guideline recommends using the new Pooled Cohort Risk Assessment Equations developed by the Risk Assessment Work Group to estimate the 10-year ASCVD risk (acute coronary syndromes, a history of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, transient ischemic attack, or peripheral arterial disease presumed to be of atherosclerotic origin) for the identification of candidates for statin therapy (see
http://my.americanheart.org/cvriskcalculator and http://www.cardiosource.org/en/Science-And-Quality/Practice-Guidelinesand-Quality-Standards/2013-Prevention-Guideline-Tools.aspx for risk calculator). These equations should be used to predict stroke as well as CHD events in non-Hispanic, Caucasian, and
African-American women and men 40 to 79 years of age with or without diabetes who have LDL-C levels 70 to 189 mg/dL and are not receiving statin therapy