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.
Atorvastatin: Statins in CVD management. Is just lipid lowering enough Dr Vivek Baliga
When it comes to management of cardiovascular diseases, are achieving lipid lowering targets sufficient. Here Dr Vivek Baliga, Consultant Internal medicine discusses the additional benefits of statins in CVD in India.
DIABETES AND CARDIOVASCULAR DISEASE - THE CONTINUUMPraveen Nagula
DIABETES IS ONE OF THE MOST COMMON NONCOMMUNICABLE DISEASES WORLD WIDE.
EVERY 6 SECONDS ONE PERSON IS AFFECTED BY DIABETES..
THEME FOR 2014-2016
LETS UNITE FOR DIABETES
Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia.
Several distinct types of DM are caused by a complex interaction of genetics and environmental factors.
Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production.
The metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual with diabetes and on the health care system.
this was the first lecture which i delivered as a doctor. it was about dyslipidemia. i hope you will find information valuable to you here. please read. let me know about your ideas. comment.
Atorvastatin: Statins in CVD management. Is just lipid lowering enough Dr Vivek Baliga
When it comes to management of cardiovascular diseases, are achieving lipid lowering targets sufficient. Here Dr Vivek Baliga, Consultant Internal medicine discusses the additional benefits of statins in CVD in India.
DIABETES AND CARDIOVASCULAR DISEASE - THE CONTINUUMPraveen Nagula
DIABETES IS ONE OF THE MOST COMMON NONCOMMUNICABLE DISEASES WORLD WIDE.
EVERY 6 SECONDS ONE PERSON IS AFFECTED BY DIABETES..
THEME FOR 2014-2016
LETS UNITE FOR DIABETES
Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia.
Several distinct types of DM are caused by a complex interaction of genetics and environmental factors.
Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production.
The metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual with diabetes and on the health care system.
this was the first lecture which i delivered as a doctor. it was about dyslipidemia. i hope you will find information valuable to you here. please read. let me know about your ideas. comment.
Cardiometabolic Disease Pathophysiology & Novel Therapies for Atherosclerosis...InsideScientific
In this webinar, Dr. Michael Sturek reviews features of macrovascular atherosclerosis and microvascular dysfunction that underlie ischemic events and the need for appropriate animal models for optimal translation.
The unabated increase in cardiometabolic disease is a main reason why coronary heart disease remains the leading cause of death worldwide. Despite the effectiveness of lipid lowering therapy in treatment of coronary atherosclerosis, calcification remains a challenging clinical problem.
Lipid lowering therapy is highly effective in treating atherosclerosis, but statins and exercise have been shown to increase coronary artery calcification. Dr. Sturek will review data showing a predominance of intracellular calcium (Ca2+) release in coronary smooth muscle cells that decreases remarkably in cells from metabolic syndrome swine and humans. The early event in coronary artery calcification, i.e. the extracellular deposit of Ca2+ crystals as hydroxyapatite, may be triggered by impaired lysosomal Ca2+ signaling. Selective, novel modulation of lysosomal Ca2+ stores may alter autophagy and matrix vesicle release to treat coronary atherosclerosis and calcification.
Diabetic Dyslipidemia
By Dr. Usama Ragab Youssif
ISMA CME Activity 2021
In Tolip EL Galala Hotel
-----------
Introduction
Physiology of lipid metabolism
Pathophysiology of diabetic dyslipidemia
Statin therapy (+/- ezetimibe) evidence and translation of evidence
Residual CV risk: excess TG
EPA therapy evidence and translation of evidence
Medical Nutrition Therapy for Cardiovascular Diseases, Krause Book 14th editionBatoul Ghosn
Prepared from the chapter of MNT of CVD from Krause's book 14 the edition 2017 as well as some part from " Modern Nutrition in health and disease" 11th edition.
Anti-Obesity Pharmacotherapy: Where are we now? Where are we going?InsideScientific
Obesity is a treatable chronic disease. With nearly 2 billion individuals worldwide classified as being overweight and 650 million as having obesity, it is critical to optimize implementation of existing treatment interventions and develop novel therapies to mitigate the obesity pandemic. Anti-obesity medications are one of the essential tools in our medical toolbox to help patients achieve their health and weight goals.
In this webinar, Dr. Jastreboff discusses current use of anti-obesity pharmacotherapy, mechanisms involved, and agents in various stages of development with considerations for next steps. The presentation aims to inspire development of innovative therapeutics while optimizing use of existing agents to address the urgent need to effectively and sustainably treat millions of individuals with obesity around the world.
Key Topics Include:
- Understand the role of anti-obesity pharmacotherapy in the treatment of obesity
- Describe current anti-obesity pharmacotherapy
- Discuss anti-obesity medications under development
Cardiovascular disease - more common in diabetic patients than in the general population
Dyslipidemia – common in patients with both types of diabetes.
Aggressive lipid treatment goals have been recommended for patients with type 2 diabetes
Diabetic Dyslipidemia is highly prevalent in the Indian diabetic population
Dyslipidemia in diabetes differs significantly with hypertriglyceridemia and small dense LDL-C
Review of the New ACC/AHA Cholesterol GuidelinesTerry Shaneyfelt
The ACC/AHA recently released updated cholesterol treatment guidelines. I review them along with what I feel are their limitations. Watch my YouTube video describing these slides: http://youtu.be/2BlUhW6Zu2E
Cardiometabolic Disease Pathophysiology & Novel Therapies for Atherosclerosis...InsideScientific
In this webinar, Dr. Michael Sturek reviews features of macrovascular atherosclerosis and microvascular dysfunction that underlie ischemic events and the need for appropriate animal models for optimal translation.
The unabated increase in cardiometabolic disease is a main reason why coronary heart disease remains the leading cause of death worldwide. Despite the effectiveness of lipid lowering therapy in treatment of coronary atherosclerosis, calcification remains a challenging clinical problem.
Lipid lowering therapy is highly effective in treating atherosclerosis, but statins and exercise have been shown to increase coronary artery calcification. Dr. Sturek will review data showing a predominance of intracellular calcium (Ca2+) release in coronary smooth muscle cells that decreases remarkably in cells from metabolic syndrome swine and humans. The early event in coronary artery calcification, i.e. the extracellular deposit of Ca2+ crystals as hydroxyapatite, may be triggered by impaired lysosomal Ca2+ signaling. Selective, novel modulation of lysosomal Ca2+ stores may alter autophagy and matrix vesicle release to treat coronary atherosclerosis and calcification.
Diabetic Dyslipidemia
By Dr. Usama Ragab Youssif
ISMA CME Activity 2021
In Tolip EL Galala Hotel
-----------
Introduction
Physiology of lipid metabolism
Pathophysiology of diabetic dyslipidemia
Statin therapy (+/- ezetimibe) evidence and translation of evidence
Residual CV risk: excess TG
EPA therapy evidence and translation of evidence
Medical Nutrition Therapy for Cardiovascular Diseases, Krause Book 14th editionBatoul Ghosn
Prepared from the chapter of MNT of CVD from Krause's book 14 the edition 2017 as well as some part from " Modern Nutrition in health and disease" 11th edition.
Anti-Obesity Pharmacotherapy: Where are we now? Where are we going?InsideScientific
Obesity is a treatable chronic disease. With nearly 2 billion individuals worldwide classified as being overweight and 650 million as having obesity, it is critical to optimize implementation of existing treatment interventions and develop novel therapies to mitigate the obesity pandemic. Anti-obesity medications are one of the essential tools in our medical toolbox to help patients achieve their health and weight goals.
In this webinar, Dr. Jastreboff discusses current use of anti-obesity pharmacotherapy, mechanisms involved, and agents in various stages of development with considerations for next steps. The presentation aims to inspire development of innovative therapeutics while optimizing use of existing agents to address the urgent need to effectively and sustainably treat millions of individuals with obesity around the world.
Key Topics Include:
- Understand the role of anti-obesity pharmacotherapy in the treatment of obesity
- Describe current anti-obesity pharmacotherapy
- Discuss anti-obesity medications under development
Cardiovascular disease - more common in diabetic patients than in the general population
Dyslipidemia – common in patients with both types of diabetes.
Aggressive lipid treatment goals have been recommended for patients with type 2 diabetes
Diabetic Dyslipidemia is highly prevalent in the Indian diabetic population
Dyslipidemia in diabetes differs significantly with hypertriglyceridemia and small dense LDL-C
Review of the New ACC/AHA Cholesterol GuidelinesTerry Shaneyfelt
The ACC/AHA recently released updated cholesterol treatment guidelines. I review them along with what I feel are their limitations. Watch my YouTube video describing these slides: http://youtu.be/2BlUhW6Zu2E
A draft of another seminar I've prepared on a key topic - the video will follow, like/follow this and I'll make sure you get to have a look! (note: the slides without the narrative are in fairness limited in value, but might pique the interest)
This update represents the first major guideline revision since the National Cholesterol Education Program released
its Adult Treatment Panel III report in 2002
"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
Blood test metrics interpretation cholesterol et alIvor Cummins
Blood test metrics explained briefly, with a summary of the conversion factors for US/European Cholesterol and Triglyceride units. See the presentation at https://www.youtube.com/watch?v=YRFRRqe0vrE
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)
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
3. 3
New Features of ATP III
Focus on Multiple Risk Factors
• Diabetes: CHD risk equivalent
• Framingham projections of 10-year CHD risk
– Identify certain patients with multiple risk
factors for more intensive
treatment
• Multiple metabolic risk factors (metabolic
syndrome)
– Intensified therapeutic lifestyle changes
4. 4
New Features of ATP III (continued)
Modification of Lipid and Lipoprotein Classification
• LDL cholesterol <100 mg/dL—optimal
• HDL cholesterol <40 mg/dL
– Categorical risk factor
– Raised from <35 mg/dL
• Lower triglyceride classification cut points
– More attention to moderate elevations
5. 5
New Features of ATP III (continued)
New Recommendation for Screening/Detection
• Complete lipoprotein profile preferred
– Fasting total cholesterol, LDL, HDL, triglycerides
• Secondary option
– Non-fasting total cholesterol and HDL
– Proceed to lipoprotein profile if TC ≥200 mg/dL
or HDL <40 mg/dL
6. 6
New Features of ATP III (continued)
New strategies for Promoting Adherence
In both:
• Therapeutic Lifestyle Changes (TLC)
• Drug therapies
7. 7
New Features of ATP III (continued)
• For patients with triglycerides ≥200 mg/dL
– LDL cholesterol: primary target of therapy
– Non-HDL cholesterol: secondary target of
therapy
Non HDL-C = total cholesterol – HDL cholesterol
12. 12
Risk Assessment
Count major risk factors
• For patients with multiple (2+) risk factors
– Perform 10-year risk assessment
• For patients with 0–1 risk factor
– 10 year risk assessment not required
– Most patients have 10-year risk <10%
13. 13
Major Risk Factors (Exclusive of LDL
Cholesterol) That Modify LDL Goals
• Cigarette smoking
• Hypertension (BP ≥140/90 mmHg or on
antihypertensive medication)
• Low HDL cholesterol (<40 mg/dL)†
• Family history of premature CHD
– CHD in male first degree relative <55 years
– CHD in female first degree relative <65 years
• Age (men ≥45 years; women ≥55 years)
†
HDL cholesterol ≥60 mg/dL counts as a “negative” risk factor; its
presence removes one risk factor from the total count.
15. 15
CHD Risk Equivalents
• Risk for major coronary events equal to that in
established CHD
• 10-year risk for hard CHD >20%
Hard CHD = myocardial infarction + coronary death
16. 16
Diabetes as a CHD Risk Equivalent
• 10-year risk for CHD ≅ 20%
• High mortality with established CHD
– High mortality with acute MI
– High mortality post acute MI
17. 17
CHD Risk Equivalents
• Other clinical forms of atherosclerotic disease
(peripheral arterial disease, abdominal aortic
aneurysm, and symptomatic carotid artery disease)
• Diabetes
• Multiple risk factors that confer a 10-year risk for
CHD >20%
18. 18
Risk Category
CHD and CHD risk
equivalents
Multiple (2+) risk factors
Zero to one risk factor
LDL Goal (mg/dL)
<100
<130
<160
Three Categories of Risk that Modify
LDL-Cholesterol Goals
19. 19
ATP III Lipid and
Lipoprotein Classification
LDL Cholesterol (mg/dL)
<100 Optimal
100–129 Near optimal/above optimal
130–159 Borderline high
160–189 High
≥190 Very high
20. 20
ATP III Lipid and
Lipoprotein Classification (continued)
HDL Cholesterol (mg/dL)
<40 Low
≥60 High
21. 21
ATP III Lipid and
Lipoprotein Classification (continued)
Total Cholesterol (mg/dL)
<200 Desirable
200–239 Borderline high
≥240 High
23. 23
Primary Prevention With
LDL-Lowering Therapy
Public Health Approach
• Reduced intakes of saturated fat and cholesterol
• Increased physical activity
• Weight control
25. 25
Causes of Secondary Dyslipidemia
• Diabetes
• Hypothyroidism
• Obstructive liver disease
• Chronic renal failure
• Drugs that raise LDL cholesterol and lower HDL
cholesterol (progestins, anabolic steroids, and
corticosteroids)
26. 26
Secondary Prevention With
LDL-Lowering Therapy
• Benefits: reduction in total mortality, coronary
mortality, major coronary events, coronary
procedures, and stroke
• LDL cholesterol goal: <100 mg/dL
• Includes CHD risk equivalents
• Consider initiation of therapy during hospitalization
(if LDL ≥100 mg/dL)
27. 27
LDL Cholesterol Goals and Cutpoints for
Therapeutic Lifestyle Changes (TLC)
and Drug Therapy in Different Risk Categories
Risk Category
LDL Goal
(mg/dL)
LDL Level at Which
to Initiate Therapeutic
Lifestyle Changes
(TLC) (mg/dL)
LDL Level at Which
to Consider
Drug Therapy
(mg/dL)
CHD or CHD Risk
Equivalents
(10-year risk >20%)
<100 ≥100
≥130
(100–129: drug
optional)
2+ Risk Factors
(10-year risk ≤20%)
<130 ≥130
10-year risk 10–20%:
≥130
10-year risk <10%:
≥160
0–1 Risk Factor <160 ≥160
≥190
(160–189: LDL-
lowering drug
optional)
28. 28
LDL Cholesterol Goal and Cutpoints for
Therapeutic Lifestyle Changes (TLC) and Drug
Therapy in Patients with CHD and CHD
Risk Equivalents (10-Year Risk >20%)
≥130 mg/dL
(100–129 mg/dL:
drug optional)
≥100 mg/dL<100 mg/dL
LDL Level at Which to
Consider Drug Therapy
LDL Level at Which to
Initiate Therapeutic
Lifestyle Changes (TLC)
LDL Goal
29. 29
LDL Cholesterol Goal and Cutpoints for
Therapeutic Lifestyle Changes (TLC) and Drug
Therapy in Patients with Multiple Risk Factors
(10-Year Risk ≤20%)
LDL Goal
LDL Level at Which to
Initiate Therapeutic
Lifestyle Changes
(TLC)
LDL Level at Which to
Consider Drug Therapy
<130 mg/dL ≥130 mg/dL
10-year risk 10–20%:
≥130 mg/dL
10-year risk <10%:
≥160 mg/dL
30. 30
LDL Cholesterol Goal and Cutpoints for
Therapeutic Lifestyle Changes (TLC) and Drug
Therapy in Patients with 0–1 Risk Factor
≥190 mg/dL
(160–189 mg/dL:
LDL-lowering drug
optional)
≥160 mg/dL<160 mg/dL
LDL Level at Which to
Consider Drug Therapy
LDL Level at Which to
Initiate Therapeutic
Lifestyle Changes
(TLC)LDL Goal
31. 31
LDL-Lowering Therapy in Patients With
CHD and CHD Risk Equivalents
Baseline LDL Cholesterol: ≥130 mg/dL
• Intensive lifestyle therapies
• Maximal control of other risk factors
• Consider starting LDL-lowering drugs
simultaneously with lifestyle therapies
32. 32
LDL-Lowering Therapy in Patients With
CHD and CHD Risk Equivalents
Baseline (or On-Treatment) LDL-C: 100–129 mg/dL
Therapeutic Options:
• LDL-lowering therapy
– Initiate or intensify lifestyle therapies
– Initiate or intensify LDL-lowering drugs
• Treatment of metabolic syndrome
– Emphasize weight reduction and increased physical
activity
• Drug therapy for other lipid risk factors
– For high triglycerides/low HDL cholesterol
– Fibrates or nicotinic acid
33. 33
LDL-Lowering Therapy in Patients With
CHD and CHD Risk Equivalents
Baseline LDL-C: <100 mg/dL
• Further LDL lowering not required
• Therapeutic Lifestyle Changes (TLC) recommended
• Consider treatment of other lipid risk factors
– Elevated triglycerides
– Low HDL cholesterol
• Ongoing clinical trials are assessing benefit of
further LDL lowering
34. 34
LDL-Lowering Therapy in Patients
With Multiple (2+) Risk Factors and
10-Year Risk ≤20%
10-Year Risk 10–20%
• LDL-cholesterol goal <130 mg/dL
• Aim: reduce both short-term and long-term risk
• Immediate initiation of Therapeutic Lifestyle
Changes (TLC) if LDL-C is ≥130 mg/dL
• Consider drug therapy if LDL-C is ≥130 mg/dL
after 3 months of lifestyle therapies
35. 35
LDL-Lowering Therapy in Patients
With Multiple (2+) Risk Factors and
10-Year Risk ≤20%
10-Year Risk <10%
• LDL-cholesterol goal: <130 mg/dL
• Therapeutic aim: reduce long-term risk
• Initiate therapeutic lifestyle changes if LDL-C is
≥130 mg/dL
• Consider drug therapy if LDL-C is ≥160 mg/dL
after 3 months of lifestyle therapies
36. 36
LDL-Lowering Therapy in Patients With
0–1 Risk Factor
• Most persons have 10-year risk <10%
• Therapeutic goal: reduce long-term risk
• LDL-cholesterol goal: <160 mg/dL
• Initiate therapeutic lifestyle changes if LDL-C is
≥160 mg/dL
• If LDL-C is ≥190 mg/dL after 3 months of lifestyle
therapies, consider drug therapy
• If LDL-C is 160–189 mg/dL after 3 months of lifestyle
therapies, drug therapy is optional
37. 37
LDL-Lowering Therapy in Patients With
0–1 Risk Factor and LDL-Cholesterol
160-189 mg/dL (after lifestyle therapies)
Factors Favoring Drug Therapy
• Severe single risk factor
• Multiple life-habit risk factors and emerging risk
factors (if measured)
38. 38
Benefit Beyond LDL Lowering: The Metabolic
Syndrome as a Secondary Target of Therapy
General Features of the Metabolic Syndrome
• Abdominal obesity
• Atherogenic dyslipidemia
– Elevated triglycerides
– Small LDL particles
– Low HDL cholesterol
• Raised blood pressure
• Insulin resistance (± glucose intolerance)
• Prothrombotic state
• Proinflammatory state
39. 39
NON HTN. DM. NON SMOKING YOUNG MALE
CHO. 268
TRIG. 168
HDL 35
LDL 198
ANS : LSM and TARGET LDL TO < 160 mgs
40. 40
Htn., Smoker, Male 48
CHO. 238
TRIG. 198
HDL 30
LDL 158
Ans. : Target LDL <100 mgs
41. 41
Major Risk Factors (Exclusive of LDL
Cholesterol) That Modify LDL Goals
• Cigarette smoking
• Hypertension (BP ≥140/90 mmHg or on
antihypertensive medication)
• Low HDL cholesterol (<40 mg/dL)†
• Family history of premature CHD
– CHD in male first degree relative <55 years
– CHD in female first degree relative <65 years
• Age (men ≥45 years; women ≥55 years)
†
HDL cholesterol ≥60 mg/dL counts as a “negative” risk factor; its
presence removes one risk factor from the total count.
42. 42
DM , Male 42 yrs. Non Smoker
CHO. 268
TRIG. 578
HDL 28
LDL 172
Ans. : Target LDL and TG
43. 43
DM Young female
CHO. 248
TRIG. 368
HDL 25
LDL 142
Ans . : Target LDL and HDL – Statin+Niacin
47. 47
Therapeutic Lifestyle Changes in
LDL-Lowering Therapy
Major Features
• TLC Diet
– Reduced intake of cholesterol-raising nutrients (same as
previous Step II Diet)
Saturated fats <7% of total calories
Dietary cholesterol <200 mg per day
– LDL-lowering therapeutic options
Plant stanols/sterols (2 g per day)
Viscous (soluble) fiber (10–25 g per day)
• Weight reduction
• Increased physical activity
48. 48
Therapeutic Lifestyle Changes
Nutrient Composition of TLC Diet
Nutrient Recommended Intake
• Saturated fat Less than 7% of total calories
• Polyunsaturated fat Up to 10% of total calories
• Monounsaturated fat Up to 20% of total calories
• Total fat 25–35% of total calories
• Carbohydrate 50–60% of total calories
• Fiber 20–30 grams per day
• Protein Approximately 15% of total calories
• Cholesterol Less than 200 mg/day
• Total calories (energy) Balance energy intake and expenditure
to maintain desirable body weight/
prevent weight gain
49. 49
Efficacy of Lifestyle Strategies for
Increasing HDL-C
Strategy Increase in HDL-C (%)
Weight reduction 5%-20%
Physical activity 5%-30%
Smoking cessation 5%
Moderate alcohol consumption 8%
Mediterranean-style diet vs. 30% fat diet* 2%
*Compared with an average American diet.
National Cholesterol Education Program. Circulation. 2002;106:3143-3421.
Roussell MA, et al. J Clin Lipidol . 2007;1:65-73.
Sacks FM, et al. Am J Med. 2002;113:13-24.
63. 63
• LDL-cholesterol goal: <100 mg/dL
• Most patients require drug therapy
• First, achieve LDL-cholesterol goal
• Second, modify other lipid and non-lipid risk
factors
Secondary Prevention: Drug Therapy
for CHD and CHD Risk Equivalents
64. 64
Patients Hospitalized for Coronary Events or Procedures
• Measure LDL-C within 24 hours
• Discharge on LDL-lowering drug if LDL-C ≥130 mg/dL
• Consider LDL-lowering drug if LDL-C is 100–129 mg/dL
• Start lifestyle therapies simultaneously with drug
Secondary Prevention: Drug Therapy
for CHD and CHD Risk Equivalents (continued)
65. 65
Progression of Drug Therapy
in Primary Prevention
If LDL goal not
achieved,
intensify
LDL-lowering
therapy
If LDL goal not
achieved,
intensify drug
therapy or refer
to a lipid
specialist
Monitor
response and
adherence to
therapy
• Start statin or
bile acid
sequestrant
or nicotinic
acid
• Consider higher
dose of statin or
add a bile acid
sequestrant or
nicotinic acid
6 wks 6 wks Q 4-6 mo
• If LDL goal
achieved, treat
other lipid risk
factors
Initiate
LDL-lowering
drug therapy
68. 68
Metabolic Syndrome (continued)
Causes
• Acquired causes
– Overweight and obesity
– Physical inactivity
– High carbohydrate diets (>60% of energy intake)
in some persons
• Genetic causes
69. 69
Metabolic Syndrome (continued)
Therapeutic Objectives
• To reduce underlying causes
– Overweight and obesity
– Physical inactivity
• To treat associated lipid and non-lipid risk factors
– Hypertension
– Prothrombotic state
– Atherogenic dyslipidemia (lipid triad)
70. 70
Metabolic Syndrome (continued)
Management of Overweight and Obesity
• Overweight and obesity: lifestyle risk factors
• Direct targets of intervention
• Weight reduction
– Enhances LDL lowering
– Reduces metabolic syndrome risk factors
• Clinical guidelines: Obesity Education Initiative
– Techniques of weight reduction
71. 71
Metabolic Syndrome (continued)
Management of Physical Inactivity
• Physical inactivity: lifestyle risk factor
• Direct target of intervention
• Increased physical activity
– Reduces metabolic syndrome risk factors
– Improves cardiovascular function
• Clinical guidelines: U.S. Surgeon General’s Report
on Physical Activity
77. 77
Specific Dyslipidemias:
Elevated Triglycerides
Causes of Elevated Triglycerides (continued)
• High carbohydrate diets (>60% of energy intake)
• Several diseases (type 2 diabetes, chronic renal
failure, nephrotic syndrome)
• Certain drugs (corticosteroids, estrogens,
retinoids, higher doses of beta-blockers)
• Various genetic dyslipidemias
79. 79
Comparison of LDL Cholesterol and
Non-HDL Cholesterol Goals for
Three Risk Categories
LDL-C Goal
(mg/dL)Risk Category
Non-HDL-C
Goal (mg/dL)
<100
CHD and CHD Risk Equivalent
(10-year risk for CHD >20%
<130
<130
Multiple (2+) Risk Factors and
10-year risk <20%
<160
<1600–1 Risk Factor <190
80. 80
Specific Dyslipidemias:
Elevated Triglycerides
Non-HDL Cholesterol: Secondary Target
• Primary target of therapy: LDL cholesterol
• Achieve LDL goal before treating non-HDL cholesterol
• Therapeutic approaches to elevated non-HDL
cholesterol
– Intensify therapeutic lifestyle changes
– Intensify LDL-lowering drug therapy
– Nicotinic acid or fibrate therapy to lower VLDL
81. 81
Specific Dyslipidemias:
Elevated Triglycerides
Management of Very High Triglycerides (≥500 mg/dL)
• Goal of therapy: prevent acute pancreatitis
• Very low fat diets (≤15% of caloric intake)
• Triglyceride-lowering drug usually required (fibrate or
nicotinic acid)
• Reduce triglycerides before LDL lowering
83. 83
Major Risk Factors (Exclusive of LDL
Cholesterol) That Modify LDL Goals
• Cigarette smoking
• Hypertension (BP ≥140/90 mmHg or on
antihypertensive medication)
• Low HDL cholesterol (<40 mg/dL)†
• Family history of premature CHD
– CHD in male first degree relative <55 years
– CHD in female first degree relative <65 years
• Age (men ≥45 years; women ≥55 years)
†
HDL cholesterol ≥60 mg/dL counts as a “negative” risk factor; its
presence removes one risk factor from the total count.
84. 84
NON HTN. ,DM, NON SMOKER
CHO. 208
TRIG. 555
HDL 35
LDL 0
ANS : FIBRATE
85. 85
HTN. , DM, MALE 34
CHO. 196
TRIG. 248
HDL 35
LDL 96
• ANS : TARGET NON HDL CHOLESTEROL
86. 86
Specific Dyslipidemias:
Low HDL Cholesterol
Causes of Low HDL Cholesterol (<40 mg/dL)
• Elevated triglycerides
• Overweight and obesity
• Physical inactivity
• Type 2 diabetes
• Cigarette smoking
• Very high carbohydrate intakes (>60% energy)
• Certain drugs (beta-blockers, anabolic steroids,
progestational agents)
87. 87
Specific Dyslipidemias:
Low HDL Cholesterol
Management of Low HDL Cholesterol
• LDL cholesterol is primary target of therapy
• Weight reduction and increased physical
activity (if the metabolic syndrome is present)
• Non-HDL cholesterol is secondary target of
therapy (if triglycerides ≥200 mg/dL)
• Consider nicotinic acid or fibrates
(for patients with CHD or CHD risk equivalents)
90. 90
Special Considerations for
Different Population Groups
Younger Adults
• Men 20–35 years; women 20–45 years
• Coronary atherosclerosis accelerated by CHD
risk factors
• Routine cholesterol screening recommended
starting at age 20
• Hypercholesterolemic patients may need LDL-
lowering drugs
91. 91
Special Considerations for
Different Population Groups (continued)
Older Adults
• Men ≥65 years and women ≥75 years
• High LDL and low HDL still predict CHD
• Benefits of LDL-lowering therapy extend to
older adults
• Clinical judgment required for appropriate use
of LDL-lowering drugs
92. 92
Special Considerations for
Different Population Groups (continued)
Women (Ages 45–75 years)
• CHD in women delayed by 10–15 years (compared
to men)
• Most CHD in women occurs after age 65
• For secondary prevention in post-menopausal
women
– Benefits of hormone replacement therapy
doubtful
– Benefits of statin therapy documented in clinical
trials
93. 93
Special Considerations for
Different Population Groups (continued)
Middle-Aged Men (35–65 years)
• CHD risk in men > women
• High prevalence of CHD risk factors
• Men prone to abdominal obesity and metabolic
syndrome
• CHD incidence high in middle-aged men
• Strong clinical trial evidence for benefit of LDL-
lowering therapy
94. 94
Special Considerations for
Different Population Groups (continued)
Racial and Ethnic Groups
• Absolute risk for CHD may vary in different racial and ethnic
groups
• Relative risk from risk factors is similar for all population
groups
• ATP III guidelines apply to:
– African Americans
– Hispanics
– Native Americans
– Asian and Pacific Islanders
– South Asians