Atherotech’s VAP+ is a simple non-fasting blood test that directly measures your cardiovascular risk and disease progression that breaks down lipid abnormalities into three categories: triglycerides, cholesterol and hereditary components. The basic lipid does NOT fully assess cardiovascular risk/disease. Often, misclassifying the high risk patients approximately 60% of the time; and inaccurately reports a falsely low LDL, the main target of therapy. Why would anyone with family history of cardiovascular disease NOT want this complete assessment at NO additional cost????
Call 202-527-1953 to find out where to get your VAP+ test done, today!
*Additional markers included in the VAP+ report are LDL-P, Lp(a), remnants (IDL, VLDL3), ApoB and Apo A1.
Dyslipidemia, specially high LDL cholesterol is the key risk factor for cardiovascular diseases. The presentation discusses metabolism and structure of lipoproteins, their screening and interpretation, risk assessment methods, targets for various lipoproteins and its step by step treatment.
Diabetes is often accompanied by high triglyceride and high cholesterol levels. Saroglitazar (Lipaglyn) is a novel molecule that not only reduces elevated TG levels; it also reduces blood glucose levels. This presentation by Dr Vivek Baliga discusses this novel molecule.
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
Dyslipidemia, specially high LDL cholesterol is the key risk factor for cardiovascular diseases. The presentation discusses metabolism and structure of lipoproteins, their screening and interpretation, risk assessment methods, targets for various lipoproteins and its step by step treatment.
Diabetes is often accompanied by high triglyceride and high cholesterol levels. Saroglitazar (Lipaglyn) is a novel molecule that not only reduces elevated TG levels; it also reduces blood glucose levels. This presentation by Dr Vivek Baliga discusses this novel molecule.
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
India has a large pool of diabetic patients
ICMR-INDIAB study – extrapolated estimations suggest 62.4 million people with diabetes and 77.2 million are prediabetic
Estimates show ~ 85.5% men and 97.8% women who are diabetic in India have concomitant dyslipidemia
the study was a pilot study done at National Institute of Ayurveda under the Phd Research Programme with an aim to find out new avenues in the managegement of Dyslipidemia - Medoroga and Coronary Heart Disease - Hridroga, thus initiating a new concept of Preventive Cardiology through Ayurveda & Panchakarma
Fasting blood sugar readings refer to the amount of glucose present in the blood of diabetics prior ...
Read more at: http://www.living-healthy-with-diabetes.com/fasting-blood-sugar.html
India has a large pool of diabetic patients
ICMR-INDIAB study – extrapolated estimations suggest 62.4 million people with diabetes and 77.2 million are prediabetic
Estimates show ~ 85.5% men and 97.8% women who are diabetic in India have concomitant dyslipidemia
the study was a pilot study done at National Institute of Ayurveda under the Phd Research Programme with an aim to find out new avenues in the managegement of Dyslipidemia - Medoroga and Coronary Heart Disease - Hridroga, thus initiating a new concept of Preventive Cardiology through Ayurveda & Panchakarma
Fasting blood sugar readings refer to the amount of glucose present in the blood of diabetics prior ...
Read more at: http://www.living-healthy-with-diabetes.com/fasting-blood-sugar.html
Diabetes
Diabetes
A disease that effects your body’s ability to produce or use insulin
Insulin is a hormone produced in the pancreas that regulates the metabolism of glucose and other nutrients.
Types of Diabetes
Type 1 diabetes is a chronic condition in which the pancreas produces little or no insulin, a hormone needed to allow sugar (glucose) to enter cells to produce energy.
Type 2 diabetes is a chronic condition that affects the way your body metabolizes sugar (glucose), your body's main source of fuel.
Incidence of Diabetes in US
Total: 25.8 million children and adults in the United States—8.3% of the population—have diabetes.
Under 20 years of age
•215,000, or 0.26% of all people in this age group have diabetes
•About 1 in every 400 children and adolescents has diabetes
Age 20 years or older
•25.6 million, or 11.3% of all people in this age group have diabetes
Age 65 years or older
•10.9 million, or 26.9% of all people in this age group have diabetes
Men
•13.0 million, or 11.8% of all men aged 20 years or older have diabetes
Women
•12.6 million, or 10.8% of all women aged 20 years or older have diabetes
Causes
Type 1: genetic predisposition and environmental factors
Viruses may trigger the disease in genetically susceptible individuals
Produce no insulin in the pancreas
Type 2:
Obesity; poor diet
Lack of physical activity
High blood pressure
Symptoms
Type 1:
Unexplained weight loss (even though you are eating and feel hungry)
Insulin Shock
Loss of consciousness (rare)
Diabetic Coma
Hypoglycemia(low blood sugar)
Blurred vision
Fatigue
Symptoms continued
Type 2:
Increased thirst and frequent urination.
Increased hunger/weight gain
Fatigue
Blurred vision
Diabetic Coma
Diagnosis and Tests of Diabetes
Random blood sugar test
Fasting Blood Glucose (FBG)
Glycated hemoglobin (A1C) test
Prevention
Type 1
Unknown way to prevent
Researchers are working on preventing the disease or further destruction of the islet cells in people who are newly diagnosed
Type 2
stay at a healthy weight/Eat healthy
Increase physical actives
Lose weight
Lower your blood sugar
Treatment
Type 1
Taking insulin
Exercising regularly and maintaining a healthy weight
Eating healthy foods
Monitoring blood sugar
Type 2
Blood sugar monitoring
Healthy eating
Home Base Business Opportunities
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A complete 8-Step 'Money Getting' Formula ($297 Value) In this High-Value Video Training Series, I'll learn the most effective ways to build a successful online business and the Core 'Must Have' principals to Effective Entrepreneurship in today’s market. These videos outline your BIGGEST money making principals all in one place Watch Video Here http://freedomofsuccess.com
Personalized therapy for cardiovascular diseasemvelasquez18
This work will show the benefits of the investigation of the DNA structure and sequences, and how it is important to have this type of studies to improve our health.
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)
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
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?
Dyslipidemia -Assessment and management based on evidence SYEDRAZA56411
This presentation is focused on cardiovascular risk assessment and application of evidence based principles in choosing right intensity statin therapy for patients with dyslipidemia
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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.
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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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
4. CVD Is an Epidemic
Cardiovascular
Disease
Metabolic
Disease
• 1 in 3 US adults has 1 or more types of CVD1
• Heart disease accounts for 25% of all US mortalities2
• 811,940 yearly deaths from CVD
• CVD kills more women each year than the next 3 causes
of death combined3
• Diabetes affects 25.8 million people of the US population
• Diabetes markedly increases the risk of MI, stroke, amputation, and death
as a result of metabolic abnormalities4
• At least 65% of people with diabetes die from some form of heart disease
or stroke5
• NCEP ATP III established diabetes as a CVD risk equivalent in mandating
aggressive antiatherosclerotic therapy4,6
NCEP ATP III=National Cholesterol Education Program Adult Treatment Panel III.
1.
2.
3.
Roger VL, et al. Circulation. 2011;123(4):e18-e209.
Gutstein DE, et al. Clin Pharmacol Ther. 2012;91(1).
WomenHeart. Available at: http://c.ymcdn.com/sites/www.womenheart.org/resource/
resmgr/docs/women,_heart_disease,_and_di.pdf. Accessed September 4, 2013.
4.
5.
6.
Beckman JA, et al. JAMA. 2002;287(19).
NDEP. Available at: http://ndep.nih.gov/media/CVD_FactSheet.pdf.
Accessed August 13, 2013.
NCEP Adult Treatment Panel III. Circulation. 2002;106(25):3143-3421.
4
5. Defining Cardiometabolic Risk
Assessing cardiometabolic risk is necessary
to establish personalized treatment strategies to improve outcomes
Metabolic Syndrome
Traditional
Risk Factors
• Abdominal obesity
• Hypertriglyceridemia
• HDL-C
• Blood pressure
• Glycemia or diabetes
• Age
• Family history
• Gender
• Blood pressure
• Cholesterol
• Diabetes
• Smoking
Nontraditional
Risk Factors
• Genetics
• Prothrombotic state
• Inflammatory profile
Cardiometabolic Risk
Evidence-based guidelines recommend a personalized treatment strategy through
cardiometabolic risk stratification and comprehensive lipid profiling.
Adapted from: Tremblay M, et al. J Can Dent Assoc. 2011;77:b125.
5
6. Accurate CVD Identification and Management
Remain a Challenge
•
•
•
•
CVD remains challenging to diagnose, treat, and prevent1
Many patients do not achieve therapeutic goals for LDL-C, HDL-C, and TGs2
Statin adherence is <50% after 4 years in patients 65 and older3
Basic lipid panel utilization of the Friedewald formula significantly
underestimates LDL-C and may lead to undertreatment of at-risk patients4
50% of men and
64% of women
who die suddenly
from heart disease
have no previous
warning signs5
50% of people
who have a CVD
event have
normal cholesterol6
Estimated values
from basic lipid
panels miss 60%
of those at risk
for CVD4
TG=triglycerides.
1.
2.
3.
Roger VL, et al. Circulation. 2011;123(4):e18-e209.
Stacy TA, Egger A. J Manag Care Pharm. 2006;12(9).
Bemmer JS, et al. JAMA 2002;288.
4.
5.
6.
Martin SS, et al. J Am Coll Cardiol. 2013.
Gutstein DE, et al. Clin Pharmacol Ther. 2012;91(1).
Sachdeva A, et al. Am Heart J. 2009;157(1):111-117 e112.
6
7. The Basic Lipid Panel Fails to Identify 60%
of At-Risk Patients
Basic Lipid Panel
Does Not Identify 60%
of Those at Risk for CVD
• BLP developed by Friedewald in 19721
• Generally agreed to be inaccurate in non-fasting
state and when
-70
• Problematic patients for BLP/Friedewald include 5
◦
◦
◦
◦
◦
◦
Frederickson class I, III, or V hyperlipoproteinemia1
Nonselective beta blocker users
Diabetes, insulin resistance, or metabolic syndrome
Liver disease
Nephrotic syndrome or chronic renal insufficiency
Hormone replacement6
% Error in LDL-C
-60
◦ Fasting 12 hours
◦ TG 150 mg/dL2-3
◦ LDL-C 100 mg/dL4
-50
-40
-30
-20
-10
0
<100 mg/dL
100-149
mg/dL
150-199
mg/dL
200-399
mg/dL
Triglycerides
1.
2.
3.
Friedewald WT, et al. Clin Chem. 1972;18(6).
Lindsey CC, et al. Pharmacotherapy. 2004;24(2).
Martin SS, et al. J Am Coll Cardiol. 2013.
4.
5.
6.
Scharnagl H, et al. Clin Chem Lab Med. 2001;39(5):426-431.
NCEP ATP III. Circulation. 2002;106(25).
Legault C, et al. J Clin Epidemiol. 1999;52(12).
7
8. Magnitude of Underestimation
in the basic lipid panel/Friedewald LDL-C
In the Johns Hopkins VLDL study of 1.3 million adults, misclassification of VLDL was significant in
the following classes of patients:
• Patients with abnormal TG levels: 25-60% should be reclassified into a higher risk category
• Patients with normal TG levels: 10-20% should be reclassified into a higher risk category
60
Discordance in BLP/Friedewald and Direct LDL-C by TG
59.4%
Strata
51.9%
50
LDL-C 70-99 mg/dL
39.1%
Error (%)
40
39.1 %
n=13,265
n=10,838
LDL-C <70 mg/dL
30
20.3%
20
10.4%
10
0
n=8042
n=2678
<100 mg/dL
n=11,456
n=10,544
100-149 mg/dL
150-199 mg/dL
n=24,988
n=19,677
200-399 mg/dL
Triglycerides
The basic lipid panel misclassifies patient risk
Martin SS, et al. J Am Coll Cardiol. 2013.
8
10. Interactive Question
What are the emerging risk factors outlined in the
national guidelines?
1. Lp(a)
2. Small LDL pattern
3. ApoB and remnant lipoproteins
4. All of the above
10
11. Evidence-Based Guidelines Recommend
Comprehensive Risk Factor Assessment
• LDL-C accounts for 30% of the risk of premature CVD, while the remaining 70%
represents residual risk factors1
• Residual risk can be attributed to LDL-C subclasses, remnant lipoproteins, and other
HDL-C components2-4
• Cardiometabolic risk stratification and personalized approach to management
are recommended2-4
National Guidelines2-5
• Direct LDL-C measurement
• Secondary targets of therapy
◦ Non–HDL-C and metabolic syndrome
• Emerging risk factors
◦ Lp(a), HDL-C subclasses, small LDL pattern, ApoB, and remnant lipoproteins
VAP+ is the first comprehensive lipid profile
to comply with NCEP ATP III, ADA, and AACE guidelines
1.
2.
3.
Kreisberg RA, Oberman A. J Clin Endocrinol Metab. 2002;87(2).
NCEP ATP III. Circulation. 2002;106(25).
Brunzell JD, et al. Diabetes Care. 2008;31(4).
4.
5.
Grundy SM, et al. Circulation. 2004;110(2).
Jellinger PS, et al. Endocr Pract. 2012;18(suppl 1):
11
12. The Comprehensive VAP+ Lipid Panel
Is Essential to Cardiometabolic Risk Stratification
• The VAP+ Lipid Panel provides the most accurate risk
assessment, enabling personalized treatment based on 3 key
indicators not measured by the basic lipid panel
Heredity
Identifies Lp(a),
a hereditary marker
of risk
Cholesterol
Directly measures
LDL-C, LDL-P,
and HDL-C
Triglycerides
Identifies TG-rich disorders, including
non–HDL-C, even in patients with
seemingly normal TG levels
12
13. HEREDITY
TRIGLYCERIDES
CHOLESTEROL
VAP+ Lipid Panel Uncovers Residual
Cardiometabolic Risk and Drives Personalized Therapy
CVD RISK ASSESSMENT
The CVD Risk Assessment
LDL
TGs
LOWER Lp(a)
gives a snapshot of the
• Consider LDL-C
Statins acid
patient’s cardiovascular
Nicotinic
risk. • goals below
Caution 3
• Resins markers on
Omega
the side indicate risk level;
• current guidelines
Cholesterol
fatty acids
absorption
• Consider
additional information in
• Fibric acid
inhibitors
nicotinic acid
the sections below further
• Low-sugar diet
• Consider risk.
Diet low in
clarifies patient baby
• aspirin if not
Exercise fat
saturated
and fried food
contraindicated
• Exercise
The VAP+ Lipid Panel offers detailed results that
enable personalized treatment to directly target
underlying problems
13
14. Global Risk Assessment Mandates
VAP+ Technology
• The VAP+ Lipid Panel uses direct measurement by ultracentrifugation;
therefore, is accurate in non-fasting or fasting patients
• All lipoproteins are physically separated and reacted with an enzymatic
cholesterol reagent, measuring all lipoproteins directly, which increases
the accuracy of the method1
• VAP+ simultaneously measures cholesterol concentrations of ALL
5 lipoprotein classes
The VAP+ Lipid Panel now includes the proprietary
Vertical Lipoprotein Particle (VLP+) technology, which allows
for accurate particle measurement
1.
Kulkarni KR. Clin Lab Med. 2006;26(4).
14
16. VAP+ Lipid Panel:
The Importance of LDL Pattern
• LDL patterns carry different CHD risks
Pattern A: Characterized by
larger, more buoyant
lipoprotein particles (LDL1,2)1
Pattern B: Characterized by
smaller, denser lipoprotein
particles (LDL3,4)1
• Although total LDL-C concentration can be similar in pattern A or B patients, pattern B
patients present with a higher concentration of LDL-P2
• Pattern B particles are more easily taken up by arterial tissue than pattern A particles 2
• Due to altered properties of the surface lipid layer, pattern B particles are more
susceptible to oxidation2
1.
2.
Austin MA, et al. Circulation. 1990;82(2).
Rizzo M, Berneis K. QJM. 2006;99(1).
16
17. Significance of LDL Particle Concentration
• This animation illustrates that 2 individuals with the same total
LDL-C can have different LDL-P concentrations, leading to different
CHD risk levels
Pattern A
B
Individuals with high LDL-P
Individuals with low
have predominantly small and dense
usually have large, buoyant, pattern A
pattern B LDL-C particles
LDL-C particles
*Note both individuals have same amount of TC.
17
18. LDL Particle Concentration Indicates Risk
• In practical application, 2 patients have identical LDL-C—which
patient is at greater risk?
Lower Risk
Higher Risk
B
20 mg/dL
A
100 mg/dL
Large LDL-C
(Pattern A)
LDL-C=100 mg/dL
LDL-P=1100 nmol/L
B
20 mg/dL
B
20 mg/dL
B
20 mg/dL
B
20 mg/dL
Small LDL-C
(Pattern B)
LDL-C=100 mg/dL
LDL-P=1800 nmol/L
Assessment of true LDL-P using the VAP+ Lipid Panel allows for isolation of the actual cause
of increased total LDL-P number to help personalize treatment and improve outcomes
18
19. Appropriate Patients to Consider for VAP+ Testing
Moderate- and
higher-risk
individuals and
those at risk
for CVD
Any patient with
NCEP ATP III
risk factors
(5 established):
• Family history of
premature CHD
• Age (men 45
years; women
55 years)
• Cigarette smoking
• Hypertension
• Low HDL-C
( 40 mg/dL)
Established
atherosclerotic
vascular disease
Diabetes mellitus
and/or metabolic
syndrome
Framingham Risk
Score (FRS)
over 5% or
Reynolds
Risk Score
An elevated
inflammatory
biomarker
19
21. Interactive Question
Which of the following is true about residual risk after
statin therapy?
1. Residual risk for CVD remains despite a significant reduction
in CV events and mortality with statin therapy.
2. Substantial residual risk persists even after patients are treated
with intensive statin therapy to reduce LDL-C.
3. High TGs and low levels of HDL-C appear to be major contributors
to residual risk, even at optimal LDL-C levels.
4. All of the above are correct.
21
22. VAP+ Lipid Panel Evidence Summary
HDL-C subclass is
an independent risk factor
The basic lipid panel
misclassifies CVD risk
• The BLP/Friedewald formula consistently
underestimates LDL-C, resulting in
undertreatment of high-risk patients1
• Framingham Heart Study: Increased
HDL3-C revealed a 40% lower risk for
CHD and 36% lower risk for hard CHD4
(primary prevention)
• Intermountain Heart Collaborative Study:
A large percentage of patients with heart
disease remain at high residual risk despite
having achieved basic lipid panel target
LDL-C treatment goals2
(secondary prevention)
• TRIUMPH Study: Low HDL3-C revealed
a 50% higher mortality risk5
(secondary prevention)
• Jackson Heart Study: Increased HDL3-C
revealed a 68% lower risk for hard CHD
and a 35% lower risk for CHD6
(primary prevention)
• Low HDL2-C reveals CV risk in 6 times as
many patients as the basic lipid panel3
(primary prevention)
1.
2.
3.
Martin SS, et al. J Am Coll Cardiol. 2013.
May HT, et al. Presented at: ACC 59th Annual Scientific Sessions; 2010.
Sailam V, et al. Clin Cardiol. 2008;31(11):542-545.
4.
5.
6.
Toth P. et al Impact of HDLC and its subfractions. 2012.
Martin SS. Presented at: AHA Scientific Sessions; 2012.
Joshi P, et al. Presented at: AHA Scientific Sessions; 2012.
22
23. VAP+ Lipid Panel Evidence Summary
Remnant lipoproteins predict heart attack risk
• Jackson Heart Study: Remnant lipoproteins are 28% more likely to reveal a significant, independent
risk factor for heart attack1 (primary prevention)
• Framingham Heart Study: Remnant lipoproteins were an independent risk factor for incident CHD
events2 (primary prevention)
• Framingham Heart Study: Pattern B revealed double the risk for hard CHD and a 40% increased risk
for CHD3 (primary prevention)
• Atherogenic lipoprotein phenotype (LDL-C pattern B) reveals double the risk for hard CHD and 40%
increased risk for CHD and is strongly associated with CIMT progression4
Elevated Lp(a) plays a significant role in atherogenesis and is closely
associated with HDL-C, VLDL-C, and TGs
• Studies by Konerman’s group utilizing the VAP+ cholesterol test have shown that Lp(a) is strongly
associated with markers of HDL-C, VLDL-C, and TGs, and highlight Lp(a)’s role in atherogenesis5
(primary and secondary prevention)
CIMT=carotid intima media thickness.
1.
2.
Khokar A, et al. J Am Coll Cardiol. 2013;61(10S).
Toth PP, et al. Presented at: ACC Scientific Sessions; 2013. Impact of Lipoprotein Remnants
on 12 Year Risk for CHD in the Framingham Offspring Population.
3.
4.
5.
Toth PP. Presented at: AHA Scientific Sessions; 2012. Impact of LDL patterns on risk for CHD
in the Framingham Offspring Population.
Maki KC, et al. Vasc Health Risk Manag. 2012;8.
Konerman M, et al. J Clin Lipidol. 2012;6(1).
23
24. VAP+ Lipid Panel Improves Outcomes
and Reduces Cost for Managed Care
• Use of the VAP+ Lipid Panel permitted WellMed Medical Group to
detect more cases of dyslipidemia than the basic lipid panel, enabling
more appropriate and effective therapy to be prescribed
and, ultimately, leading to better outcomes1,2
◦ Repeated VAP testing and therapy adjustments led to lower LDL-C, higher
HDL3-C, reduced inpatient (IP) stays, and fewer emergency department (ED) visits
Utilization and Cost Comparisons
IMPROVED
PATIENT
OUTCOMES
REDUCED COSTS
TO MANAGED
CARE BY
35%
VAP
Test
Group
Control
Test
Results
P-Value
Mean total cost
year 1
$4307.70
$5146.02
-1.34*
0.1157
Mean total cost
year 2
$4852.62
$7413.18
-2.24*
0.0255
Mean ED cost
both years
$22.24
$33.15
-1.92*
0.0561
Mean IP cost
both years
$732.80
$876.20
-1.80*
0.0722
Cost
*t-test.
1.
Atherotech Inc. Available at: http://www.atherotech.com/information/viewinformation.asp?informationid=179. Accessed August 13, 2012.
2.
McAna JF, et al. Popul Health Manag. 2012;15(1).
24
26. Our Healthy Heart Patient Education Program
Our Healthy Heart is a unique service offered by
Atherotech at no additional charge with a
VAP+ Lipid Panel.
The service provides patients with personalized
lifestyle modification education, compliance
strategies, and coaching from licensed health
coaches to promote heart health through the
continuum of care.
Our licensed health coaches can design a
personalized program based on physician
recommendations, patient needs, and
VAP+ results.
Call 1-866-VAP-TEST or 1-866-827-8378
toll-free to enroll your patient.
26
27. Atherotech Offers Customizable Disease
State Panels
These disease state panels are provided as
examples only. Physicians should only order
tests that are medically necessary and
reasonable for the diagnosis or treatment of a
patient for which reimbursement is claimed. All
tests included in Atherotech panels or physiciancreated panels may be ordered individually.
Through proprietary technologies, including
the VAP+ Lipid Panel, Atherotech supports a
full offering of disease state panels that can
be customized by the clinician.
CARDIOMETABOLIC AND GENETIC TESTS FROM ATHEROTECH
CVD Risk Panel
•
•
•
•
•
•
VAP+ Lipid Panel
CMP
Lp-PLA2
Hs-CRP
Homocysteine
Cystatin C
CVD Treatment
Panel
•
•
•
•
•
•
•
•
VAP+ Lipid Panel
CMP
Lp-PLA2
Hs-CRP
Homocysteine
Cystatin C
TSH
Uric acid
Diabetes/Metabolic
Syndrome Panel
•
•
•
•
•
•
•
•
VAP+ Lipid Panel
CMP
A1C
GlycoMark
GGT
Uric acid
Cystatin C
Insulin
Heart Failure
Panel
•
•
•
•
•
VAP+ Lipid Panel
BMP
NTproBNP
Galectin 3
Cystatin C
Myalgia Panel
•
•
•
•
•
VAP+ Lipid Panel
B12
TSH
Vitamin D
Uric acid
27
28. In Conclusion
Comprehensive care is essential to effectively manage cardiometabolic risk and
improve outcomes
Basic lipid panels have led to misclassification of as many as 60% of
patients, potentially resulting in ineffective treatment for patients most at risk
Evidence-based guidelines recommend cardiometabolic risk stratification via
comprehensive cholesterol profiling so a personalized treatment strategy can
be implemented
The VAP+ Lipid Panel uncovers residual cardiometabolic risk, which provides
actionable information to improve patient outcomes
Atherotech provides over 100 routine and cardiometabolic specialty tests and
customizable disease state panels to offer clinicians a single source laboratory
Atherotech goes beyond diagnostics to offer personalized provider and patient
education for disease management
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