Transcript Pathophysiology and Risk Factors of C.A.D.

Cardiovascular Risk Factors
&
Coronary Artery Disease
Overview

Cardiovascular Diseases

Atherogenesis and response to Injury
(Endothelial Dysfunction)

Manifestations and Diagnosis of CAD

Treatment of CAD

Risk Factors Contributing to CAD
– Modifiable vs. Non-modifiable
CAD: Statistics





CAD is the largest killer of American males and females
13 million Americans have CAD
1.1 million MI’s per year
Every 26 seconds  an American will suffer from a coronary event
Every 60 seconds  an American will die because of a coronary
event
 42% of those having a coronary event will die from it
 350K people die per year because of a coronary event in the
Emergency Department before even being admitted to the hospital
 Death Rate in 2001:
 177 in 100,000
5
CAD: Demographics and Statistics
 84% of those who die from CAD are 65 or older
 If under the age of 65, 80% mortality rate with the first myocardial





infarction
Within 1 year of initial MI:
 25% of men and 38% of women will die
Within 8 years of initial MI:
 50% of men and women under 65 will die
An average of 11.5 years of life are lost due to an MI
IMPORTANT:
 50% of men and 64% of women who have died suddenly via
CAD DID NOT HAVE ANY PREVIOUS SYMPTOMS
Sudden Death:
 Those with a previous history of MI have a 5-6 times Sudden
Death rate compared to the general population
6
The Leading Causes of Death
From Cardiovascular Disease
Data from American Heart Association, 2006.
Cardiovascular diseases in Saudi
Arabia
 the third most common cause of hospital-based
mortality second to accident and senility.
 (35 percent) were due to cardiovascular disease.
 Vascular injury accumulates in adolescence, making
it necessary for primary preventive measures to be
taken from childhood.
WHO report, 2008
Cardiovascular Diseases

Arteriosclerosis – loss of elasticity of the arteries;
thickening and hardening of artery walls.

Atherosclerosis – process where fatty material is
deposited along walls of arteries. This material thickens,
hardens, and can eventually block the artery.
Atherosclerosis is just one type of Arteriosclerosis.

Our understanding of the development and progression
of atherosclerosis (atherogenesis) is still incomplete
Vascular Anatomy

Endothelium: barrier between blood and arterial
wall

3 layers in arterial wall:
– Tunica Intima - connective tissue; where
lesions form
– Tunica Media - smooth muscle

advanced atherosclerosis characterized by
proliferation of smooth muscle cells here
– Tunica Adventitia - connective tissue; highly
vascularized to provide nutrients
Endothelial
Function
Endothelial
Dysfunction
Regulates
vasomotion
Inadequate
Regulates
thrombosis
vasodilation
Regulates
transport of
substances to and
from vascular space
Regulates
growth and
apoptosis of vascular
wall
Regulates
oxidation
LDL
Prothrombotic
Altered
permeability
Increased
secretion of
growth factors
Increased
LDL
oxidation of
Atherogenesis
Response to Injury

Arterial Injury
– Can result from smoke, hypertension, cholesterol,
glycated substances, vasoconstriction, homocysteine
or infectious agents
– Normal endothelial function is not repaired by
inherent mechanisms

Endothelial Dysfunction and Inflammatory Response
 Arterial homoeostasis is altered by injury, results in
inflammatory response
 Increased adhesiveness endothelial cells lose
selective permeability
Atherogenesis
 Platelet aggregation
 Platelets adhere to damaged endothelium
and form small blood clots on vessel wall
(mural thrombi)
 Release growth factors and vasoconstrictor
substances
 Can cause obstruction to blood flow
Atherogenesis

LDL oxidation

Excess oxidized LDL particles accumulate in arterial
wall, attracting monocytes and other cells into intima

Monocytes mature into macrophages and cause
proliferation of smooth muscle cells and promote
uptake of more lipids, particularly LDL

These cells move from the media to the intima,
becoming foam cells, producing fatty streaks or
lesions

Continued release of vasoactive substances and
growth factors
Atherogenesis

Foam cells
 Release cholesterol into extracellular space

Fatty streaks
 Earliest visually detectable lesion of
atherosclerosis
 As the process continues, smooth muscle
cells accumulate in the intima and form a
fibrous plaque
Response to Injury

Fibromuscular plaque
 With continued accumulation, lesion progresses in
size and appearance to Fibromuscular plaque with
an Atheroma (cholesterol core)

Remodeling
 Outward growth of artery & increased lumen size
 Lumen size increases to compensate for
atherosclerotic plaque
 If plaque bulk continues to increase, lumen diameter
is decreased and blood flow obstruction occurs
Atherogenesis

Plaque rupture, thrombus formation, incorporation
 Layered appearance to lesion and increased plaque
progression
 Rupture may result from local stress or chemical
factors and exposes contents or lesion to blood
 Plaques that are most vulnerable to rupture typically
have a large lipid core, thinned fibrous cap, and
outward remodeling of arterial wall

Advanced Atherosclerotic Plaque
Progression of Atherosclerosis
Coronary artery at
lesion-prone location
Adaptive
thickening
(smooth muscle)
Type II (Lesion)
Type III (Preatheroma)
Small pools of
extracellular
lipid
Macrophage
foam cells
Intima
Media
Type IV
(Atheroma)
Core of
extracellular
lipid
Type V
(Fibroatheroma)
Type VI
(Complicated lesion)
Fibrous
thickening
Adapted from Stary in Fuster et al (eds). Atherosclerosis and Coronary Artery Disease 1996.
Thrombus
fissure &
hemtoma
Atherogenesis




Does not occur in a predictable linear pattern
Some lesions develop slowly and are stable for long
periods of time, others develop quickly
Partial regression of fatty, soft lesions is possible with
aggressive risk reduction
Endothelial dysfunction can be reversed
– Exercise, dietary fat intake control, decreasing
stress, maintaining optimal blood pressure and
blood glucose levels
Manifestations of Atherosclerosis

The Heart
– Myocardial Ischemia
– Angina
– Myocardial Infarction

Brain

Legs
Manifestations of Atherosclerosis
Myocardial Ischemia – ischemic cascade
 LV
stiffening & decreased diastolic filling
(diastolic dysfunction)
 Impaired
LV systolic emptying
 ECG
changes associated with altered
repolarization
Pectoris – transient, referred cardiac
pain resulting from ischemia
 Angina
Manifestations of Atherosclerosis
Angina – Types:

Silent ischemia: no pain

Anginal Equivalent: shortness of breath, diaphoresis
etc.

Typical Angina: occurs with exertion, emotions &
relieved with rest or NTG

Atypical Angina: similar symptoms, but no exertion etc

Stable Angina: reproducible, predictable

Unstable Angina: new onset, increased freq, intensity,
duration, or occurs at rest
Manifestations of Atherosclerosis
Myocardial Infarction

Diagnosis: 2 of 3 criteria:
1) Chest pain > 30 minutes
2) ECG – Q waves / ST segment elevation/ T wave
inversion
3) Cardiac enzymes:

Creatine phosphokinase (CK) Normal = 0-195

Troponin T – Normal < 0.03
Manifestations of Atherosclerosis
Myocardial Infarction
Signs
& Symptoms:
– Angina, GI upset, Dyspnea, Diaphoresis,
Syncope
Treatment:
– Relieve symptoms (nitroglycerin, painkillers)
– Reperfusion
Manifestations of Atherosclerosis
Myocardial Infarction
 STEMI vs. NSTEMI:
– ST Elevation MI – ST elevation of 1 mm or
more in contiguous leads or new LBBB
– Non-ST Elevation MI – ST depression or T
wave inversion lasting greater than or equal
to 24 hours
Differential Diagnosis chest pain
Cardiac
Stable angina
Unstable angina
Acute MI
Pericarditis
Vascular
Aortic dissection
Pulmonary embolism
Pulmonary hypertension
Pulmonary
Pleuritis/pneumonia
Tracheobronchitis
Spontaneous pneumothorax
Differential Diagnosis chest pain
Gastrointestinal
GERD
PUD
GB disease
Pancreatitis
MSK
Costochondritis
Cervical disc disease
Infectious
Herpes Zoster
Psychological
Panic disorder
Remember:
 Patients may have no pain and may only complain of
episodic Shortness of Breath, weakness, Dizziness,
Collapse, Sweating or Nausea and Vomiting.
Remember:
 Atypical symptoms do not necessarily rule out
ACS.
 One study found the syndrome in 22% 0f 596
Patients presented to A/E with sharp or
stabbing pain.
Lee TH, Cook EF, Weisberg M, Sargent RK, Wilson C, Goldman L. Acute chest pain in the emergency room.
Identification and examination of low-risk patients. Arch Intern Med 1985;145:65-9.
Ischaemic heart disease
Manifestations
 Sudden death
 Myocardial infarction
 Acute coronary syndrome
 Stable angina pectoris
 Heart failure
 Arrhythmia
 Asymptomatic
Ischaemic heart disease Definition
 An imbalance between the supply of oxygen and the
myocardial demand resulting in myocardial ischaemia.
Activity induces O2 demands beyond the supply
restrictions imposed by a partially occluded coronary
artery
 Angina pectoris
Symptom not a disease
Chest discomfort associated with abnormal
myocardial function in the absence of myocardial
necrosis
ANGINA
Characteristics of “typical” or “classic”
 Pressure, tightness, squeezing, heaviness, or
choking
 Radiates down left arm, back, and/or jaw
 Occurs with physical activity, emotional stress,
cold weather, heavy meals
 Last few minutes or until activity ceases
 May be relieved by rest or nitroglycerine.
 May be associated with nausea, vomiting, or
diaphoresis
ATHEROSCLEROSIS
PAD
STABLE ANGINA
UNSABLE ANGINA
IHD
CVD
ACUTE CORONARY SYNDROME
MYOCARDIAL INFARCTION
NON STE MI
STE MI
ISCHAEMIC CARDIAC PAIN
No ST Segment Elevation
Negative Serum
Cardiac Markers
Unstable Angina
Positive Serum
Cardiac Markers
Non-Q Wave MI
ST Segment Elevation
Positive Serum
Cardiac Markers
Q Wave MI
Spectrum of Acute Coronary Syndromes
Stable
Angina
Unstable
Angina
Non-Q
wave MI
Non ST
Elevation ACS
Q wave
MI
ST Elevation
MI
ECG - ST
ECG - ST
CK-MB ‫مهم‬
Troponin ‫مهم‬
‫االنزيمات مهمه جدا‬
‫اعرف كل انزيم ومده‬
‫ظهوره ومتى يتخفي‬
CRP
Cannon CP. 1999
‫مهمه‬
Acute inferior MI
Old Inferior MI
Drug Treatment in CHD and post MI ‫مهمه جدا‬
◘ Aspirin
◘ Clopidogrel (Plavix) (Evidence:combined with Aspirin
for post Acute Coronary Syndrome up to one year)
◘ Beta Blocker
◘ Statins
◘ ACE-Inhibitor or ARB
◘ Calcium Channel Blocker (Diltiazem)
Symptomatic Drugs will not affect the mortality
◘ Isosorbide Dinitrate
◘ GTN Sublingual
Manifestation of Atherosclerosis

Brain
 Transient ischemic attack (TIA)
 Cerebrovascular accident (stroke)

Legs
 Intermittent claudication
Graded Exercise Test (GXT)
Used to assess...


Ischemia
–
ST segment changes
–
Arrhythmia
Functional Capacity
–

MET’s
Efficacy of medical or surgical
intervention
Myocardial Perfusion Imaging
(Thallium scan)
Used to assess...
 Ischemia
 Ventricular
–
Ejection Fraction
 Myocardial
–
Function
Viability
Reversible vs non-reversible
Echocardiography
Used to assess...

Myocardial Structures
–

MR, TR, AR
Ventricular Function
–
EF
–
Wall motion abnormalities

Effusions

Thrombus

Ischemia
Cardiac Angiography
Used to assess...

Coronary arteries

Pressures within cardiac chambers

Valve function

Ventricular function
Prevention is the key
1.
2.
3.
4.
5.
6.
7.
8.
CVD - Is it preventable ?? - Very much Yes.
The risk assessment must start very early
At the age of 20 years itself
Healthy life style and hearty eating habits
Regular physical exercise from young age
Maintaining ideal weight and hour glass waist
Avoiding tobacco and reducing alcohol
There are enough guidelines – Implementation ?
47
Risk Factor Modification
Treat to Target
Medical Management
Balancing the Supply and Demand Equation
Lower the Demand
 Beta Blockers





Decrease heart rate
Decrease preload

Calcium Channel
Blockers

Decrease preload

Increase diastole
Nitrates
Nitrates


Decrease
contractility
Increase the Supply
 Beta Blockers
Increase collateral
circulation
Calcium Channel
Blockers

Decrease vascular
resistance
Percutaneous Coronary Intervention
(PCI)
Indications for Angioplasty (+/- stenting)

Electively for chronic stable angina

Urgently for unstable angina

Emergently for myocardial infarction

1 or 2 vessel disease

NEVER for left main disease
Coronary Artery Bypass Graft
Surgery (CABG)
Indications

Left main disease > 50 %

Proximal 3 vessel disease

Multivessel disease with left ventricular
dysfunction

Lifestyle limiting angina unresponsive to
medical therapy or PCI
Non-modifiable and Modifiable
Non-Modifiable Risk Factors

Family History
– Twice the risk of MI if one first-degree relative with MI
– Triple the risk of MI if 2+ first-degree relatives with MI
– Risk is strongest if MI occurred at age 55 or less

Advancing Age
– Risk of CAD Increases as we get older

Gender
– Men are at risk at an earlier age than women
– Women’s risk of heart disease increases after
menopause and soon equals men’s
Modifiable Risk Factors

Tobacco Smoking

Dyslipidemia

Hypertension

Obesity

Sedentary Lifestyle

Diabetes

Emerging Risk Factors
Tobacco Smoking

The MOST preventable risk factor

Smokers have 2 to 5 times the risk of CAD as
nonsmokers

Risk factor if one is currently smoking, has quit
within the past 6 months, or has exposure to
environmental tobacco smoke
Tobacco Smoking
 Increase
–
workload to heart
Increased HR and BP
 Endothelial
dysfunction
–
Increased vasoconstriction
–
Decreased HDL
–
Increased LDL and Triglycerides
–
Increased LDL oxidation
–
Increased platelet aggregation
–
Decreased O2 carrying capacity of red blood cells
Dyslipidemia

2 main types of lipids:
 Cholesterol
 Triglycerides (TGs)

Lipids are an essential component of healthy
body functioning, including:
 Structural component of cell walls
 Hormones
 Energy source
Dyslipidemia
 Much research to support the link between
abnormal serum lipid levels and CAD
 LDL =  risk of CAD
 HDL =  risk of CAD
 TGs =  risk of CAD
Dyslipidemia

Abnormal lipid levels are known to be the basis
of the atherosclerotic process

Endothelial Dysfunction
 Elevated cholesterol levels

Reduce vasodilation

Increase thrombosis
 Elevated triglyceride levels

Mechanism is unclear
Lipid Targets for CAD
2009 Canadian Cholesterol Guidelines
Primary Targets:
LDL-C
< 2.0mmol/L or 50% reduction
Alternate: Apolipoprotein
B < 0.80 g/L
Lipid Targets for CAD
2009 Canadian Cholesterol Guidelines
Secondary Targets: (once LDL cholesterol is at goal)

Total Cholestrol to High-Density Lipoprotein (HDL)
cholesterol ratio less than 4.0

Non HDL cholesterol < 3.5 mmol/L

Triglycerides < 1.7 mmol/L

Apolipoprotein B to apolipoprotein AI ratio < 0.8

High-sensitivity C-reactive protein (CPR) < 2 mg/L
Hypertension

Primary risk factor for CAD

Hypertension is associated with three to four times
increased risk for CAD, MI and CVA & PVD

Hypertension as a precursor or consequence of
endothelial dysfunction?
 Vasoconstriction (increases SBP)
 Vascular wall injury

Increased platelet aggregation
 myocardium

increased wall stress

increased myocardial O2 demand
U.S.
Department of
Health and
Human
Services
National
Institutes
of Health
National Heart,
Lung, and
Blood Institute
National Heart, Lung, and Blood
Institute
National High Blood Pressure
Education Program
The Seventh Report of the
Joint National Committee on
Prevention, Detection,
Evaluation, and Treatment of High
Blood Pressure (JNC 7)
Classification and Management
of BP for adults
BP
SBP*
classificati
mmHg
on
Normal
<120 &
Lifestyle
DBP*
modificati
mmHg
on
<80
Initial drug therapy
Without compelling
indication
Encourage
Prehyperte 120–139 or 80–89
nsion
Yes
No antihypertensive
drug indicated.
Stage 1
140–159 or 90–99
Hypertensi
on
Yes
Thiazide-type diuretics
for most. May consider
ACEI, ARB, BB, CCB,
or combination.
Stage 2
Hypertensi
on
Yes
>160
or >100
With compelling
indications
•*Treatment determined by highest BP category.
Drug(s) for
compelling
indications. ‡
Drug(s) for the
compelling
indications.‡
Other
Two-drug combination for
antihypertensive
†
most (usually thiazide-type drugs (diuretics,
diuretic and ACEI or ARB
ACEI, ARB, BB,
or BB or CCB).
CCB) as needed.
•†Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension.
•‡Treat patients with chronic kidney disease or diabetes to BP goal of <130/80 mmHg.
Blood Pressure Targets
2010 Canadian Hypertension Guidelines

Non-Diabetics
<140/90 mmHg

Diabetics or persons with chronic kidney
disease
<130/80 mmHg
Obesity

The risk for CVD is greater in person’s with
central (android) obesity than those with
peripheral (gynoid) obesity

Obesity is often associated with …
 Diabetes
 Hypertension
 Dyslipidemia
 Inactivity
Obesity

Body Mass Index (BMI)


Measured in Kg/m2
ACSM BMI Targets
Underweight
<18.5
Normal
18.5-24.9
Overweight
Obese
25.0-29.9
>30
Obesity

Waist Circumference

ACSM Waist Circumference Targets
Men
< 102 cm
Women
< 88 cm
Sedentary Lifestyle

Lower fitness level is associated with increased risk of
CAD in men and women

The relative risk of CAD associated with physical
inactivity is comparable to that observed for cigarette
smoking, hypercholesterolemia and hypertension

Persons who are physically inactive after a heart attack
have significantly high mortality rates than active
individuals
Sedentary Lifestyle
Physical activity reduces the risk of CAD through:

Improved balance between myocardial O2 supply and
demand

Decreased platelet aggregation

Decreased susceptibility to malignant ventricular
arrhythmias

Improved endothelial tone

Beneficial effect on other CAD risk factors (ie. diabetes,
dyslipidemia, hypertension, obesity, stress)
Diabetes

People with diabetes have 2 to 7 times increased risk of
developing CAD than people without diabetes

Mechanism of atherosclerosis is unclear
 Endothelial damage


Increased platelet aggregation

Insulin promotes synthesis of lipids and uptake
of lipids by smooth muscle
Excess sugar in vessels damages the lining making it
vulnerable to plaques and clots
Diabetes
Careful control of blood sugar levels reduces the
risk of developing the complications of diabetes
Targets for diabetic control
ACSM
Canadian
FBG <200 mg/dL
FBG 4-7 mmol/L
2 hr pc BS <200mg/dL
2 hr pc BS 5-11 mmol/L
HgbA1C <0.07
Stress


Psychosocial factors associated with CAD risk:
–
Type A personality
–
Hostility/Anger
–
Depression/Anxiety
3 to 4 times increased risk of death in first year
following MI
Stress (Canadian)
Influence CAD risk via 2 main mechanisms:


Catacholamine release
–
increased BP
–
increased HR
–
vasoconstriction
–
increased O2 demand
Decreased adherence to lifestyle
modification recommendations
Atherogenic Diet

Diets high in fruits, vegetables, whole grains
and unsaturated fatty acids have lower risk for
CAD

This influence goes beyond what is explained
by other risk factors that may be related to diet.
Emerging Risk Factors

Nontraditional factors that are associated with
increased risk of CVD, but a causal link has not yet
been proved with certainty
The Four Big Ones
 Poor oral health
 Dietary trans fat intake

Adhesion molecules
Cytokines
Infectious agents
 C-Reactive Protein
 Lipoprotein (a)
 Fibrinogen
 Homocysteine
Clinical Diagnosis of Metabolic Syndrome
‫مهمه جدا‬
Any 3 of the following

Abdominal Obesity: Weight Circumference:
Men
≥ 102 cm
Women
≥ 88 cm

Triglycerides ≥ 1.7 mmol/L (150 mg/dL) Or on medication

HDL cholesterol
men < 1.05 mmol/L (40 mg/dL)
women < 1.30 mmol/L (50 mg/dL)
Or on medication for HDL-C

Blood Pressure ≥ 130/85 or on antihypertensive Medication

Fasting Glucose ≥ 100 mg/dl (5.6 mmol/L)
or any medication for high blood glucose
Diagnosis and Management of the metabolic syndrome.
Scott M et al Circulation, American Heart Association, Sept 12, 2005
Central Obesity
Weight Reduction
Exercise
Endothelial
dysfunction/
Microalbuminuria
Glucose Intolerance
Insulin Sensitizer
ACE / ARB
Metformin
Dyslipidaemia
Syndrome
STATINS
Prothrombotic State
ASPIRIN
Glitazones
Hypertension
Metabolic
Proper Control
Proinflammatory State
Cardiovascular Disease
Circulation. 2004:109:433-438 JAMA. 2002:2709-2716
STATINS
Am J Cardiol 2003;92:1414-1418
Dr.Hussein Saad
ATP III Framingham Risk Scoring
ATP III: Assessment of Risk
For persons without known CHD, other forms
of
atherosclerotic disease, or diabetes:
 Count the number of risk factors.
 Use Framingham scoring for persons with 2 risk
factors* to determine the absolute 10-year CHD
risk.
*For persons with 0–1 risk factor, Framingham calculations are not
necessary.
Expert Panel on Detection, Evaluation, and Treatment of
High Blood Cholesterol in Adults. JAMA. 2001;285:2486-2497.
www.lipidhealth.org
Framingham Risk SCORE
Is a risk assessment tool that has been derived
from data in the Framingham Heart Study.
The various degrees of risk associated with five
categories:
•
•
•
•
•
AGE
TOTAL CHOLESTEROL LEVEL
HDL-C LEVEL
SMOKING
Systolic Bp
The Framingham Study. JAMA 1986;256:2835-8
ATP III Framingham Risk Scoring
Assessing CHD Risk in Men
Step 4: Systolic Blood Pressure
Step 1: Age
Years
20-34
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
Points
-9
-4
0
3
6
8
10
11
12
13
Systolic BP
(mm Hg)
<120
120-129
130-139
140-159
160
HDL-C
(mg/dL)
60
Points
-1
50-59
0
40-49
1
<40
2
Age
Total cholesterol
HDL-cholesterol
Systolic blood pressure
Smoking status
Point total
Step 7: CHD Risk
Step 2: Total Cholesterol
TC
Points at
at Points at
(mg/dL)
Age 20-39
70-79
<160
0
160-199
4
200-239
7
240-279
9
280
11
Step 3: HDL-Cholesterol
Step 6: Adding Up the Points
Points
Points
if Untreated if Treated
0
0
0
1
1
2
1
2
2
3
Points at
Points at
Points
Age 40-49 Age 50-59 Age 60-69 Age
0
0
3
2
5
3
6
4
8
5
Step 5: Smoking Status
at
70-79
Nonsmoker
Smoker
0
1
1
2
3
Points at
Points at
Age 20-39
0
8
0
0
0
1
1
Points at
Point Total 10-Year Risk
Risk
<0
<1%
0
1%
1
1%
2
1%
3
1%
4
1%
5
2%
6
2%
7
3%
8
4%
9
5%
10
Points at
Points 6%
Point Total 10-Year
11
12
13
14
15
16
17
8%
10%
12%
16%
20%
25%
30%
Age 40-49 Age 50-59 Age 60-69 Age
0
5
0
3
0
1
0
1
Note: Risk estimates were derived from the experience of the Framingham Heart Study,
a predominantly Caucasian population in Massachusetts, USA.
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults.
JAMA. 2001;285:2486-2497.
www.lipidhealth.org
ATP III Framingham Risk Scoring
Step 1: Age
Men
Years
20-34
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
Women
Points
-9
-4
0
3
6
8
10
11
12
13
Years
20-34
35-39
40-44
45-49
50-54
55-59
60-64
65-69
70-74
75-79
Points
-7
-3
0
3
6
8
10
12
14
16
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. JAMA. 2001;285:2486-2497.
© 2001, Professional Postgraduate Services®
www.lipidhealth.org
ATP III Framingham Risk Scoring
Step 2: Total Cholesterol
Men TC
79
(mg/dL)
Points at
Age 20-39
Points at
Age 40-49
Points at
Age 50-59
<160
160-199
200-239
240-279
280
0
4
7
9
11
0
3
5
6
8
0
2
3
4
5
TC
(mg/dL)
Points at
Age 20-39
Points at
Age 40-49
Points at
Age 50-59
<160
160-199
200-239
240-279
280
0
4
8
11
13
0
3
6
8
10
0
2
4
5
7
Women
79
Points atPoints at
Age 60-69 Age 700
1
1
2
3
0
0
0
1
1
Points atPoints at
Age 60-69 Age 700
1
2
3
4
0
1
1
2
2
Note: TC and HDL-C values should be the average of at least two fasting
lipoprotein measurements.
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. JAMA. 2001;285:2486-2497.
www.lipidhealth.org
ATP III Framingham Risk Scoring
Step 3: HDL-Cholesterol
Men
HDL-C
(mg/dL)
60
Women
Points
-1
HDL-C
(mg/dL)
60
Points
-1
50-59
0
50-59
0
40-49
1
40-49
1
<40
2
<40
2
Note: HDL-C and TC values should be the average of at least two
fasting lipoprotein measurements.
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. JAMA. 2001;285:2486-2497.
www.lipidhealth.org
ATP III Framingham Risk Scoring
Step 4: Systolic Blood Pressure
Men
Systolic BP
Points
(mm Hg) if Untreated
<120
0
120-129
0
130-139
1
140-159
1
160
2
Points
if Treated
0
1
2
2
3
Women
Systolic BP
(mm Hg)
<120
120-129
130-139
140-159
160
Points
Points
if Untreated if Treated
0
0
1
3
2
4
3
5
4
6
Note: The average of several BP measurements is needed for an accurate
measurement of baseline BP. If an individual is on antihypertensive treatment,
extra points are added.
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. JAMA. 2001;285:2486-2497.
www.lipidhealth.org
ATP III Framingham Risk Scoring
Step 5: Smoking Status
Men
79
Nonsmoker
Smoker8
Points at
Age 20-39
Points at
Age 40-49
Points at
Age 50-59
0
5
0
3
0
1
Points at
Age 20-39
Points at
Age 40-49
Points at
Age 50-59
0
7
0
4
0
2
Points at Points at
Age 60-69 Age 700
1
0
Women
79
Nonsmoker
Smoker9
Points at Points at
Age 60-69 Age 700
1
0
Note: Any cigarette smoking in the past month.
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. JAMA. 2001;285:2486-2497.
www.lipidhealth.org
ATP III Framingham Risk Scoring
Step 6: Adding Up the Points
(Sum From Steps 1–5)
Age
Total cholesterol
HDL-cholesterol
Systolic blood pressure
Smoking status
Point total
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. JAMA. 2001;285:2486-2497.
www.lipidhealth.org
ATP III Framingham Risk Scoring
Step 7: CHD Risk for Men
Point Total
Risk
<0
0
1
2
3
4
5
6
7
8
9
10
10-Year Risk
Point Total
<1%
1%
1%
1%
1%
1%
2%
2%
3%
4%
5%
6%
11
12
13
14
15
16
17
10-Year
8%
10%
12%
16%
20%
25%
30%
Note: Determine the 10-year absolute risk for hard CHD (MI and coronary death) from
point total.
Expert Panel on Detection, Evaluation, and Treatment of High Blood
Cholesterol in Adults. JAMA. 2001;285:2486-2497.
www.lipidhealth.org