CORONARY ARTERY

DISEASE
ITS &
PREVENTION
CORONARY ARTERY
DISEASE

Coronary artery disease is the most common
form of heart disease in all over the world.

A narrowing of the coronary arteries prevents
adequate blood supply to the heart muscle in
this condition.

Usually caused by atherosclerosis, it may
progress to the point where the heart muscle is
damaged due to lack of blood supply.

Such damage may result in infarction,
arrhythmias, and heart failure.
CORONARY ARTERY DISEASE IS
ALSO KNOWN AS;

 ATHEROSCLEROTIC
CARDIOVASCULAR DISEASE
(ASCVD)
 CORONARY ATHEROSCLEROSIS
 CORONARY HEART DISEASE
 ISCHAEMIC HEART DISEASE
 CORONARY
ATHEROSCLEROSIS
 CORONARY ATHEROSCLEROSIS is the
abnormal accumulation of lipid or
fatty substances or fatty atheroma
(plaque) in the lumen of coronary
artery
RISK
FACTORS

Modifia Non
ble Modifia
ble
MODIFIABL
E

 Cigarette smoking, tobacco use

 Hypertension
 Diabetes mellitus
 Physical inactivity or sedentary
lifestyle
 Obesity
NON
MODIFIABLE
 Family history of premature CAD
in first degree relatives.
 Increasing age
 Gender(male)
 Race(non white populations)
Emerging risk
factors:
 Metabolic syndrome(Syndrome
X)
 High Triglyceride
 Apo Lipoprotein B( increase fat
and cholestrol)
 Dietary trans fat intake
 Poor oral health
 Fibrinogen
 Homocysteine(type of amino
acid
 Urine
microalbuminuria/creatinine
Synergy of risk
factors:

 The CAD death risk in men

who smoke, have DBP>90 mm
Hg, TC>250 mg/dl, the actual risk
is more than all the three risk
factors are added
 Thus there is multiplicative
effect of multiple risk factors
acting in concert.
 Also control of one risk factor
provides substantial benefit in
PATHOPHYSIOLO
GY
 Normal arterial wall has three
layers:
 Intima- limited by internal elastic
lamina
 Media- between internal and
external elastic lamina
 Adventitia

 Intima is the site at which the

atherosclerotic lesions form
PATHOPHYSIOLO
GY  ?? ETIOLOGICAL FACTORS

 INJURY TO THE ENDOTHELIAL CELL LINING THE

ARTERY

 INFLAMMATION AND IMMUNE REACTIONS

 LDL OXIDATION: ACTS AS FREE
RADICALS AND
INITIATES INFLAMMATORY PROCESS

 OXIDIZED LDL ENTERS THE ARTERY INTIMA &

THERE IS
ACCUMULATION OF LIPIDS IN THE INTIMA OF
ARTERIAL
 T LYMPHOCYTES AND MONOCYTES
THAT BECOMES AS MACROPHAGES
INFILTRATE THE AREA TO INGEST THE
LIPIDS AND BECOME
FOAM CELL

 PROLIFERATION OF SMOOTH MUSCLE

CELLS WITH IN THE VESSEL

 FORMATION OF FIBROUS CAP OVER

FATTY CORE (ATHEROMA)

 PROTRUSION OF ATHEROMA IN TO
THE LUMEN OF VESSEL
 NARROWING AND OBSTRUCTION

 IF CAP (catabolite activator protein) IS THIN

THE LIPID CORE MAY GROW CAUSING IT TO
RUPTURE

 HEMORRHAGE INTO PLAQUE ALLOWING

THROMBUS TO
DEVOLOP

 THROMBUS OBSTRUCT THE BLOOD FLOW

LEADING TO
SUDDEN CARDIAC DEATH OR MYOCARDIAL
INFARCTION
 The process of atherosclerosis
begins in childhood and has
clinical manifestations in late
adulthood
 The process develops over years
to decades and progression is
not linear and smooth but
discontinuous with periods of
quiescence and rapid evolution.
IHD – Clinical
Spectrum Chronic
 Stable Angina
 Silent Ischemia
 Mixed Angina
 Microvascular
Angina
(Syndrome X)
 Stunned &
Hibernating
Acute
 Unstable Angina
 Acute
Myocardial
Infarction
(NSTEMI,
STEMI)
ANGINA
PECTORIS
 Angina pectoris is a clinical syndrome
usually characterized by central chest
pain, discomfort or breathlessness that
is precipitated by exertion or any
stress and promptly relieved by rest or
nitrate.
 It may occur when there is imbalance
between myocardial oxygen supply
and demand.
 Coronary atheroma is the commonest
cause of angina.
 Variant angina
 Also called prinzmetal angina.
 Pain at rest with reversible ST segment
elevation thought to be caused by
coronary artery vasospasm
 PRINZMETAL
OR VARIANT
ANGINA

 Prolonged bouts of chest

pain at rest with EKG ST
seg. elevation.
Pathophysiology: profound spasm of one of
the three major epicardial coronary arteries.
A = Marked transitory ST Elevation during a
2
bout of severe chest pain 1
Microvascular
angina
 Also known as syndrome X
 Patient have chest pain with ECG
change
 In this condition stress test (ETT) is
positive
 But does not have any blockage in
epicardial coronary artery in
angiogram.
 The pain is due to blockage or
spasm in cardiac
Pathophysiology: Dynamic small vessel constriction
(vasospasm) 2
 Silent
ischaemia

 Objective evidence of ischaemia

(such as electrocardiographic
changes with a stress test) but
patient has no symptoms
 Commonly seen in diabetic
patients.
 Silent
Ischemia
Is the objective
evidence-ST
segment shifts-
of
myocardial
ST seg.
depression ischemia which
is not
associated with
angina or angina
equivalents.
Iceberg’s sign

Angi
na
2
5
ANGINA PAIN
FEATURES
 Squeezing burning tightening aching
pain
or discomfort across chest
 The pain often spread to neck,
jaw, arms, shoulders, throat,
back or even teeth
 Angina pain starts with exertion
which is mostly predictable.
 It is relieved with rest or after
taking nitrate.
ACUTE CORONARY
SYNDROME(ACS)
 ACS is a term that encompasses
both unstable angina and
Myocardial Infarction (MI).
 After rupture of an ulcerated or
fissured plaque, there is a dynamic
process whereby degree of
obstruction may either increase
leading to complete vessel
occlusion and MI, or regress due to
endogenous fibrinolysis.
Unstable
angina
 New onset or rapidly worsening
angina or angina on minimal
exertion or angina at rest in the
absence of myocardial damage.
 Also called preinfarction angina
 Symptoms occur frequently and
last longer than stable angina
 Pain may occur at rest.
 The culprit lesion is usually an
ulcerated or fissured atheromatous
plaque with adherent platelet rich
thrombus and local coronary artery
MYOCARDIAL
INFARCTION
 Myocardial infarction refers to the
dynamic process in which a region of
the heart experience a severe
prolonged lack of oxygen supply
due to complete occlusion of
coronary artery with subsequent
necrosis or death to myocardial
tissue.
 The process of infarction progress
over several hours.
 IS CORONARY ARTERY
DISEASE
PREVENTABLE?
WHAT CAN WE DO TO PREVENT
CAD?
 Lifestyle changes / Health
behaviours
Lifestyle changes that may be useful in
coronary disease include:

•Smoking cessation
•Exercise
•Healthy diet
•Stress management
•Weight control / Obesity reduction
Control of risk
factors
 Control of Hypertension
 Control of diabetes
 Management for
dyslipidaemia
Stres
s
 Psychosocial factors associated with
CAD risk:
– Type A personality ( odd, eccentric
thinking or behaviour)
– Hostility/Anger
– Depression/Anxiety

 3 to 4 times increased risk of death in

first year following MI
Stres
s
Influence CAD risk via 2 main
mechanisms:
 Catacholamine release
– increased BP
– increased HR
– vasoconstriction
– increased O2 demand
 Decreased adherence to lifestyle
modification recommendations
Healthy
Diet
 Dietshigh in fruits, vegetables, whole
grains, fish and unsaturated fatty acids
have lower risk for CAD
Good and Bad Cholesterol
Actually, some cholesterol is necessary for proper body function.
But dietary saturated fat and cholesterol both raise levels of LDL
"bad" cholesterol. High levels of LDL cholesterol can cause plaque
to build up in arteries, leading to heart disease and stroke. HDL is
a "good" cholesterol in that it helps eliminate bad cholesterol from
blood. It is possible to lower LDL cholesterol and raise HDL
cholesterol with diet.
Serve Up Heart-Healthy Food
When it comes to fruits and vegetables, pick up the pace! Multiple
servings throughout the day can help lower LDL "bad" cholesterol.
Moreover, these foods have antioxidants that can be beneficial. Also,
eating more vegetables and fruits often results in eating fewer high-
fat foods. This can lower blood pressure promote weight loss.
Think Fish For Heart Health
Fish is generally exceptionally heart healthy because it is high in
healthy omega-3 fatty acids and low in saturated fat. It is the
omega-3 fatty acids that help lower blood levels of triglycerides.
Especially emphasize fatty fish. Keep in mind that deep oil frying of
any food diminishes the health benefits.
Start the Day With Whole Grains
Oatmeal or whole-grain cereal have fiber and complex carbohydrates
that help to feel fuller for longer, so a person is less inclined to
overeat later in the day. These breakfasts help reduce LDL "bad"
cholesterol and can help with our weight control.
Go Nuts for Cardiovascular Health
Nuts help to lower cholesterol because they are high in
monounsaturated fat. This form of fat lowers LDL "bad" cholesterol
while maintaining HDL "good" cholesterol levels. This can lower
the risk of heart disease. Only eat a handful, though, because nuts
are high in calories, especially if they are coated in sugar or
chocolate.
Unsaturated Fats Protect the Heart
Our daily fat needs are only about a third of our daily calories.
However, the form of fat makes a difference. Unsaturated fats (in
canola, olive, and sunflower oils) lower LDL "bad" cholesterol
levels. Saturated fats (in butter and palm oil) and trans fats
increase LDL cholesterol. All fats have calories. Moderation is the
key.
Eat More Beans, Fewer Potatoes
Carbohydrates are important for energy production. However, there
are differences in the quality of carbohydrates, too. Whole grains like
beans, quinoa, whole-wheat pasta, and brown rice are high in fiber
that can help lower cholesterol. Whole grains also keep you feeling
full longer. The carbohydrates in pastries, white rice, white bread, and
potatoes boost blood sugar levels rapidly. This can lead you to feel
hungry sooner, potentially leading to overeating.
 Obesit
 Body Mass Index (BMI)
y 
Measured in weight in Kg
/height in m2
 BMI Targets
Underweig <18.5
ht Normal 18.5-
24.9
Overweigh 25.0-
29.9
t Obese
Definition of central obesity >30
in South
asians :
– Waist circumference of Men >90cm or
36 inches,
Women >80cm or 32
Sedentary Lifestyle &
Exercise
Regular exercise- at least 30 minutes , 3
or 4 times a week.
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.
Blood pressure
target

 Normal <120 / 80
 Prehypertens (120/80 to 139/89
ive mm Hg) (140/90 to
 Stage 1 159/99 mm Hg)
 Stage 2 (≥160/100 mm Hg)

*JNC 7
Lipid Targets for
CAD
Primary Targets for very high risk
patients*:
 LDL-C < 1.8mmol/L (70 mg/dl) or <50%
reduction (< 100mg/dl in moderate
risk patients)
 NonHDL-C ≤ 2.6 mmol/L (100
mg/dl)
(< 130mg/dl in moderate risk patients)
*ESC
 Alternate:
2015
guideline
Apolipoprotein B < 0.80 g/L
*National lipid association Can J Cardiol 29 (2013)
 Lipid Targets for
CAD
Secondary Targets: (once LDL
cholesterol is at goal)
 Total Cholesterol to High Density
Lipoprotein (HDL) cholesterol ratio less
than 4.0
 Non HDL cholesterol < 3.5 mmol/L
 Triglycerides < 1.7 mmol/L (150 mg/dl)
 Apolipoprotein B to apolipoprotein AI ratio
< 0.8
 High-sensitivity C-reactive protein (CPR) <
2 mg/L
Can J Cardiol 2009; 25(10):
 Diabete
s
 Peoplewith 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

 Excesssugar in vessels damages the

endothelial lining making it vulnerable
Diabete
s
Careful control of blood sugar levels
reduces the risk of developing the
complications of diabetes

Targets for diabetic control-as

near normal as
possible
Canadian guideline:
FBG 4-7 mmol/L
2 hr pc BS 5-11 mmol/L
Emerging Risk
Factors
 Nontraditional factors that are associated with
increased risk of CAD, but a causal link has
not yet been proved with certainty
– Poor oral health – Adhesion molecules

– Dietary trans fat – Cytokines

intake – Fibrinogen
– Homocysteine – High sensitive C-
– Lipoprotein A reactive
protein
– Infectious agents
Lifestyle interventions to reduce
TC & LDL-C levels

 Reduce •Reduce excessive

dietary body
saturated weight
fat •Increase physical
 Reduce dietary activity
trans fat •Utilize Soy
 Reduce protein
dietary products
**ESC guideline
cholesterol on
dyslipidaemia
 Increase 2015
dietary
fibres
 Utilize
Drugs to lower
LDL
 Statins – atorvastatin,
rosuvastatin, simvastatin,
 Ezetimibe

 Investigational agent-
evolocumab & alirocumab
(PCSK9 inhibitors)- >50%
reduction in LDL-c and nonHDL-
c levels
Lifestyle interventions to
reduce TG levels
 Reduce excessive body weight
 Reduce alcohol intake
 Reduce intake of mono and
disaccharides
 Reduce total amount of dietary
carbohydrate
 Increase habitual physical activity
 Utilize supplements of n-3
polyunsaturated fat
 Replace saturated fat with mono
Drugs to lower
Tg
 Fenofibrate
 Gemfibrozil, colestipol,
cholestyramine etc
Lifestyle interventions to
increase HDL-C levels
 Reduce dietary trans fat
 Increase habitual physical activity
 Reduce excessive body weight
 Reduce dietary carbohydrate and
replace them with unsaturated fat.
 Use alcohol with moderation
 Prefer carbohydrate with low
glycaemic index and high fibre
content
 Quit smoking
 Reduce intake of mono and
Drugs to raise
HDL-c
 Currently none in clinical use.
 Investigational agent-
anacetrapib, evacetrapib, -
150% increase in HDL-c.
SUMMAR
Y
 Control of -
 Dyslipidaemia, Hypertension
& DM
 Healthy behaviours-
 Smoking cessation
 Weight control
 Exercise
 Healthy diet
 Stress free life
Thank you
all !!