this article discusses about coronary artery disease, its symptoms, presentations, risk factors, pathophysiology in short and primary prevention. this article is intended to present to a group of physicians in various disciplines other than cardiology.

1. CORONARY ARTERY DISEASE
&
ITS PREVENTION
DR MD ASHRAF UDDIN CHOWDHURY
FCPS (MEDCINE), MD (CARDIOLOGY)
CENTRAL POLICE HOSPITAL
DHAKA

2. 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.

3. CORONARY ARTERY DISEASE IS ALSO
KNOWN AS;
ATHEROSCLEROTICCARDIOVASCULAR
DISEASE (ASCVD)
CORONARYATHEROSCLEROSIS
CORONARY HEART DISEASE
ISCHAEMIC HEART DISEASE

4. CORONARY ATHEROSCLEROSIS
 CORONARY ATHEROSCLEROSIS is the
abnormal accumulation of lipid or fatty
substances or fatty atheroma (plaque) in the
lumen of coronary artery

5. RISK FACTORS
Non
Modifiable
Modifiable

6. MODIFIABLE
 Atherogenic dyslipidaemia
 Cigarette smoking, tobacco use
 Hypertension
 Diabetes mellitus
 Physical inactivity or sedentary lifestyle
 Obesity

7. NON MODIFIABLE
 Family history of premature CAD in first
degree relatives.
 Increasing age
 Gender(male)
 Race(non white populations)

8. Emerging risk factors:
 Metabolic syndrome
 HighTriglyceride
 Apo Lipoprotein B
 Dietary trans fat intake
 Poor oral health
 Fibrinogen
 Homocysteine
 Urine microalbuminuria/creatinine
ratio (CKD)
 High sensitivity CRP
 Impaired fasting glucose

9. 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 persons with multiple
risk factors

10. PATHOPHYSIOLOGY
 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

11. PATHOPHYSIOLOGY
 ?? ETIOLOGICAL FACTORS
 INJURYTOTHE ENDOTHELIALCELL LININGTHE ARTERY
 INFLAMMATIONAND IMMUNE REACTIONS
 LDL OXIDATION: ACTS AS FREE RADICALS AND
INITIATES INFLAMMATORY PROCESS
 OXIDIZED LDL ENTERSTHE ARTERY INTIMA &THERE IS
ACCUMULATIONOF LIPIDS INTHE INTIMA OFARTERIAL
WALL

13.  T LYMPHOCYTESAND MONOCYTESTHAT
BECOMESAS MACROPHAGES INFILTRATETHE
AREATO INGESTTHE LIPIDS AND BECOME
FOAM CELL
 PROLIFERATIONOF SMOOTH MUSCLE CELLS
WITH INTHEVESSEL
 FORMATION OF FIBROUS CAP OVER FATTY
CORE (ATHEROMA)
 PROTRUSION OF ATHEROMA INTOTHE
LUMEN OFVESSEL

14.  NARROWING AND OBSTRUCTION
 IF CAP ISTHINTHE LIPID CORE MAY GROW CAUSING ITTO
RUPTURE
 HEMORRHAGE INTO PLAQUE ALLOWINGTHROMBUSTO
DEVOLOP
 THROMBUS OBSTRUCTTHE BLOOD FLOW LEADINGTO
SUDDEN CARDIAC DEATH OR MYOCARDIAL INFARCTION
 ANGINA AND OTHER SYMPTOMS

16.  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.

18. IHD – Clinical Spectrum
Chronic
 Stable Angina
 Silent Ischemia
 Mixed Angina
 Microvascular Angina
(Syndrome X)
 Stunned & Hibernating
Acute
 Unstable Angina
 Acute Myocardial
Infarction (NSTEMI,
STEMI)
 Sudden Cardiac Death
Prinzmetal Angina
18

19. 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.

20. Variant angina
 Also called prinzmetal angina.
 Pain at rest with reversible ST segment elevation
thought to be caused by coronary artery
vasospasm

21. 21
 Prolonged bouts of chest pain at rest
with EKG ST seg. elevation.
PRINZMETAL OR
VARIANT ANGINA
A = Marked transitory ST Elevation during a bout of severe
chest pain
B =Thirty min. after A (Normal EKG)
Pathophysiology: profound spasm of one of
the three major epicardial coronary arteries.

22. 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 microvasculature.

23. 23
Pathophysiology: Dynamic small vessel constriction (vasospasm)
(positive stress testing)

24. Silent ischaemia
 Objective evidence of ischaemia (such as
electrocardiographic changes with a stress
test) but patient has no symptoms
 Commonly seen in diabetic patients.

25. Is the objective
evidence-ST segment
shifts- of
myocardial ischemia
which is not
associated with
angina or angina
equivalents.
25
Silent Ischemia
ST seg. depression
Iceberg’s sign
Angina

26. 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.

28. 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.

29. 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 spasm.

30. 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.

32. Progression of coronary plaque over time Clinical
Findings
32
Acute Coronary Syndromes
Sudden Cardiac Death
Acute silent
occlusive
process
Angina
pectoris
Thrombogenic
risk factors
Atherogenic
risk factors
Endothelial dysfunction
20 years 60 years
Age

33. IS CORONARY ARTERY DISEASE
PREVENTABLE?
WHAT CANWE DOTO PREVENT CAD?

34. 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

35. Control of risk factors
 Control of Hypertension
 Control of diabetes
 Management for dyslipidaemia

36. 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

37. Stress
Influence CAD risk via 2 main mechanisms:
 Catacholamine release
– increased BP
– increased HR
– vasoconstriction
– increased O2 demand
 Decreased adherence to lifestyle modification
recommendations

38. Healthy Diet
 Diets high in fruits, vegetables, whole grains, fish
and unsaturated fatty acids have lower risk for
CAD

39. 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.

40. 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.

41. 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.

42. 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.

43. 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.

44. 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.

45. 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.

46. Obesity
 Body Mass Index (BMI)
 Measured in weight in Kg /height in m2
 BMITargets
Underweight <18.5
Normal 18.5-24.9
Overweight 25.0-29.9
Obese >30
Definition of central obesity in South asians :
– Waist circumference of Men >90cm or 36 inches,
Women >80cm or 32 inches

47. 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. diabetes,
dyslipidaemia, hypertension, obesity, stress)

48. Blood pressure target
 Normal <120 / 80
 Prehypertensive (120/80 to 139/89 mm Hg)
 Stage 1 (140/90 to 159/99 mm Hg)
 Stage 2 (≥160/100 mm Hg)
*JNC 7

49. Lipid Targets for CAD
PrimaryTargets for very high risk patients*:
 LDL-C < 1.8mmol/L (70 mg/dl) or <50% reduction
(< 100mg/dl in moderate risk patients)
 Non HDL-C ≤ 2.6 mmol/L (100 mg/dl)
(< 130mg/dl in moderate risk patients)
 Alternate: Apolipoprotein B < 0.80 g/L
CanJ Cardiol 29 (2013) 151–167.*National lipid association Annual
*ESC guideline
2015

50. Lipid Targets for CAD
SecondaryTargets: (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
CanJ Cardiol 2009; 25(10): 567-579.

51. 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 endothelial
lining making it vulnerable to plaques and clots

52. Diabetes
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
HbA1C <7

53. 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
– Dietary trans fat intake
– Homocysteine
– Lipoprotein A
– Infectious agents
– Adhesion molecules
– Cytokines
– Fibrinogen
– High sensitive C-reactive
protein

54. Lifestyle interventions to reduce TC &
LDL-C levels
 Reduce dietary
saturated fat
 Reduce dietary trans
fat
 Reduce dietary
cholesterol
 Increase dietary
fibres
 Utilize functional
foods enriched with
phytosterols
•Reduce excessive body
weight
•Increase physical activity
•Utilize Soy protein
products
**ESC guideline on
dyslipidaemia 2015

55. Drugs to lower LDL
 Statins – atorvastatin, rosuvastatin,
simvastatin,
 Ezetimibe
 Investigational agent- evolocumab &
alirocumab (PCSK9 inhibitors)- >50%
reduction in LDL-c and nonHDL-c levels

56. 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 or poly
unsaturated fat.
**ESC guideline on
dyslipidaemia 2015

57. Drugs to lower Tg
 Fenofibrate
 Gemfibrozil, colestipol, cholestyramine etc

58. 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 disaccharides
**ESC guideline on dyslipidaemia 2015

59. Drugs to raise HDL-c
 Currently none in clinical use.
 Investigational agent- anacetrapib,
evacetrapib, - 150% increase in HDL-c.

60. SUMMARY
 Control of -
 Dyslipidaemia, Hypertension & DM
 Healthy behaviours-
 Smoking cessation
 Weight control
 Exercise
 Healthy diet
 Stress free life

61. Important Trials that showed
role of statins in CAD
 AVERT(atorvastatin versus revascularization treatment)-
incidence of ischaemic evects was 36% lower in atorvastatin
group compared with revascularization group(PTCA)
 ASTEROID (a study to evaluate effects of rosuvastatin on
intravascular ultrasound derived coronary atheroma burden)–
9.1% reduction in atheroma volume in heavy plaque burden area
of coronary artery.
 JUPITER (Justification for the use of statins in primary
prevention: an intervention trial evaluating rosuvastatin)– this
trial was stopped prematurely as it was seen unequivocally
rosuvastatin reduces morbidity and mortality than placebo in
primary prevention.
 SATURN- study of coronary atheroma by intravascular
ultrasound: effects of rosuvastatin versus atorvastatin. Both were
effective in reducing coronary atheroma.

62. Thank you all !!

63. This presentation was prepared for a group of physicians working in
various disciplines in a large generalhospital.Very often they ask me
whether he or she have CAD and what they should do to avert this deadly
disease. Here I have discussed how to diagnose coronary artery disease
clinically, its pathophysiology in short and how to prevent it (primary
prevention). Investigations and management was not discussed in this
presentation. If anyone find this presentation helpful, I shall be very happy.
I convey my thanks to people who made some of these slides, pictures and
also thanks in advance to those who intend to use these.
Thanking you,
Dr md ashraf uddin chowdhury
FCPS, MD (Cardiology)
Clinical and interventional cardiologist.
ashraf_k45@yahoo.com