1) Ischaemic heart disease (IHD) results from a lack of oxygen supply to the heart muscle due to narrowed coronary arteries. It presents as stable angina, unstable angina, or myocardial infarction. 2) Coronary arteries supply oxygenated blood to the heart muscle. Blockages in these arteries due to atherosclerosis can cause angina or infarction depending on the severity and location of the blockage. 3) Myocardial infarction occurs when a blockage completely cuts off blood flow, causing death of heart muscle tissue. It is classified as non-ST elevation or ST-elevation MI depending on ECG findings. Treatment involves reperfusion through thrombolysis or angioplasty as well

1. Ischaemic Heart Disease (IHD)
Dr.A.T.M.Mahfuzul Hoque
M D (Cardiology)
Asst. Prof.
Department of Cardiology
Dhaka Medical College& Hospital

2. Definition & clinical presentation of IHD :
Def. of IHD: Disease of the heart muscle
resulting from myocardial ischaemia
Clinical presentation:
1) Stable Angina
2) Unstable Angina
3) Myocardial infarction (MI) -
* Non ST elevation MI
* ST elevation MI

3. CORONARY CIRCULATION
Two major coronary
arteries
1. Right coronary
artery
*Arises from- RSV
*Supplies- SA node,
AV node & bundles,
RV , LV inferior wall

4. CORONARY CIRCULATION
2. Left coronary artery
Arises from- LSV
Two branches-
a). Anterior descending
Supplies- IVS & anterior
wall of LV
b). Left circumflex
*Lateral & posterior wall of
LV

5. CAD IHD Angina pectoris
Definition of Coronary Artery Disease
All patients with
coronary artery
disease
(atherosclerosis) Cardiac disease as a result of
myocardial ischemia
(imbalance between oxygen
requirements and supply)
Symptoms of ischemia = angina pain
1. At rest = unstable angina
2. During exercise = stable angina

6. Coronary insufficiency is
characterized by:
Myocardial
requirements
Myocardial
supply
An Imbalance between requirements and
supply leading to Myocardial Ischemia

7. Causes of Coronary
Insufficiency:
Spasm
Atheroma
(90% of cases)

8. Stable plaque Plaque rupture or fissuration
Thrombus formation
Coronary atherosclerosis can
lead to myocardial ischemia
Myocardial ischemia with
Moderate/severe
exertion
Chronic Ischemic Disease
Myocardial
necrosis
Prolonged myocardial
ischemia with less
exertion/rest
Acute Ischaemic Events

9. Stable angina
Unstable angina Myocardial
Infarction
Stable plaque Plaque rupture or fissuration
Thrombus formation
Myocardial ischemia with
stable ischemic threshold
Myocardial
necrosis
Prolonged myocardial
ischemia with decreased
ischemic threshold
Coronary atherosclerosis can lead
to myocardial ischemia

10. ACS Pathophysiology
Disruptions of coronary artery
plaque -> platelet
activation/aggregation
/activation of coagulation
cascade -> endothelial
vasoconstriction ->intraluminal
thrombus/embolisation ->
obstruction -> ACS
Severity of coronary vessel
obstruction & extent of
myocardium involved
determines characteristics of
clinical presentation

12. Presentation of IHD
Stable angina
Unstable angina
Acute myocardial infarction (Acute MI)
* Non ST elevation MI (NSTEMI)
* ST elevation MI (STEMI)
Acute coronary syndrome (ACS)

13. Stable angina/Angina pectoris
Def. Chest discomfort due to transient
inadequate blood supply to the heart
(usually increased on exertion & relieved
by rest or sublingual GTN)
Characteristics of anginal pain :
* Location & Radiation
* Character
* Relation to exercise/provoking factors
* Duration of pain

14. Diagnosis
Clinical features (symptoms & sign)
Investigations:
* ECG: Resting ECG, Stress ECG
* Echocardiography
* Myocardial perfusion imaging (MPI)
* Coronary angiogram (CAG): CT CAG,
CAG

15. Acute coronary syndrome
It includes-
*Unstable angina- Ischaemia with no
myocardial damage
*Non ST elevation MI- with minimal damage /
partial thickness damage
(Non Q wave MI)
*ST elevation MI- Full thickness damage
(Q wave MI)

16. Unstable angina (UA):
Definition:
• Recent onset Angina
• Angina occuring with increasing
frequency
• Angina occurring with less exertion or at
rest
• Angina not rapidly relieved by S/L GTN

17. Unstable angina (UA):
Pathogenesis:
1. Plaque rupture &
2. Thrombus formation,
leading to incomplete &
intermittent coronary occlusion
with presence of collateral
channels. No myocardial necrosis

18. Unstable angina (UA):
Diagnosis of UA:
Clinical presentation: Typical chest pain
(Prolonged chest pain- Pain > 15 minutes)
Investigations:
ECG- May be normal / ST depression & /
T wave inversion

19. Electrical Signs of ischemia
ST-segment depression
P
Q
R
S
T
ST-segment
depression is present
if there is (at least):
• 1 mm of depression
• 80 ms’ duration
ST-segment
depression is an
objective sign of
reversible ischemia
mm
ms

20. Electrical Signs of ischemia
Other signs
Negative T wave, symmetrical
and pointed

21. Unstable angina (UA):
Investigations:
Cardiac enzymes/ Biochemical markers-
Usually normal
Echocardiography-
Wall motion abnormality

22. Echocardiography

23. Echocardiography

24. Coronary angiogram

26. Unstable angina (UA)
Treatment :
A. Medical management
B. Surgical management
A. Medical management Includes:
General management: Bed rest, O2, I/V line,
cont. ECG monitoring,
Drugs:
1) Nitrates- S/L & Oral, if needed I/V
2) Anti platelets
* Aspirin- 300 mg stat & 75 mg daily
* Clopidogrel- 300 mg stat & 75 mg daily

27. Unstable angina (UA):
3) I/V Morphine- For chest pain
4) Anticoagulants- * Low molecular weight Heparin
(Enoxaparin, Dalteparin)
* Unfractionated Heparin
5) Beta blockers- Metoprolol, Atenolol
6) Calcium antagonists- Diltiazem, Verapamil
7) Lipid lowering agents- Statins
Coronary intervention: PTCA / PCI with stenting
Surgical treatment: Coronary artery bypass graft
(CABG)

28. Myocardial infarction
Def:
Necrosis of a portion of heart muscle as a
result of an acute interruption of coronary
blood supply
PATHOLOGY:
Rupture of an atheromatous plaque, leads
to deposition of intra-coronary thrombus,
which leads in turn to coronary occlusion &
consequent necrosis of myocardium

29. Two types: Depending on ECG criteria
(ST elevation / Q wave)
1. Non ST elevation MI / Non Q wave MI
2. ST elevation MI / Q wave MI
Acute myocardial infarction

30. Non ST elevation MI (Non Q wave MI)
Pathophysiology-
* Plaque rupture & thrombus formation
* Incomplete & intermittent coronary
occlusion with presence of collateral
channels & some myocardial necrosis

31. Non ST elevation MI (Non Q wave MI)
Diagnosis:
A. Clinical presentation: Typical chest pain
B. Investigations:
* ECG- May be normal, ST depression & /
T wave inversion
* Cardiac enzymes/biochemical markers-
Elevated
* Echocardiography- Abnormal wall motion
* Coronary angiogram- CA occlusion

32. Non ST elevation MI (Non Q wave MI)
Treatment :
A. Medical management
B. Surgical management
Medical management: Includes- Hospitalization
* General management: O2, I/V line, ECG monitor
Drugs:
1) Nitrates- S/L, Oral. If needed I/V
2) Anti platelets- Aspirin, Clopidogrel
3) Anticoagulants- Heparin
* Low molecular weight Heparin (Enoxaparin)
* Unfractionated Heparin

33. Non ST elevation MI (Non Q wave MI)
Medical management….Contd:
4) Morphine I/V
5) Beta blockers
6) Calcium antagonists
7) Lipid lowering agents (Statins)
Coronary intervention: PTCA with stenting
B. Surgical treatment: Coronary artery bypass graft
(CABG)

34. MYOCARDIAL INFARCTION
ST Elevation MI
Def:
Necrosis of a portion of heart muscle as a
result of an acute interruption of coronary
blood supply
PATHOLOGY:
Rupture of an atheromatous plaque
Deposition of intra-coronary thrombus
Coronary occlusion
Necrosis of myocardium

35. Universal definition of myocardial
infarction
A combination of criteria is required to meet the diagnosis of acute
MI, namely the detection of an increase and/or decrease of a cardiac
biomarker, preferably high-sensitivity cardiac troponin, with at least
one value above the 99th percentile of the upper reference limit and
at least one of the following:
(1) Symptoms of ischaemia.
(2) New or presumed new significant ST-T wave changes or left
bundle branch block on 12-lead ECG.
(3) Development of pathological Q waves on ECG.
(4) Imaging evidence of new or presumed new loss of viable
myocardium or regional wall motion abnormality.
(5) Intracoronary thrombus detected on angiography or autopsy

36. Types
Type 1 MI
Type 1 MI is characterized by
atherosclerotic plaque rupture, ulceration,
fissure, erosion or dissection with resulting
intraluminal thrombus in one or more
coronary arteries leading to decreased
myocardial blood flow and/or distal
embolization and subsequent myocardial
necrosis.

37. Types-Contd
Type 2 MI
Type 2 MI is myocardial necrosis in which a
condition other than coronary plaque instability
contributes to an imbalance between myocardial
oxygen supply and demand. Mechanisms
include coronary artery spasm, coronary
endothelial dysfunction, tachyarrhythmias,
bradyarrhythmias, anaemia, respiratory failure,
hypotension and severe hypertension, injurious
effects of pharmacological agents and toxins.

38. Risk factors
The presence of any risk factor is
associated with doubling the risk of an MI.
Non Modifiable
Age
Gender
Family history

39. Modifiable
Smoking
Diabetes
Hypertension
Hyperlipidemia
Obesity
Physical Inactivity

40. MYOCARDIAL INFARCTION ( STE MI)
SYMPTOMS:
Prolonged chest pain (> 30 minutes)
Retrosternal, severe, compressing/
constricting/ tightness/heaviness
Radiates to- throat, jaw,
arms, epigastrium,back
Breathlessness
Nausia & vomiting
Anxiety (fear of impending death)
Syncope/collapse

41. MYOCARDIAL INFARCTION ( STE MI)
PHYSICAL SINGS:
1. Signs of sympathetic activation: eg
Pallor, sweating, tachycardia
2. Signs of vagal activation: eg
Vomiting, bradycardia
3. Pulse- Rate: Normal / Brady / tachy.
Rhythm: regular/irregular
Volume: Normal/small.
4. JVP- Normal / may be raised (RV infarct)

42. MYOCARDIAL INFARCTION (STE MI)
4. BP- May be normal / Hypotension or shock
5. Apex beat- Normal / feeble
6. Heart sound- Soft SI & S2. S3, S4 (if HF)
7. Murmur-
* Apical PSM (MR)-
due to papillary muscle dysfunction / rupture
* Lower parasternal PSM (VSR)-
due to ventricular septal rupture

43. MYOCARDIAL INFARCTION (STE MI)
contd.
8. Basal crepetation (pulmonary edema)
9. Pericardial rub (pericarditis)
10. Fever, leucocytosis, raised ESR
(myocardial necrosis)

44. MYOCARDIAL INFARCTION (MI)
D/D :
1) Unstable angina
2) Pericarditis
3) Aortic dissection
4) Pneumothorax
5) Pleurisy
6) Massive pulmonary embolism
7) Esophageal, other upper GI & biliary tract
disease

45. DIAGNOSIS:
1. Clinical features
• Symptoms
• Signs
2. Investigations-
• ECG
• Serum enzymes/Biochemical markers
• Blood counts
• CXR
• Echo

46. INVESTIGATIONS
1.ECG:
* ST segment elevation
* Pathological Q wave
* T wave inversion
a) Infrior MI: changes in
II, III, aVF
b) Anterior MI: VI- V6
c) Anteroseptal MI: VI-
V4 d)
d) Anterolateral MI. I,
aVL & V4- V6
e) Posterior MI: VI & V2
f) RV infarction: V4 R

47. INVESTIGATIONS
2) SERUM ENZYMES/
Biochemical markers:
a. Troponin T, Troponin I
Advantage- Rapid release
Early diagnosis
b. Creatine Kinase (CK)-
heart, brain & skeletal
muscle ,
CK-MB - cadiospecific
Rises within 6 hrs of onset.
Reaches peak in 18-24 hrs
Becomes normal after 72
hrs

48. INVESTIGATIONS
c. SGOT/AST:
Rises 12 hrs.
Peak 24-36 hrs,
Normal 3-5 days
d. LDH:
Rises later after MI
Peak- after 24-48 hrs
Normal after 1-3
weeks

49. INVESTIGATIONS
E) Blood count:
Leucocytosis
Raised ESR
F) Chest X-ray-
To detect pulmonary edema
G) Echocardiography:
RWMA
LV function
LV thrombus
Pericardial effusion
MR, VSR

50. MANAGEMENT OF ACUTE MI
A) ST segment elevation MI (STEMI)
Hospitalization in CCU & immediate initial
treatment:
1.Bed rest, I/V access, cont. ECG monitor-
2.02 inhalation (2-4 L/m)
3.Sublingual nitroglycerine
4.Anti platelet
300 mg soluble Aspirin (chew/crush)
300 mg Clopidogrel

51. MANAGEMENT OF ACUTE MI
4. Relief of pain with Morphine (3-5 mg i/v
every 5-15 minutely until relief of pain)
5. IV anti emetic: (Prochlorperazine)
8. Reperfusion : Pharmacological
a) IV thrombolytics
* Streptokinase- 1.5 million units in 100
ml of saline i/v over I hour
* Others- Urokinase, Alteplase (tPA)

52. INTRAVENOUS THROMBOLYSIS
Inclusion criteria:
 Symptoms of AMI
 ECG:
* ST elevation- I mm in limb leads & 2 mm in chest leads
(in 2 or more contiguous leads)
* New LBBB
 Time to therapy from onset of angina:
12 hr or less (< 6 hr more beneficial)
1st hr is the golden hr
Door to needle time (aim < 30 m)

53. INTRAVENOUS THROMBOLYSIS
Contraindication
1. Active internal bleeding
2. Previous sub arachnoid or intra
cerebral haemorrhage
3. Uncontrolled HTN (BP- 180/100 or >)
4. Recent surgery (Within 1 month)
5. Recent trauma including traumatic
resuscitation
6. Active PUD / any active bleeding
7. Pregnancy

54. MANAGEMENT OF ACUTE MI
b) Invasive procedure
1. Primary PTCA (percutaneous
transluminal coronary angioplasty)
with stenting
1. CABG (coronary artery by pass graft)

55. MANAGEMENT OF ACUTE MI
AFTER STABILIZATION….
DRUG:
1) Antiplatelet- Aspirin- 75 mg/day after meal
Clopidogrel- 75 mg/day
2) Beta-Blocker- Metoprolol- 50 mg/day
Atenolol- 25-50 mg/day
Carvedilol- 6.25-25 mg/day

56. MANAGEMENT OF ACUTE MI
Contd…
3. ACE inhibitors & ARBs-
Captopril, Ramipril
Valsartan, Losartan
4. Nitrates- Oral / IV
5. Lipid lowering agents-
Atorvastatin, Simvastatin
6.Treatment of complications: If any

57. COMPLICATIONS OF MI
I. Arrhythmia:
a. Ventricular- Ventricular ectopics
Ventricular tachycardia
Ventricular fibrillation
b. Supreventricular- SV Ectopis
Atrial flutter, SVT
Atrial fibrillation
c. Others- Sinus tachycardia
Sinus bradycardia

58. COMPLICATIONS OF MI
2. Heart block-
1st degree, 2nd degree & Complete HB
3. Bundle branch block-
LBBB, RBBB, Bi & Tri fascicular block
4. Heart failure- LVF, RVF (RVI)

59. COMPLICATIONS OF MI
5. Hypotension, cardiogenic shock
6. Mechanical complications-
MR,VSR, Cardiac rupture
7. Thrombo embolism
8. Pericarditis

60. COMPLICATIONS OF MI
Late complications-
1. Post MI angina, Re infarction
2. LV Aneurysm
3. Late arrhythmias
4. Thrombo embolism (systemic,
pulmonary)
5. Dressler’s syndrome
6. Heart failure

61. Secondary prevention:
1. Life style/ Risk factor modification
2. Drugs to be continued for indefinite
period
Aspirin/Clopidogrel
Beta-Blocker
Lipid lowering agent
ACE inhibitors

62. Future plan of management
For further evaluation-
CAG-To see coronary artery anatomy
* Accordingly 2 types of treatment
A) Medical management
* Drug treatment & /
* PTCA (Balloon angioplasty with stenting)
B) Surgical treatment- CABG

65. Interventional treatment
PTCA (Ballooning) Stenting
CABG