Ischemic Heart Disease

Dr. Mehzabin Ahmed

 IHD
• The most common disease of the heart and is caused by
myocardial ischemia
• Four main syndromes are caused by the disease of the
coronary arteries
– Chronic manifestations
• Stable angina
• (May cause cardiac failure in some with a long standing
history/ with repeated infarctions)

– Acute manifestations
• Unstable angina
• Myocardial infarction
• Sudden cardiac death
 Angina

• It is an episodic pain that takes place when there is a

demand for increased myocardial work in the presence
of impaired perfusion by blood.
• Types:
– Stable
– Unstable
– Printzmetal
 Stable angina
• Stable angina is caused by low flow in an
atherosclerotic coronary artery
• There is at least one high grade stenosis (over 50% of
the lumen).
• Drug therapy may modify the stenosis- if the plaque is
eccentric.
• Repeated episodes result in fine fibrosis in the
myocardium with death of individual muscle fibres.
• Development of collaterals (anastomotic channels)
compensates for the stenosis
 Acute Ischemic Heart Disease
• Acute ischemic heart disease is largely caused by
complications in the atheromatous plaques like

– Superficial ulceration Thrombus formation

– Plaque fissuring Hemorrhage into the plaque
• Such complications occur in low grade stenosis,
and no history of angina on exertion.
• The patient may present with massive infarction
leading to sudden cardiac death.
 Pathogenesis
• Complex and dynamic interaction among:
1. Fixed atherosclerotic narrowing of
coronary arteries (fixed coronary obstruction)
• 2. Intraluminal thrombosis overlying a
disrupted atherosclerotic plaque (acute
plaque changes)
• 3. platelet aggregation
• 4. and vasospasm.
 Role of fixed coronary obstruction
• Progressive encroachment of the lumen leading to stenosis
(chronic, fixed obstruction).
• 75% or more reduction in the cross –sectional area of the
lumen of one or more of the major coronary arteries
generally causes symptomatic ischemia (Angina) induced
by exercise
• 90% can lead to inadequate flow even at rest.
• Repeated episodes of impaired flow may lead to
development of fine fibrosis in the myocardium with death
of individual cardiac muscle fibers. Slowly developing
occlusions may stimulate collateral vessels (anastomotic
vessels) to compensate for areas of vascular stenosis
which protect against distal myocardial ischemia and
infarction.
• End with stable angina or cardiac failure.
• Acute disruption of a partially stenosing plaque precipitate acute
coronary syndromes in many patients; The event may be:
– Rupture or fissuring, erosion or ulceration –followed by thrombosis,
– Hemorrhage into the plaque with enlargement of the plaque
• Several influences are important in disruption of plaque
including :
• A. Intrinsic, plaque structure and composition
• B. Extrinsic, blood pressure, adrenergic stimulation; peak
incidence of MI at 6AM to 12noon!,emotional stress, platelet
reactivity.
• - 2/3 of plaques that rapture with subsequent occlusive thrombosis
caused occlusion of only 50% or less before plaque rapture, and 85%
had initial stenosis less than 70%.
• Abrupt plaque change followed by thrombosis is the precipitating factor
for most acute coronary syndromes.
Acute coronary thrombosis
Unstable angina (Crescendo angina)
• Unstable angina is caused by fissuring of
the atherosclerotic plaques
• The angina is of sudden- onset and
increases in frequency and severity.
• The process of thrombus formation is
initiated (started) and total occlusion may
occur resulting in myocardial infarction.
 Myocardial infarction
• Acute myocardial infarction may be regional or
circumferential subendocardial
• Regional infarction (90% of cases) involves one
segment of the ventricular wall.
– Complete occlusions cause full thickness (transmural) infarcts.
– Reperfusion (by lysis of the thrombus /collateral supply) limit
the infarct to the subendocardium.
• Circumferential (10%) involves the subendocardial
zone. It is due to general hypoperfusion of the main
coronary arteries (as in hypotension in a high grade
stenosis).
• The site of myocardial
infarction depends on
which vessel is
involved

•Arteries
–Right Coronary A - Inferior wall MI (posterior)
–Left Coronary A - Main artery - Massive anterolateral wall MI
•Left Anterior Descending A - Antero- septal MI
•Circumflex Coronary A - Lateral MI
 Morphological changes
• Myocardial infarction induces acute inflammation, followed by
organization and scarring ( the end result is the conversion of the
infarcted area into a collagenous scar in 6-8 weeks)
Time Event Comment
0- 12 hrs No visible change Cardiac enzymes are raised
12- 24 hrs Area of pale infarct There is intercellular edema
24- 72 hrs Infarct becomes soft & pale Infracted area shows coagulative
necrosis & inflammatory infiltrate is
seen, mostly neutrophils &
macrophages
3- 10 days Infracted area shows yellow The red border was due to the
colored dead tissue granulation tissue
surrounded by a hyperemic
red border
Weeks- A white scar is seen at the Healing takes place by deposition of
months site of the infarct collagenous / fibrous tissue
 Sudden cardiac death
• Sudden cardiac death (no warning
symptoms or death shortly after the onset of
symptoms)
• It is due to either
– Infarction- may be massive or may precipitate
fatal arrhythmias
– Arrhythmias- Usually ventricular fibrillation
 Complications of MI- Immediate
1)  Contractile dysfunction-healing of the infarction is
by fibrosis, which has poor contractility
2)  Severe myocardial pump failure (cardiogenic
shock)- due to a massive infarction
3)  Arrhythmia- abnormal patterns of rate and rhythm
of the cardiac contraction
4)  Myocardial rupture- in the first week after the
infarct the infarcted area is weak and can rupture.
It may result in hemopericardium and cardiac
tamponade
5)  Pericarditis- inflammation of the pericardium
Cardiac
rupture

Hemopericardium

Papillary muscle rupture

following infarction
 Complications of MI- Delayed
1)  Ventricular aneurysm- the weakened ventricular
wall may bulge outwards to form a sac
2)  Progressive heart failure- the heart function
cannot cope with the body’s demand for the blood
supply
3)  Mural thrombi- formation of thrombus in the
cardiac wall
4)  Papillary muscle dysfunction- it results from
involvement of the papillary muscles by the
infarction and results in the ineffective closure of
the valves causing regurgitation.
5) Dressler’s syndrome – it is an immune mediated
pericarditis associated with high ESR. May
develop 2-10 months after an acute event.
 Mural thrombi

Ventricular
aneurysm