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 colored dead tissue surrounded by a hyperemic red border

The red border was due to the granulation tissue

Weeks- months

A white scar is seen at the site of the infarct

Healing takes place by deposition of 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 tamponade5)  Pericarditis- inflammation of the pericardium

Cardiac rupture

Hemopericardium

Papillary muscle rupture following infarction

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.

Complications of MI- Delayed

Ventricular aneurysm

Mural thrombi