0630 - pathology of MI - AHF

Question 1

What is cell injury?

Answer 1

Cell injury occurs when cells are stressed so severely that they are no longer able to adapt, e.g. oxygen deprivation, toxins, infectious agents, physical trauma; can be reversible or irreversible.

Question 2

What are the 3 main ways oxygen deprivation to the cells occurs?

Answer 2

• occlusion of blood flow
• reduced transportation of oxygen e.g. reduced Hb
• increased demand for oxygen e.g. during exercise

Question 3

What is ischaemia and what does it compromise?

Answer 3

Ischaemia is decreased or losses of blood supply from the impeded artery, or reduced venous drainage. It compromises the supply of oxygen and metabolic substrates (e.g. glucose).

Question 4

When does infarction occur? Where can it occur?

Answer 4

It occurs in any tissue in which there is sufficient ischaemia to cause tissue death or necrosis. Infarction may be arterial (e.g. complete blockage by thrombosis or embolism; often wedge-shaped, pale due to decreased blood supply but will be red if there was reperfusion) or venous (e.g. mechanical compression of vascular supply; red as blood blocked into organ).

Question 5

What is necrosis and what are the different types?

Answer 5

The morphologic changes that follow cell death in living tissue; changes due to denaturation of intracellular proteins and enzymatic degradation of the cell; can bee seen macroscopically and microscopically.

Question 6

Define ischaemic heart disease.

Answer 6

Generic designation for closely-related syndromes arising due to myocardial ischaemia; 90% due to coronary artery atherosclerosis; leading cause of death in males and females, but death rate has fallen by 50%; clinical manifestations divided into 4 main syndromes:

• angina (stable: has a regular pattern, can predict when pain will occur; unstable: no pattern, may occur without exertion; prinzmetal: spasm in a coronary artery)
• sudden death
• MI
• chronic ischaemic heart disease with heart failure

Question 7

What is the pathogenesis of ischaemic heart disease?

Answer 7

Risk of developing IHD depends on the number, distribution and structure of atheromatous plaques; the degree of narrowing they cause; and how quickly the plaques evolve (if slowly, protective collateral vascular channels will develop). IHD will develop if coronary perfusion is diminished relative to myocardial demand.

Question 8

What are the acute coronary syndromes? How do they arise?

Answer 8

• unstable angina
• sudden cardiac death
• MI

They are precipitated by conversion of a stable atherosclerotic plaque to an unstable one; this mechanism is poorly understood, but rupture/fissuring, erosion/ulceration and haemorrhaging leading to thrombus formation and arterial occlusion involved.

Question 9

Outline some risk factors for MI.

Answer 9

• male
• atherosclerosis (increasing risk for MI; 90% of MI associated with atherosclerosis)

1. hypertension
2. smoking
3. diabetes
4. hypercholesterolaemia

Question 10

What is the pathogenesis of MI?

Answer 10

• coronary arterial occlusion
• acute plaque change
• platelets undergo adhesion, aggregation, activation
• vasospasm
• extrinsic pathway of coagulation activated and thrombus size increases
• complete occlusion of artery within minutes
• increased myocardial demand
• haemodynamic compromise
• presence/absence of collateral vessels

Response:

Coronary artery occlusion à ischaemia to myocardium à functional (loss of contractility within 60 sec), biochemical (cessation of glycolysis within seconds), morphological consequences (ischaemia lasting 20 - 40 min leads to necrosis; complete necrosis in 6 hrs)

Question 11

Explain the difference between transmural and subendocardial infarction.

Answer 11

Transmural: full thickness ischaemic necrosis of the ventricular wall; involves a single coronary artery; ST elevation on ECG (“STEMI”)

Subendocardial: ischaemic necrosis limited to inner 1/3 of ventricular wall; may involve several coronary arteries

Question 12

What are the macroscopic and microscopic findings in MI?

Answer 12

Question 13

Relate complications of MI to pathological changes occurring in the heart.

Answer 13

If we understand the pathophysiology of MI, we can predict the timing of post-MI complications, and anticipate them so as to prevent and diagnose early. From outside to inside:

• contractile dysfunction
• abnormalities of LV function
  1. may lead to hypotension, pulmonary oedema
• cardiogenic shock
• conducting system (arrhythmias)
• arrhythmias usually due to cardiac muscle irritability secondary to ischaemia
• MI can directly affect bundle of His in septum
• pericardium
• pericarditis associated with transmural infarct
• pericardial space
• haemopericardium (escape of blood from ventricles into pericardial cavity)
• cardiac tamponade (constriction of heart with decreased diastolic filling)
• myocardium
• rupture due to mechanical weakening as a result of myocardial necrosis
  1. ventricular free wall
  2. ventricular septum
  3. papillary muscle
• extension (new necrosis adjacent to existing infarct)
• expansion (weak necrotic muscle stretches and infarct enlarges without further necrosis)
• ventricular aneurysm (localised swelling of arterial wall due to expansion of infarct and healing by fibrosis; bulges during systole)
• endocardium
• mural thrombus (local inflammation of endocardium)
• papillary muscles/valves
• dysfunction leading to mitral regurgitation
  1. rupture
  2. fibrosis, shortening
  3. ventricular dilation

Timeline of complications:

1. arrhythmia (immediate)
2. contractile dysfunction (within 60 sec)
3. pericarditis (2 - 3 days)
4. myocardial rupture (3 - 7 days)
5. mural thrombosis with risk of embolism (10 days - 3 months)
6. aneurysm

Question 14

Following a massive MI, the maximum risk of myocardial rupture is between.

A. 1 - 2 hours

B. 1 - 2 days

C. 3 - 7 days

D. 10 - 12 days

E. 1 - 3 months

Answer 14

C.