L5 Ischemic Heart Disease

Question 1

Evolution of Atherosclerosis?

Answer 1

Thickening of vessel wall

Loss of elasticity

Fatty Streak –> Atheroma

Question 2

Composition of an Atheroma

Answer 2

Surface = Fibrous cap (firm & white)

Smooth muscle cells

Dense connective tissue

Deeper/core = Soft/fluid (white/yellow)

Lymphocytes

Disorganized cholesterols

Lipid-laden macrophages

Cell debris

Question 3

Causes of Atherosclerosis?

Answer 3

Lipid insulation/infiltration hypothesis

Reaction to injury hypothesis: Plaques form as a response to arterial endothelial injury

Question 4

Consequences of Atehrosclerosis

Answer 4

Plaque Complications:

Disruption

Erosion

Rupture

Embolism

Calcification –> arteries stiffen

Aneurysmal Dialation

Arterial wall undergoes pressure atrophy

Loss of elastic tissue –> wall weakness and dialation

Question 5

Causes of Ischemic Heart Disease

Answer 5

1. Fixed atherosclerotic coronary artery narrowing: >75% (stable Angina)
2. Acute plaque change/disruption –> ACUTE CORONARY SYNDROME
3. Vasospasm/vasoconstriction of the coronary artery

Question 6

_____________:

• Paroxysmal (sudden & violent) & recurrent attacks of chest pain
  
  • pressure, tightness, constricting, squeezing feeling
• Transient (15 seconds to 15 mins) myocardial ischemia
• Short of inducing the myocardial necrosis of a myocardial infarction

Answer 6

Angina Pectoris:

• Paroxysmal (sudden & violent) & recurrent attacks of chest pain
  
  • pressure, tightness, constricting, squeezing feeling
• Transient (15 seconds to 15 mins) myocardial ischemia
• Short of inducing the myocardial necrosis of a myocardial infarction

Question 7

Angina Pectoris (Stable vs. Unstable vs. Prinzmetal)

Answer 7

• Stable/Classic Angina:

Most Common Form

Chest Pain induced by exertion, relieved by rest

Asc. w/ chronic stenosing atherosclerosis

No plaque disruption

• Unstable Angina

Chest pain w/ increasing frequency

Less exertion needed/ occuring at rest

Induced by plaque disruption

Ischemia falls short of threshold for infarction

• Prizmetal Angina:

Uncommon

Random episodic chest pain @ rest

Due to coronary artery spasm (not atheroschlerosis or stenosis)

Question 8

____________________:

Unstable angina + MI + Sudden cardiac death => Ischemic myocardial change sufficient to cause necrosis

Precipitated by an abrupt/acute plaque change/disruption –> thrombosis

Answer 8

Acute Coronary Syndrome:

Unstable angina + MI + Sudden cardiac death => Ischemic myocardial change sufficient to cause necrosis

Precipitated by an abrupt/acute plaque change/disruption –> thrombosis

Question 9

Why is Acute Coronary Syndrom more likely in moderately stenosed vessels?

Answer 9

More likely in moderately stenosed atherosclerotic vessels rather than in severely stenosed (>75%) vessels.

1. Have a complex configuration.
2. Have a soft core =>More likely to disrupt

Less likely in severely stenosed atherosclerotic vessels:

Slow plaque buildup

Stimulates development of COLLATERAL VESSELS

Protective against unstable angina/ MI

Question 10

Pathogenesis of a Myocardial Infarction?

Answer 10

• Necrosis begins beneath the endocardial surface in the center of the ischemic zone (last to receive blood from coronary arteries)
• If the circulation is not restored:
  
  • Necrosis radiates through the adjacent myocardium
  • 3 -6 hours infarct reaches it’s full size
• Narrow zone of myocardium immediately beneath the endocardium is spared from necrosis (oxygenated by diffusion from the ventricle)

Question 11

Two Types of Myocardial Infarction?

Answer 11

Question 12

Biochemical Changes/ Cardiac Enzymes indicative of Myocardial Infarction

Timing of each?

Answer 12

Creatine Kinase (CK)/ CK-MB)

Elevated following exercise in absence of ischemia

Establish re-infarction => levels reset in 72 hours

Timing:

Rise 2-4 hours

Peaks 24-48 hours

Normal 72 hours

Troponins:

More commonly used

Not normally present in circulation

Higher the level, higher risk of death

Timing:

Rises 2-8 hours

Peaks 24 hours

Return to normal in 10 days

Question 13

Dangers of too quick reperfusion in myocardial infarction?

Answer 13

REPERFUSION INJURY:

Due to quick reoxygenation of injured cells

reperfusion accelerates disintegration of necrosed myocytes

=> dying cells die faster, healthy ones saved

WBCs infiltration => generate oxygen derived free radicals that damage the myocardium

Microvascular injury: Microvasculature becomes leaky

Question 14

___________________:

Viable but injured myocardium w/ abnormal biochemical function remains non-contractile for a few days

=>patients need supportive therapy.

Answer 14

S_TUNNED MYOCARDIUM:_

Viable but injured myocardium w/ abnormal biochemical function remains non-contractile for a few days

=>patients need supportive therapy.

Question 15

Complications of Myocardial Infarction?

Answer 15

Question 16

______________:

Unexpected death due to cardiac causes

___________ or within 1 to 24 hours of symptom onset

80%: ______

10-15%: _______

5%: ___________

Answer 16

Sudden Cardiac Death

Unexpected death due to cardiac causes

w/o symptoms or within 1 to 24 hours of symptom onset

80%: Atherosclerotic Coronary Artery Disease (ASCAD)

10-15%: Cardiomyopathies

5%: Valvular cardiac disease

Question 17

_________________:

Compromised ventricular function => heart failure due to accumulated ischemic myocardial damage (Past MI or Coronary artery bypass)

Answer 17

Chronic IHD with cardiac failure( Ischemic Cardiomyopathy)

Compromised ventricular function => heart failure due to accumulated ischemic myocardial damage (Past MI or Coronary artery bypass)