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Ischemic Heart Disease Flashcards

1
Q

Define Ischemic Heart Disease

A

Imbalance between supply and demand for oxygen and nutrients and removal of metabolites

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2
Q

What is the leading cause of death and disability in the USA?

A

Ischemic Heart Disease (IHD)

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3
Q

What most commonly causes IHD?

A

≥ 90%: reduced coronary blood flow due to atherosclerotic narrowing

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4
Q

Causes of decreased blood flow?

A
  • Fixed atherosclerotic narrowing
  • Acute plaque change
  • Thrombosis overlying ruptured plaque
  • Vasospasm
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5
Q

What coronary arteries are most commonly affected by fixed obstruction?

A

First several centimeters of the LAD, left circumflex, and entire length or right coronary artery

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6
Q

How does the degree or anatomic narrowing/occlusion lead to different types of ischemia?

A

Narrowing of >70% causes symptomatic ischemia with exercise

>90% stenosis causes ischemia at rest

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7
Q

What are risks associated with acute plaque change?

A

Ruptures/fissures/ulcers that can expose underlying thrombogenic substances

Hemorrhage into atheroma

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8
Q

What are some intrinsic factors that influence acute plaque change?

A

Large areas of foam cells

Thin fibrous cap

Most dangerous leasions are the moderately stenoic, lipid rich atheromas (soft core)

Abundant inflammation

Few smooth muscle cells

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9
Q

What are some extrinsic factors that contribute to acute plaque change?

A

Adrenergic stimulation

Upon awakening

Emotional

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10
Q

What is coronary thrombosis?

What are the problems associated with total occlusion vs. incomplete occlusion?

A

Coronary thrombosis - partial or total occlusion superimposed on a partially stenotic plaque

Total occlusion can cause acute transmural MI or sudden death

Incomplete occlusion (mural thrombus) can lead to unstable angina, acute subendocardial infarction, or sudden death

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11
Q

What can stimulate vasoconstriction?

A
  • Adrenergic agonists in circulation
  • Locally released platelet contents
  • Endothelial dysfunction leading to impaired secretion of endothelial relaxing factors
  • Mediators released from mast cells
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12
Q

Four basic syndromes of IHD?

A
  • Angina pectoris
  • Myocardial infarction
  • Chronic ischemic heart disease
  • Sudden cardiac death
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13
Q

What is Angina Pectoris?

A

Paroxysmal and recurrent attacks of chest pain caused by transient myocardial ischemia (15 seconds to 15 minutes) - no necrosis

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14
Q

What are the three patterns or Angina Pectoris presentation?

A

Stable - produced by physical activity or emotional excitement - attributed to chronic stenosis coronary aortic sinus

Prinzmetal - due to coronary artery spasm, at rest

Unstable - occurs with progressively increasing frequency and progressively less effort - often at rest and of prolonged duration

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15
Q

What is often the event that induces Unstable angina pectoris

A

Induced by disruption of plaque with superimposed partial thrombosis (often a prodrome of acute MI)

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16
Q

What is a Myocardial Infarction?

A

Death of cardiac muscle due to ischemia

17
Q

What are risk factors associated with MI?

What are the most common causes of MI?

A

M>F

  • Risk factors: increasing age and predisposition to atherosclerosis
  • Pathogenisis
    • 90% - acute plaque change - thrombosis and occlusion of coronary artery
    • 10% - vasospasm, emboli or unexplained
18
Q

What are the characteristics of a Transmural MI?

A
  • Full thickness of ventricular wall
  • Confined to distribution of one vessel
  • Fixed coronary obstruction with superimposed acute plaque change and complete obstructive thrombosis
19
Q

What are the characteristics of a Subendocardial MI?

A
  • Necrosis limited to inner 1/3
  • May extend laterally beyond perfusion of one vessel
  • Fixed coronary obstruction with acute plaque change but with non-occlusive thrombus or lysis of thrombus or hypotension
20
Q

What is the myocardial response to…

60 seconds of ischemia?

20-40 minutes of ischemia?

Early thrombolytic therapy (3-4 hours) after ischemia?

Loss of blood supply?

A

60 seconds of ischemia: loss of contractility

20-40 minutes of ischemia: irreversible damage

Early thrombolytic therapy (3-4 hours) after ischemia: Reperfusion and limited size of infarct

Loss of blood supply? reversible damage in early stages

* Arrhythmias can lead to sudden death

21
Q

Which area of the blood vessel (in relation to the obstruction) is first to necrose?

A

The area farthest away from the obstruction

22
Q

Frequency of involvement of coronary arteries in MI?

A

LAD: most often (40-50%)

RCA: next most often (30-40%)

LCA (left circumflex): Least common (15-20%)

23
Q

Myocardial infarction: Gross morphology

<12 hours:

12-24 hours:

1-14 days:

>2 weeks:

A

<12 hours: pale areas 2-3 hours post occurance

12-24 hours: Dark red-blue mottling (stagnant blood)

1-14 days: early: sharply defined yellow-tan area; late: hyperemic peripheral zone (increased blood flow)

>2 weeks: Gray-white scar begins to form

24
Q

Histology of MI

4-12 hours:

12 hours - 7 days:

7 -14 days:

>2 weeks:

A

4-12 hours: wavy fibers

12 hours - 7 days: coagulative necrosis (neutrophils, lack of nuclei, macrophages at border)

7 -14 days: Granulation tissue well established

>2 weeks: Progressively more collagen deposition - eventually dense fibrous scar

25
Q

Reperfusion injury associated with acute MI usually occurs after what treatments? Prevention of necrosis occurs with reperfusion within __ minutes

A

Thrombolysis, balloon angioplasty, or bypass grafts

20 minutes

26
Q

Possible causes of reperfusion injury

A
  • Oxygen free radicals released from leukocytes
  • Microvascular injury causes hemorrhage and endothelial swelling that occludes capillaries
  • Platelet and complement activation

*Microscopically: Necrosis with contraction bands due to influx of calcium

27
Q

How do you diagnose MI?

A

Chest pain

Rapid weak pulse, dyspnea due to pulmonary edema

ECG patterns

Lab evaluation of cardiac enzymes, C-reactive protein

Approximately 10-15% without symptoms

28
Q

What are some potential complications of MI?

A

Contractile dysfunction

Cardiogenic shock (pump failure) with damage to 40% or more

Arrhythmia

Myocardial rupture (shunts)

Pericarditis

29
Q

What types of mycocardial rupture are associated with MI?

A

Free wall - hemopericardium, tamponade, aneurysm

Ventricular septum - Lt to Rt shunt

Papillary muscle due to mitral regurgitation

30
Q

What are some later complications of MI?

A

Ventricular aneurysm

Progressive heart failure

Papillary muscle dysfunction secondary to scarring

31
Q

Long term prognosis of acute MI depends on…

A

Quality of left ventricular function and the extent of vascular obstruction

32
Q

What makes chronic IHD different than acute IHD?

A

Usually in elderly patients with progressive heart failure due to ischemic myocardial damage - myocardial dysfunction

33
Q

What is the morphology associated with Chronic IHD?

A

Heart is enlarged and heavy with left ventricular hypertrophy and dilation, coronary atherosclerosis, scars, subendocardial myocyte vacuolization

34
Q

Sudden Cardiac Death is most often due to…

A

IHD and its first manifestation (80-90%)

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