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MD3001 > Ischaemic Heart Disease > Flashcards

Ischaemic Heart Disease Flashcards

1
Q

True or False: Cardiovascular Disease is still the most common cause of death (out of all diseases)

A

True

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2
Q

Why are rates of CV disease in different areas of the country ?

A

Due to different levels of social deprivation

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3
Q

Are women and men equal when it comes to CV death ?

A

No, women have a lower rate of CV death

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4
Q

Identify the main effects of IHD.

A

1) Chronic coronary insufficiency
- Angina (this is the pain of myocardial ischemia. IHD usually becomes symptomatic only when the luminal cross-sectional area of the affected vessel is reduced by more than 75%, leading to coronary insufficiency)

2) Unstable coronary disease (likely due to clot of plaque)
- Myocardial infarction
- Sudden ischemic coronary death

3) Heart Failure
Contractile impairment in these people is due to irreversible loss of myocardium (previous infarcts) and hypoperfusion of surviving muscle, which leads to chronic ventricular dysfunction

4) Arrhythmia
- Acute ischaemic
- Scar related

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5
Q

State another name of ischaemic heart disease.

A

Atherolscerotic heart disease

Coronary heart disease

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6
Q

Define endocardium and epicardium coronary arteries.

A 
epicardium = outer surface of the heart
endocardium = inner surface of the heart
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7
Q

Why is the difference between endocardium and epicardium relevant in ischemic heart disease ?

A

Subendocardial (beneath the endocardium or between the endocardium and myocardium) region is water-shed area of perfusion and first to become ischaemic

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8
Q

Identify the main epicardial coronary arteries.

A

The left and right coronary arteries and their branches

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9
Q

Identify the main imaging techniques used for coronary artery imaging.

A
  • Coronary Angiography
  • CT
  • MR imaging
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10
Q

Identify the main causes of IHD.

A

Caused by “Risk Factors”

  • Age
  • Hypertension
  • Hypercholesterolaemia
  • Smoking
  • Diabetes
  • Obesity
  • Physical inactivity
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11
Q

Describe the histology of coronary atherosclerosis.

A
  • Intimal fibrous cap
  • Central core rich in lipids (necrotic center)
  • Patchy and raised white to yellow 0.3-1.5cm
  • Fatty streaks: may be elongated streaks (1cm or longer) or fatty dots (< 1 mm)
  • Foam cells + T lymphocytes
  • Cholesterol crystals in tunica intima
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12
Q

Describe the contents of a fatty streak. What is a fatty streak ?

A

Foam cells + T lymphocytes
Mature fibro-fatty Atheroma, first grossly visible lesion in the development of atherosclerosis (can be precursor to plaque)

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13
Q

Describe the main stages in the pathology of the formation of atherosclerotic coronary artery disease.

A
  1. Fatty Streak
  2. Chronic endothelial injury / dysfunction
  3. Lipids and macrophages play a role
  4. Smooth muscle proliferation
  5. Formation of a fibro-lipid plaque ((fibrous cap (collagen from vascular smooth muscle cells) + fat (lipid contained in macrophages))
  6. Injury to the plaque (plaque disruption)
    -Plaque rupture
    -Plaque erosion
    Leads to formation of a thrombus (roof of fibrous cap has become disrupted and contents are thrombogenic)
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14
Q

What is the role of lipids in atherosclerosis ?

A

Hyperlipidaemia (LDL cholesterol) results in:
– Impairs endothelial function
– Accumulates within intima
– Causes oxidative modification of LDL:
• After oxidation, ingested by macrophages via SCAVANGER receptors = foam cells (hence immobilised)
• Chemotactic for monocytes
• Inhibit the motility of macrophages
• Stimulates release of cytokines
• Cytotoxic to endothelial and smooth muscle cells

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15
Q

What is the role of macrophages in atherosclerosis ?

A
  • Monocytes which have migrated from lumen to tunica intima get activated as macrophages
  • Secrete IL1 (Interleukin-1), TNF (Tumor necrosis factor), MCP1 (Monocyte chemotactic protein 1) and growth factors
  • Engulf oxidised LDL = foam cells
  • Foamy cells accumulate together, start raising lumen of artery (brown yellow line, FATTY STREAK)
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16
Q

What is the role of smooth muscle cells in atherosclerosis ?

A

Migrate from tunica media to tunica intima where they may act as phagocytes (engulf lipids which come from lumen to tunica intima)
Proliferate
Once die, rutpture and the cholesterol ingested becomes crystalised
Smooth muscle cells in tunica intima start organising, (depositing collagen and ECM ?)

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17
Q

Distinguish between stenosis and occlusion of an artery.

A

Stenosis is a decrease in blood flow through the artery, occlusion is a complete blockage of blood flow through the artery.

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18
Q

How is total occlusion of left anterior descending artery compensated for by the body ?

A

Filled by Collaterals from the Right Coronary Artery

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19
Q

Identify the main symptoms of angina.

A

– Gripping central chest pain
– Radiation to arm and jaw
– Clear and precise relationship to exercise
– Goes off in 2-10 mins after discontinuation of exercise
– Worse after food (because of decreased blood flow to gut). Worse in cold
– No autonomic features
– Flat of hand/fist to describe pain

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20
Q

Is angina a disease ?

A

No, angina is a symptom

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21
Q

What is the main cause of angina ?

A

Sub-Endocardial ischaemia (mismatch of blood supply (i.e. coronary blood flow) to demand (i.e. myocardial oxygen consumption)), because of epicardial stenosis

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22
Q

What is the main difference on an ECG with angina ?

A

ST depression

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23
Q

Define ischemia.

A

Insufficient supply of blood to an organ, usually due to a blocked artery.

24
Q

What proportion of narrowing of the lumen diameter signifies limitation of max blood supply ?

A

50% of narrowing of the lumen diameter usually signifies limitation of maximal flow.

25
Q

What other factors, besides degree of narrowing, affect blood flow ?

A

Length of narrowing

26
Q

How is the coronary circulation normally controlled ?

A

• Two regulatory systems with two control mechanisms
– Autoregulation (myogenic control)
– Metabolic regulation

27
Q

Explain the processes of autoregulation (myogenic control) and metabolic regulation of blood flow.

A

– In response to changes in arterial pressure
• Arterial pressure↑, arterioles constrict to reduce flow
• Arterial pressure↓, arterioles dilate to increase flow
As a result, blood flow remains the same irrespective of BP (only insofar as BP doesn’t increase or decrease too much, refer to slide 28 of this lecture)
– Constriction due to auto-regulation is through myogenic response (↑ arterial pressure results in stretch-activated Ca2+ channels causing Calcium influx into smooth muscle, and thus depolarization of smooth muscle) (not so much dilation)
– Constriction due to auto-regulation has also been hypothesized to be due to ↑arterial pressure increases O2 and “washes out” local factors (metabolic regulation)

28
Q

How does exercise affect myocardial blood flow ?

A

-CBF can rise up to five fold (400 ml/min/100g) to accommodate a 20 fold increase in total body O2 consumption
BUT little change in a near maximal O2 extraction and a rise in heart rate where per beat CBF is constant can account for 1/3 of the increase seen (so HR doesn’t account for most of it.)
-Vasodilation during exercise account for increase in CBF

29
Q

Explain the process of metabolic regulation of blood flow during exercise.

A

Use a lot of ATP when exercising which produces more ADP which produces more AMP membrane produces more adenosine (membrane permeable, gets out of the cell, and causes vasodilation)

30
Q

Define coronary flow reserve.

A

Maximum increase in blood flow through the coronary arteries above the normal resting volume (difference between autoregulated flow and flow with maximum vasodilation)

31
Q

Graph coronary flow reserve.

A

Refer to slide 33 on this lecture.

32
Q

List the main determinants of myocardial oxygen consumption.

A

Mass of tissue (e.g. ventricular hypertrophy increases it)

Factors which are variable per unit mass of tissue:

  • Tension development - LV (higher tension means higher stronger force of contraction through Frank Starling mechanism. Stronger force of contraction requires more oxygen)
  • Contractility (same as above, but also postive inotropes will increase myocardial oxygen consumption)
  • HR

Factor which is fixed per unit mass of tissue:
-Basal activity (= 10-20%)

33
Q

Given that positive inotropes increase myocardial oxygen consumption, will negative inotropes decrease myocardial oxygen consumption ?

A

No, because if a negative ionotrope is given, the body will still require the same CO to be achieved.
The veinous return will increase and stretch the heart (achieved by increasing L ventricular V and increasing L ventricular
wall tension), so reduction of O2 consumption is completely offset.

34
Q

Is coronary flow reserve constant ? How is this relevant clinically ?

A

No, coronary flow reserve may change from time to time (especially for smaller vessels, less than 200 microns)
Clinically: that is the basis of variable angina

35
Q

Distinguish between fixed stenosis with variable coronary flow reserve and fixed stenosis with fixed coronary flow reserve.

A

With fixed stenosis occurs with fixed coronary flow reserve, the same intensity of the same exercise will always either cause pain, or not (not once yes once on).

When fixed stenosis occurs with variable coronary flow reserve, the same intensity of the same exercise can sometimes cause pain (angina) and sometimes not.

36
Q

Does the collateral circulation have fixed or variable coronary reserve ?

A

Variable (because they’re small vessels, less then 200 microns)

37
Q

Describe the main tests/imaging used for the investigation of chest pain.

A

• Test of Inducible ischaemia
– Exercise stress test (look for ST depression)
– Dobutamine stress echo (look for reduction in function)
– Myocardial perfusion imaging with either exercise or phamacological stress
– Cardiac magnetic resonance imaging (cMR)

• Anatomical assessment
– CT coronary angiography (to confirm angina)
– Invasive angiography

• Anatomic and functional
– Invasive angiography and fractional flow reserve (FFR) (give adenosine and see if P drops)
– cMR
– Novel CT

38
Q

What are the possible treatment options in angina ? What is the aim of each option ?

A

• Drugs
– Reduce Myocardial Oxygen consumption
– Reduce variability of coronary flow reserve (e.g. vasodilators)

• Percutaneous Coronary Intervention (stents and balloons)
– Improve coronary flow reserve

• Coronary Artery Bypass Grafting (CABG)
– Improve coronary flow reserve

39
Q

Identify the vessels used for the main kinds of coronary artery bypass grafting.

A

For RCA- Saphenous vein

For LAD- LIMA (left internal mammary)

40
Q

Name drug classes which contribute to:

  • Reduce myocardial oxygen consumption
  • Reduce variability of coronary flow
A
  • Reduce myocardial oxygen consumption: beta blockers, Ivabridine
  • Reduce variability of coronary flow: vasodilators including organic nitrates (venodilation and arterial vasodilation), calcium channel blockers (arterial vasodilation)
41
Q

Describe the clinical presentation of an MI.

A 
• Chest Pain 
– severe 
– crushing radiating to jaw and arm
• Associated “Autonomic” symptoms (nausea, sweating, terror)
• Breathlessness
42
Q

What are the main causes of MI ?

A

1) Plaque rupture
2) Plaque erosion
3) Coronary embolism
4) Coronary artery spasm/drug
5) Coronary anomaly
6) Spontaneous coronary dissection

43
Q

How does plaque rupture and epicardial coronary occlusion occur ?

A

Atherosclerotic plaque ruptures, contents leak out, resulting in platelet aggregation and arterial thrombosis.
These events include expression of MMPs by macrophages, which break down the cap of the plaque, allowing blood to come in. They also express tissue factor, which is an essential cofactor for the activation of the extrinsic pathway of coagulation.

44
Q

Identify some factors which can modify the presentation of an MI.

A
  • Time of day (more common in early mornings and in winter)
  • Inflammatory activity
  • Infection (esp. Respiratory)
  • Elevation of blood pressure (More common with elevations of BP such as extreme exercise)
  • Catacholamines
45
Q

What can we classify myocardial infarctions ?

A

BY SITE OF INFARCTION (PATHOLOGY)
– Full thickness, transmural
– Sub endocardial

BY ECG (CLINICAL)
– ST Elevation myocardial infarction (STEMI)
– Non-ST elevation myocardial infarction (non- STEMI)

BY CAUSE
– Type 1-5

46
Q

How do the clinical (full thickness transmural and subendocardial) and pathological (STEMI and non-STEMI) classifications of an MI fit together ?

A

STEMSI implies full thickness, transmural MI

NSTEMI will include subendocardial infraction but does NOT exclude transmural infarctions in regions remote from ECG (e.g; back of the heart)

47
Q

Describe the types of MIs when classified by cause.

A

Type 1:
spontaneous MI related to ischemia due to primary coronary event (e.g. plaque erosion or rupture, fissuring, dissection)

Type 2:
MI secondary to ischemia due to increase oxygen demand or decreased supply

Type 3:
Sudden unexpected cardiac death with symptoms suggestive of myocardial ischemia

Type 4:
MI associated with percutaneous coronary intervention or stent thrombosis

Type 5:
MI associated with cardiac surgery

48
Q

Describe the process of MI diagnosis.

A

Both of the following

• A Clinical History with:
– ECG Changes, defining sub-classification of:
STEMI
NSTEMI

• And raised cardiomyocyte markers in blood

  • Troponin T or I (this is the main one)
  • Creatine kinase MB isoform (CKMB)
  • Creatine Phosphokinase (CPK)
  • AST
  • Myoglobin
49
Q

Why are there raised cardiomyocytes in the bood in an MI ?

A

Because the membrane is not working properly, so they have leaked

50
Q

Describe STEMI management and therapy.

A

1) Antiplatelet agents
- Aspirin + Clopidogrel

2) Immediate revascularisation
-By Primary PCI (Percutaneous Coronary Intervention)
(a while ago, thrombolysis)

3) After anti-platelets agents and revascularisation (i.e. adjunctive therapy)
– Beta blockers (reduce myocardial infarction)
– Statin drugs (reduce cholesterol – plaque passivation)
– ACE inhibitors (usually a couple of days later to inhibit dilation of the left ventricle)

51
Q

List possible complications of STEMI immediately, early, and late.

A

• Immediate
– Ventricular Arrhythmia and death
– Acute Left Heart Failure

• Early
– Myocardial Rupture
– Mitral valve insufficiency
– Ventricular Septal defect
– Mural thrombus and embolisation

• Late
– LV dilatation and heart failure
– Arrhythmia
– Recurrent myocardial infarction

52
Q

Identify causes of NSTEMI.

A

– Threatened STEMI
– Small branch occlusion
– Occlusion of well collateralised vessel
– Lateral STEMI in territory not well seen by ECG

53
Q

Does NSTEMI affect any populations in particular ?

A

Yes, more common in elderly

54
Q

Which of STEMI or NSTEMI is more common ? which is on the rise ?

A

STEMI more common

NSTEMI getting more frequent (STEMI less common)

55
Q

What does NSTEMI imply, in terms of cardiac damage ?

A

NSTEMI implies sub-endocardial ischaemia

56
Q

Describe treatment of NSTEMI.

A

• Antiplatelet therapy (Aspirin and clopidogrel)
• Anti-ischaemics (beta blockers and nitrates)
• Statind rugs
• ACE inhibitors
• Coronary angiography and (delayed) revascularisation
– Early if symptoms continue
– Early if Troponin raised
– Risk score (eg GRACE, to assess risk of heart attack)

MD3001 (75 decks)

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