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MD3001 > Ischaemic heart disease > Flashcards

Ischaemic heart disease Flashcards

1
Q

Learning outcomes

A
  • Describe the causes of ischaemic heart disease
    1. Describe the macroscopic features of coronary artery atheroma
    1. Describe the clinical and pathological features of acute myocardial infarction
    1. Describe the complications of acute myocardial infarction
    1. Describe the clinico-pathological features of chronic ischaemic heart disease
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2
Q

What is ischaemic heart disease?

What does it lead to?

A
  • Ischaemic heart disease is where the blood vessels supplying the heart (coronary vessels) are narrowed or blocked
  • This results in a mismatch of blood supply (coronary blood flow) to demand (myocardial oxygen consumption)
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3
Q

what does chronic coronary insufficiency cause?

A

angina

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4
Q

what are different types of unstable coronary disease?

A

acute coronary syndromes
myocardial Infantin
unstable angina
sudden ischaem ic coronary death

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5
Q

epicardial

A

outer surface of heart

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6
Q

endocardial

A

inner surface of heart

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7
Q

subendocardial region

A

water shed area of perfusion and first to becomes ischaemic

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8
Q

posterior descending artery infarction type?

A

true posterior infarction

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9
Q

left anterior descending artery infarction?

A

anterior MI

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10
Q

circumflex coronary infarction?

A

lateral MI

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11
Q

What are 3 different names for Ischaemic heart disease (IHD)?

A
  • Ischaemic heart disease (IHD) is also known as:
    1) Atherosclerotic heart disease
    2) Coronary heart disease
    3) Coronary artery disease
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12
Q

What are 4 the main cardiac effects of Ischaemic heart disease?

A

1) Chronic coronary insufficiency
* Causes 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)
* Can lead to:
* 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
* Due to acute ischaemia
* Scar related

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13
Q

What is the epicardium?

What is the endocardium?

What is the subendocardial space?

Why is it relevant in IHD?

A
  • Epicardium = outer surface of the heart (consistent with visceral layer of serous pericardium)
  • Endocardium = inner surface of the heart
  • Subendocardial space is the area beneath the endocardium or between the endocardium and myocardium
  • The subendocardial space is the water-shed area of perfusion and first to become ischaemic
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14
Q

What is the main cause of angina?

A
  • Subendocardial ischaemia due to epicardial coronary artery stenosis and is the main cause of angina
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15
Q

What are the main epicardial coronary branches?

A
  • The main epicardial coronary arteries are the left and right coronary arteries and their branches
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16
Q

What are the 3 main imaging techniques used for coronary artery imaging?

A
  • Main imaging techniques used for coronary artery imaging:
    1) Coronary Angiography
    2) CT
    3) MR imaging
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17
Q

What are 7 risk factors of IHD?

A
  • Risk factors of IHD:
    1) Age
    2) Hypertension
    3) Hypercholesterolaemia
    4) Smoking
    5) Diabetes
    6) Obesity
    7) Physical inactivity
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18
Q

What is hypercholesterolaemia?

How does this affect endothelial function?

Where does LDL accumulate in this condition?

What does this cause?

What happens when Macrophages ingest LDL?

What are these chemotactic for?

What happens to the motility of macrophages?

What does this stimulate the release of?

How do these effect endothelial and smooth muscle cells?

A
  • Hypercholesterolaemia is a form of hyperlipidaemia, where there is too much bad LDL cholesterol in the blood
  • This impairs endothelial function
  • In this condition, LDL cholesterol accumulates in the tunica intima, which causes oxidative modification of LDL
  • When macrophages in the tunica intima ingest oxidised LDL cholesterol via scavenger receptors, they become foam cells
  • These foam cells are very chemotactic for monocytes, which come into the tunica intima and become macrophages
  • Ingesting the LDL cholesterol will inhibit motility in the macrophages
  • This stimulates the release of cytokines, which are cytotoxic to endothelial and smooth muscle cells
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19
Q

What are the 3 roles of macrophages in the development of atherosclerosis?

A
  • Role of macrophages in development of atherosclerosis:
    1) Macrophages engulf oxidised LDL to from Foam cells
    2) They secret various factors, such as Interleukin 1 and Growth factors, which will be chemotactic for more monocytes
    3) Macrophages can form a fatty streak, which is the first grossly visible (to the naked eye) lesion in the development of atherosclerosis
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20
Q

Role of smooth muscles in the development atherosclerosis.

What does the fatty streak mature into?

What 3 steps is this done in?

A
  • The fatty streak matures into fibrofatty atheroma
  • Steps of this process:
    1) The smooth muscle enters the tunica intima, which help in formation of collagen on the surface of fibrous tissue, causing a fibrous cap
    2) In the centre of the atheroma, foam cells will eventually die, the LDL cholesterol will crystalise and will group together in the centre forming a lipid necrotic debris
    3) It is now a full formed fibrofatty atheroma
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21
Q

What is morphology?

What is the morphology of atherosclerosis?

A
  • Morphology is the visual study of anomalies caused by diseases
  • Morphology of atherosclerosis is an atheromatous (fibrofatty, fibro-lipid) Plaque which:
    1) Is patchy and raised white to yellow 0.3-1.5cm
    2) Has a core of lipid
    3) Has a fibrous cap
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22
Q

What are the 6 sites atheromas can occur from most likely to least likely?

A
  • 6 sites atheromas can occur from most likely to least likely:
    1) Abdominal aorta
    2) Coronary arteries
    3) Popliteal arteries
    4) Descending thoracic aorta
    5) Internal carotid arteries
    6) Vessels of the circle of Willis
23
Q

What are 5 complications that can rise due to atheroma?

A
  • 5 complications that can rise due to atheroma:
  • Calcification
  • Rupture or ulceration
  • Haemorrhage
  • Thrombosis
  • Aneurysmal dilation (when the ascending aortic diameter reaches or exceeds 1.5 times the expected normal diameter)
24
Q

Distinguish between stenosis and occlusion of an artery.

A
  • Stenosis is a narrowing of a vessel
  • Occlusion is a complete or partial blockage/closure of a blood vessel
25
Q

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

A
  • Total occlusion of left anterior descending artery compensated for by filling from the collaterals of the Right Coronary Artery
26
Q

What is the main cause of angina?

How does an ECG with angina present differently?

A
  • Subendocardial ischaemia due to epicardial coronary artery stenosis is the main cause of angina
  • ECGs with angina have an ST depression
27
Q

What is ischaemia?

A
  • Ischaemia is Insufficient supply of blood to an organ, usually due to a blocked artery.
28
Q

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

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

A
  • 50% of narrowing of the lumen diameter usually signifies limitation of maximal flow.
  • Length of narrowing can also significantly affect blood flow
29
Q

Do organs auto-regulate blood flow?

How do organs auto-regulate blood flow?

A
  • Organs auto-regulate blood flow independent of innervation/hormonal control, despite the central decision about where we constrict vasculature to modify total peripheral resistance
  • Organs auto-regulate blood flow through Active and reactive hyperaemia
  • 2 intrinsic ways we can maintain safe blood flow when blood pressure increases:
30
Q

What 2 intrinsic ways can we maintain safe blood flow when blood pressure increases?

A

1) Myogenic theory (acute flow auto-regulation)
* Stretch induces vascular depolarisation of smooth muscle due to increase in arterial pressure
* This limits the blood flow that can move through the vessel, preventing damage to the vessels
* This is a myogenic response, where stretch activated Ca2+ channels trigger the process of contraction

2) Metabolic theory (acute flow autoregulation)
* An increase in arterial pressure increases O2 and washes out local factors e.g Breakdown of ATP to ADP and AMP, which can be converted to adenosine in the blood
* High degree of oxygen delivery to smooth muscle is likely to trigger constriction mediated effects in the vasculature, leading to an occlusion of the blood supply downstream, as there is enough oxygen present
* This constriction can reduce flow and protect the vessel walls from being damages

31
Q

How does exercise effect cardiac blood flow and total body oxygen consumption?

A
  • Cardiac blood flow can rise up to five-fold (400 ml/min/100g) during exericse
  • This is to accommodate a 20-fold increase in total body O2 consumption
32
Q

What accounts for most of the increase in cardiac blood flow?

A
  • Vasodilation accounts for most of the increase in cardiac blood flow (Increase in HR where per beat CBF is constant accounts for about 1/3rd of the increase in cardiac blood flow)
33
Q

What is O2 extraction fraction (OEF)?

How does this change during exercise?

A
  • Oxygen extraction fraction (OEF) is defined as the ratio of blood oxygen that a tissue takes from the blood flow to maintain function and morphological integrity
  • During heavy exercise, approximately 70–80% of the oxygen delivered to the active muscles may be extracted.
  • This demonstrates that there is a reserve of oxygen in the blood that can be utilized immediately to meet the needs of the contracting muscles at the onset of exercise.
34
Q

What is coronary flow reserve?

How does degree of stenosis affect coronary flow reserve?

A
  • Coronary flow reserve is the maximum increase in blood flow through the coronary arteries above the normal resting volume (difference between autoregulated flow and flow with maximum vasodilation)
  • Greater stenosis will lead to a decreased coronary flow reserve
35
Q

What are 5 factors that determine myocardial oxygen consumption?

A
  • Factors that determine myocardial oxygen consumption:

1) Mass of tissue
* Ventricular hypertrophy increases mass of tissue

  • Factors which are variable per unit mass of tissue:

2) Tension development
* Higher tension means higher maximum force of contraction through Frank Starling mechanism.
* A stronger maximum force of contraction requires more oxygen

3) Contractility
* A stronger maximum force of contraction requires more oxygen
* Positive inotropes will increase myocardial oxygen consumption

4) HR

  • Factor which is fixed per unit mass of tissue:

5) Basal activity
* heart accounts for 10-20% of oxygen consumption at rest

36
Q

Is coronary flow reserve constant?

How is this linked to variant angina?

A
  • Coronary flow reserve is not constant and may change from time to time (especially for smaller vessels, less than 200 microns)
  • This underpins the cause of variant angina, where coronary artery spasms (vasospasms) can cause supply ischaemia to the heart
37
Q

Does the collateral circulation have fixed or variable coronary reserve?

A
  • Collateral circulation has variable coronary reserve, because they’re small vessels (less than 200 microns)
38
Q

How does the appearance of angina differ between fixed stenosis with variable coronary flow reserve and fixed stenosis with fixed coronary flow reserve?

A
  • If fixed stenosis occurs with fixed coronary flow reserve, the same intensity of exercise will always either cause pain or not
  • If fixed stenosis occurs with variable coronary flow reserve, the same intensity of exercise can sometimes cause angina, and sometimes not
39
Q

What are the 3 different types of treatment options for angina?

What is the aim of each option?

What vessel are used for CABG?

A
  • 3 different types of treatment options for angina and aims of each treatment:

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

2) Percutaneous Coronary Intervention (stents and balloons)
* Improve coronary flow reserve

3) Coronary Artery Bypass Grafting (CABG)
* Improve coronary flow reserve
* For the Right coronary artery (RCA), the saphenous vein is used
* For the Left anterior descending artery (LAD), the left internal mammary artery is used (LIMA)

40
Q

What 4 types of drugs are used to treat angina?

What effect do they each have?

A
  • 4 types of drugs are used to treat angina:

1) Beta Adrenoceptor Blockers (Beta-blockers)
* Reduce Heart Rate and reduces Blood Pressure
* i.e. Reduce work of heart and myocardial oxygen consumption

2) Nitrates (GTN – Glyceryl Trinitrate)
* Venodilation → Reduced LV size → decreased wall tension (Reduces work)
* Small effect on epicardial stenosis
* Arterial Dilator that improves blood supply - Reduces variability of coronary flow

3) Calcium Channel blockers
* Some reduce HR
* Small effect on epicardial dilatation (mixed)
* Arterial dilator that improves blood supply - Reduce variability of coronary flow

4) Ikf Channel Inhibitors (F-type funny Na+ channel inhibitors)
* Selective heart rate reduction by inhibiting channels in SA node
* Example is Ivabradine
* Reduce variability of coronary flow

41
Q

What are the 3 main types of tests/imaging used for investigation of chest pain?

A
  • 3 main tests/imaging used for investigation of chest pain:

1) Test of Inducible ischaemia (the presence of new regional abnormalities in contractile function at peak exercise that were not present at rest)
* Exercise stress test (look for ST depression)
* Dobutamine stress echo (look for reduction in function)
* Myocardial perfusion imaging with either exercise or pharmacological stress
* Cardiac magnetic resonance imaging (cMR)

2) Anatomical assessment
* CT coronary angiography (to confirm angina)
* Invasive angiography

3) Anatomical and functional assessment
* Invasive angiography and fractional flow reserve (FFR) (give adenosine and see if pressure drops)
* FFR measures pressure differences across a coronary artery stenosis to determine the likelihood that the stenosis impedes oxygen delivery to the heart muscle
* cMR scan (cardiovascular Magnetic resonance scan)
* Novel CT scan

42
Q

What are the clinical presentations of MI?

A
  • Clinical presentations of MI:

1) Chest Pain
* Severe
* Crushing radiating to jaw and arm

2) Associated “Autonomic” symptoms (nausea, sweating, terror)

3) Breathlessness

43
Q

What are 6 primary coronary causes of MI?

A
  • 6 primary coronary causes of MI:

1) Plaque rupture –
* Rupture is the disruption of a fibrous cap over a lipid core.
* The overlying thrombus is in continuity with the lipid core

2) Plaque erosion –
* Superficial disruption of a fibromuscular plaque without a core.
* An acute thrombus in direct contact with the intima in an area of denuded endothelium

3) Coronary embolism

4) Coronary artery spasm/drug

5) Coronary anomaly

6) Spontaneous coronary dissection

44
Q

How does coronary occlusion occur from plaque rupture?

A
  • Atherosclerotic plaque ruptures, contents leak out, resulting in platelet aggregation and arterial thrombosis.
  • Platelets express prothrombinase complex leads to more thrombi forming, which can totally occlude a coronary artery
45
Q

What are 5 factors which can modify the presentation of an MI?

A
  • Factors which can modify the presentation of an MI:
    1) Time of day (more common in early mornings and in winter)
    2) Inflammatory activity
    3) Infection (esp. Respiratory)
    4) Elevation of blood pressure (More common with elevations of BP such as extreme exercise)
    5) Catecholamines e.g neurotransmitters
46
Q

What are 3 ways we can classify myocardial infarctions?

A
  • 3 ways we can classify myocardial infarctions:

1) By site of infraction (pathology)
* Full thickness, transmural (occurring across entire surface of heart) - A transmural myocardial infarction refers to a myocardial infarction that involves the full thickness of the myocardium
* Sub endocardial - A subendocardial infarct results in necrosis exclusively involving the innermost aspect of the myocardium.

2) By ECG (clinical)
* ST Elevation myocardial infarction (STEMI) – implies full thickness, transmural MI
* Non-ST elevation myocardial infarction (non- STEMI / NSTEMI) - NSTEMI will include subendocardial infraction but does not exclude transmural infarctions in regions remote from ECG (e.g; back of the heart)

3) By cause
* Type 1-5

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

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

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

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

4) Type 5:
* MI associated with cardiac surgery

47
Q

What are the 2 steps in the diagnosis of MI?

A
  • The steps in the diagnosis of MI:

1) Clinical History with:
* ECG Changes, defining sub-classification of STEMI or NSTEMI

2) Raised cardiomyocyte markers in blood
* Troponin T or I (this is the main one)
* Creatine kinase MB isoform (CKMB)
* Creatine Phosphokinase (CPK)
* AST
* Myoglobin

48
Q

Why are there raised cardiomyocytes markers in the blood in an MI?

A
  • There are raised cardiomyocytes markers in the blood in an MI because the membrane is not working properly, so they have leaked
49
Q

Describe the 3 stages of STEMI management and treatment

A
  • 3 stages of STEMI management and treatment:
    1) Antiplatelet agents
  • Aspirin + Clopidogrel or other anti-platelet

2) Immediate revascularisation
* By Primary PCI (Percutaneous Coronary Intervention) e.g thromblysis - clot dissolving

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

50
Q

What are the immediate (2), early (4), and late (3) complications of STEMI?

A
  • The immediate, early, and late complications of STEMI:

1) Immediate
* Ventricular Arrhythmia and death
* Acute Left Heart Failure

2) Early (day 2 – 7)
* Myocardial Rupture
* Mitral valve insufficiency
* Ventricular Septal defect
* Mural thrombus and embolization

4) Late (more than 7 days)
* LV dilatation and heart failure
* Arrhythmia
* Recurrent myocardial infarction

51
Q

Where is NTSTEMI more common?

Is NSTEMI or STEMI more frequent?

What does NSTEMI imply?

A
  • NSTEMI are more frequent in the elderly
  • STEMI are more common than NSTEMI, but NSTEMI are getting more frequent
  • NSTEMI implies sub-endocardial ischaemia
52
Q

What are 4 causes of NSTEMI?

A
  • 4 causes of NSTEMI:
    1) Threatened STEMI
    2) Small branch occlusion (partially occluded epicardial coronary artery)
    3) Occlusion of well collateralised vessel
    4) Lateral STEMI in territory not well seen by ECG
53
Q

How does STEMI and NSTEMI treatment differ?

What are the 5 steps in treatment NSTEMI?

A
  • NSTEMI treatment same as STEMI, except immediate vascularisation isn’t needed
  • Steps in treatment NSTEMI:

1) Antiplatelet therapy (Aspirin and clopidogrel)

2) Anti-ischaemics (beta blockers and nitrates)

3) Statin drugs

4) ACE inhibitors

5) Coronary angiography and (delayed) revascularisation
* Early if symptoms continue
* Early if Troponin raised
* Risk score (eg GRACE, to assess risk of heart attack)

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