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LSS Cardiovascular System > 20 Coronary Heart Disease, Angina, MI and Embolism > Flashcards

20 Coronary Heart Disease, Angina, MI and Embolism Flashcards

1
Q

Q: How does coronary artery disease present? (7) Main?

A

A: o Sudden cardiac death ***
o Acute coronary syndrome
– Acute myocardial infarction
– Unstable angina
o Stable angina pectoris (chest pain or discomfort due to coronary heart disease)
o Heart failure
o Arrhythmia (as a result of heart muscle scarring eg heart attack)

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2
Q

Q: Name 4 determinants of risk factors for CHD. Name 4 of the risks can that lead to CHD. What percentage of CHD cases are down to these?

A

A: Tobacco use,
physical inactivity,
harmful use of alcohol,
unhealthy diet

accounts results in:

– Hypertension
– Obesity
– Diabetes mellitus
– Hyperlipdaemia

~80%

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3
Q

Q: CVD is the leading cause of death in? (3) Common CVD?

A

A: -developed and low/medium income countries

  • <70yr
  • women worldwide

CHD

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4
Q

Q: What is Myocardial Ischaemia? 2 broad categories? Describe in terms of coronary arteries. When do they each tend to occur?

A

A: o Mismatch between myocardial oxygen
supply and demand

o Primary reduction in blood flow- eg coronary arteries are blocked
=> occurs in stable angina

o Inability to increase blood flow to match
increased metabolic demand- eg coronary arteries have narrowed
=> tends to occur in those with acute heart attacks

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5
Q

Q: Graphs to show functional anatomy of coronary circulation- pressure changes:

  • aorta to capillaries
  • response to flow dependant dilation
  • response to changes in intravascular pressure
  • response to metabolites
A

A: REFER

X = conductive arteries -> prearterioles -> arterioles

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6
Q

Q: What are the 2 components of coronary arteries? How does the structure of arteries change as they enter the heart? (2) How is resistance divided? (2)

A

A: -epicardial component
-intramyocardial component

The big conduit arteries divide into smaller arterioles and these then divide into the myocardium

Overall coronary resistance is divided 50% in the large arteries and 50% in the smaller arteries and capillaries

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7
Q

Q: What is the role of coronary circulation? (3)

A

A: 1. To make sure that over a wide range of perfusion pressures, flow remains constant - AUTOREGULATION

  1. To make sure that coronary blood flow matches myocardial demand
  2. deliver oxygen and nutrients and remove toxic waste products
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8
Q

Q: What can occur to coronary circulation to change it? (2) 3 examples.

A

A: -arterioles can change
-capillary resistance can change

  • Arterioles dilate in response to changes in blood pressure
  • they are subject to vasoconstriction and vasodilation due to the autonomic nervous system
  • Changes in capillary resistance is responsive to myocardial metabolic stimuli
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9
Q

Q: What are epicardial coronary arteries? dependant on?

A

A: are mainly conductance vessels - dependent on arterial blood pressure

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10
Q

Q: What is the effect of epicardial stenosis on resting coronary resistance? How is this compensated? result?

A

A: (Usually the resistance in the smaller arteries in the myocardium and the larger arteries outside the myocardium is equal)

If you have stenosis in the epicardial compartment - the resistance in the epicardial component INCREASES

This can be compensated to a degree by an increase in the diameter of the intramyocardial resistance vessels - thus decreasing the resistance in the intramyocardial component to maintain flow

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11
Q

Q: Graph to show how coronary blood flow changes with percent stenosis. (2)

A

A: As we increase the stenosis, the resting blood flow remains unchanged because of the response of the intramyocardial arterioles

After around 70% stenosis, the coronary blood flow decreases rapidly

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12
Q

Q: What can trigger a sympathetic stimulus? leads to? (2) result?

A

A: Lots of things can trigger a sympathetic stimulus which leads to an increase in heart rate and blood pressure hence leading to an increase in coronary flow

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13
Q

Q: What is coronary flow reserve? Ability of? Draw a graph showing this against percentage diameter stenosis. What does this graph show?

A

A: ratio of resting blood flow: blood flow achieved under maximal stress

ability of the coronary circulation to adapt to an increasing demand in the face of an increasing epicardial coronary stenosis

  • This ratio is on the y axis on the right : in 3 to 5 range
  • REFER

once reach 50 severity= ability to increase blood flow in face of stenosis reduces => impairment of coronary flow reserve

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14
Q

Q: Draw a graph for percentage stenosis against coronary vasodilator reserve. What does it show? (2) Where does this happen?

A

A: REFER

  • we’re looking at the ability of the coronary circulation to dilate in the face of a narrowing coronary artery
  • you find that the ability to maintain the requisite amount of flow needed under stressful conditions starts to become impaired around 50% stenosis

This is what happens in people with stable coronary disease

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15
Q

Q: How does the stenosis severity threshold differ between changes in resting blood flow and the expression of exertional symptoms?

A

A: threshold at which peak ability to increase flow under high demand situations is at a lower level of stenosis severity than stenosis severity that was required to reduce resting flow = people can present with exertional symptoms at a lower threshold of stenosis severity than that required to reduce resting blood flow

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16
Q

Q: Explain the ischaemic cascade. (7)

A

A: 1. heart in normal condition where blood flow is matched to demand

  1. as stenosis gets more and more severe-> get situations of mismatch
  2. begets impairment of perfusion
  3. heart can’t pump well if perfusion is abnormal/ insufficient
  4. leads primarily to change in diastolic function, relaxation of the heart
  5. when relaxation function is impaired, systolic function (contractile) becomes impaired
  6. after that-> see changes on resting/surface ECG electrocardiogram
  7. last feature patients experience as part of cascade is symptom of angina pectoris
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17
Q

Q: What is the clinical diagnosis of angina pectoris based on? It is? (2) Provoked by? (3) Relieved by?

A

A: Clinical diagnosis based on the constellation of symptoms

It is a tight feeling in the chest which can diffuse across the jaw, shoulders, back or arms

It can be provoked by physical exertion, emotional stress or anxiety

It can be relieved by rest

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18
Q

Q: What does the investigation of stable CAD achieve? (2-1,3) What determines what tests are run?

A

A: stable coronary artery disease

To confirm the clinical diagnosis
-Demonstrate myocardial ischaemia

To assess risk of future adverse cardiovascular events

  • Burden of myocardial ischaemia
  • Anatomic severity of coronary artery disease
  • LV function

choice of test is dependant on clinical probability of CHD

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19
Q

Q: How can the tests for CHD (and CAD) be divided? (2) What does each do? How are they further divided?

A

A: functional and anatomical

Functional - demonstrate that there is an imbalance between supply and demand - look for ischaemia

Anatomical - look at anatomical severity of the narrowing within the artery then make an inference about how it is compromising flow

  • invasive
  • non invasive
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20
Q

Q: CHD tests (stable CAD). How do you view stenoses?
How do you determine the degree to which flow is impaired?
What do non invasive tests involve? (3)
Imaging techniques include? (3)

A

A: A catheter can be inserted into the radial or femoral artery and moved along to the left main coronary artery to identify the stenoses that you see

Computational fluid dynamics can be used to determine the degree to which flow is impaired // radioactive tracers and scans

Non-invasive tests can involve giving stressing agents to create situations of increased oxygen demand
You can give inotropic agents (beta agonists), vasodilators or get the patient to exercise

Imaging techniques include: echocardiography, MRI or nuclear perfusion imaging

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21
Q

Q: What are the 3 treatment strategies for Stable CAD (CHD)?

A

A: o Prevent atherosclerosis progression and risk of
death/MI
o Reduce myocardial oxygen demand
o Improve blood supply

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22
Q

Q: Stable CAD treatment (CHD). How do you prevent atherosclerosis progression and risk of death/MI? (3)

A

A: – Education
– Lifestyle modification
– Aspirin, statins, ACE inhibitors = main drugs

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23
Q

Q: Stable CAD treatment (CHD). How do you reduce myocardial oxygen demand? (3)

A

A: – HR (b blockers, Ca antagonists, If blockers)
– wall stress (ACE inhibitors, Ca antagonists)
– Metabolic modifiers

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24
Q

Q: Stable CAD treatment (CHD). How do you improve blood supply? (2)

A

A: – Vasodilators (nitrates, nicorandil, Ca antagonists)

– Revascularisation (PCI, CABG)

25
Q

Q: What are the clinical features of MI? (4)

A

A: - severe chest discomfort going to throat down to arms

  • abrupt on set
  • occurring at rest
  • often associated with sweating, nausea, vomiting
26
Q

Q: Describe the development of acute MI. (8) Result?

A

A: 1. atherogenic plaque develops

  1. causes obstruction of lumen of coronary artery
  2. development of necrotic core within plaque
  3. fibrous cap over plaque= very thin
  4. various mechanisms can cause it to rupture
  5. when it ruptures it exposes thromobogenic components of plaque to blood
  6. promotes clot formation (process: thrombosis)
  7. thrombus occludes artery and stops blood flow to that part of heart muscle supplied by blocked vessel

= primary reduction in blood flow leading to myocardial infarction

27
Q

Q: What can lead to abnormal inflammation? 2 types.

A

A: abnormalities of vessel wall and abnormal blood flow conditions => leads to abnormal inflammation which can be:
– Systemic
– Local (in plaque)

28
Q

Q: What are the mechanisms underlying MI? Cause? (3) Most common? When can thrombosis occur? (2)

A

A: Myocardial cell death arising from interrupted blood flow to the heart

  • Coronary plaque rupture (most common) 70-80%
  • Coronary plaque erosion
  • Coronary dissection (calcific nodule= sharp point of calcium that can protrude into lumen-> thrombus formation = rare)
  1. Thrombosis can occur even in the absence of plaque rupture
  2. Plaque erosion could be sufficient to cause thrombus formation
29
Q

Q: What are the mechanisms of myocardial death? (2)

A

A: (occlusion not removed)

Oncosis (a form of accidental or passive cell death that is often considered a lethal injury)

Apoptosis

30
Q

Q: What is thrombus formation dependant on? (3) What puts you at increased risk of thrombosis?

A

A: Virchow’s Triad

  • Abnormal vessel wall (endothelial dysfunction,
    inflammation, atherosclerosis)
  • Abnormal blood flow (endothelial dysfunction, turbulent flow at bifurcations and stenoses,
    stasis)
  • Abnormal blood constituents (endothelial
    dysfunction, hypercoagulability, abnormal
    platelet function, altered fibrinolysis, metabolic,
    hormonal factors)

If you have an impaired endothelium then you have increased risk of thrombosis (endothelial dysfunction is common in all 3 factors)

31
Q

Q: What are the 2 thrombosis types? Describe- rich in? common in? benefit from?

A

A: White Thrombus
o Platelet rich
o Common in arterial thrombosis (high pressure/ turbulent circulation)
o Benefit from antiplatelet therapy

Red Thrombus
o Fibrin rich, with trapped erythrocytes
o Common in venous or low pressure situations (stasis)
o Benefit from anticoagulant or antifibrinolytic therapy

32
Q

Q: What are the effects of coronary stenosis on haemodynamics? (3)

A

A: In the narrowing there is an area of high shear where the blood accelerates as you go through the stenosis

The energy dissipates as you go through the stenosis so you end up with a pressure drop

The areas of low and oscillatory shear stress in the areas distal to the high shear are important in mediating endothelial dysfunction and accelerating atherogenesis

33
Q

Q: What is a key factor that triggers the coagulation cascade? Where is it made? (3) What can they lead to?

2 other factors that trigger coagulation cascade? What are they?

A

A: TISSUE FACTOR

  • can be made from the cellular constituents of the atherosclerotic plaque
  • or by the ischaemic heart muscle itself
  • circulating inflammatory cells can also act as a humoural source of tissue factor

Tissue factors triggers a cascade of factor activation leading to coronary thrombosis

Factor 10a and Factor 2a are important molecular targets for number of drugs in management of MI

34
Q

Q: How is MI defined?

A

A: Detection of a rise or fall in a biomarker (TROPONIN) with at least one value >99th percentile reference limit AND at least one of:

  1. Symptoms suggestive of ischaemia
  2. New or presumed new ST-T changes or LBBB on ECG
  3. Development of pathological Q waves on ECG
  4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  5. Identification of intracoronary thrombus or angiography or autopsy
35
Q

Q: What is cardiac troponin? How many isoforms? Which ones are highly specific to cardiac muscle? When is it released? therefore?

A

A: Cardiac troponin (cTn) is part of the thin filament of the sarcomere

There are THREE isoforms: I, T and C

Troponin I and T are highly specific to cardiac muscle

This troponin is released as a result of proteolytic cleavage during myocardial ischaemia

So, troponin I and T can be related to cardiac cell death

36
Q

Q: What happens in terms of troponin levels after the onset of symptoms of MI? How long can troponin be detected after MI?

A

A: After the onset of symptoms, cardiac troponin levels rise and then fall after a period of time

Troponin can be detected for 2 weeks after MI

37
Q

Q: What are the 2 types of acute coronary syndrome? Describe. How are they seen on an ECG? Difference? (2)

A

A: ST ELEVATION ACUTE CORONARY SYNDROME
= complete blockage of a coronary artery due to an occlusive thrombus
-ST elevation

NON ST ELEVATION ACUTE CORONARY SYNDROME
= partial occlusion which embolises distally into the microcirculation resulting in myocardial cell death and troponin elevation
-no ST elevation
-ST depression or changes in the T wave (e.g. inversion) or even a normal ECG

  • those with ST elevation are rushed straight to cardiac catheterisation lab
  • with out- can have medical intervention then taken to cardiac cath lab within 24hrs of presentation
38
Q

Q: How do you treat STEACS? How long does it take? What do you want to achieve?

A

A: Primary Percutaneous Coronary Intervention (PPCI) for ST Elevation Acute Coronary Syndrome (STEACS)

A guide wire is passed through the coronary thrombus and over the wire a balloon is passed and a stent is deployed which allows recanalisation of the vessel

This can be done in 10 mins

You want to get to the blocked vessel as soon as possible

39
Q

Q: What happens when a coronary artery is blocked for too long? Process (2).

A

A: start to get heart death

  1. The myocardial necrosis zone will start at the inner layers of the myocardium
  2. and progress as a wave front to spread through the entire extent of the myocardium if the coronary artery wasn’t quickly recanalised
40
Q

Q: Which part of the heart is most at threat when a coronary artery is blocked? why? Process (4). What does it become?

A

A: The subendocardium is particularly under threat because this is the main work horse of the heart - start with subendocardium infarction if damage is limited to inner layers

  1. The arterial inflow is on the outer surface of the heart and it runs through the myocardium to get to the endocardium
  2. Intramyocardial pressures are GREATER than subepicardial pressures and this threatens to increase the difference between supply and demand
  3. So the subendocardium gets hit worst and first when there is an occlusion
  4. This then spreads and becomes a transmural myocardial infarction (encompasses entire thickness of heart muscle wall)
41
Q

Q: What is reperfusion injury? If the artery is occluded and not recanalised, what happens? What does reperfusing do? How can this be altered?

A

A: The act of opening an artery can be associated with damage to the heart muscle - reperfusion injury

If we occlude an artery and don’t recanalise it, 70% of the heart muscle will die

If we were to reperfuse it, you could reduce the amount of heart muscle death to around 40%

if we use a number of strategies to attenuate this reperfusion injury process, we can reduce the extent of the heart attack even further

42
Q

Q: What can you get post MI? depends on? (2) What does this involve? (3) Accompanied with? (2) What do you want to try and do? How? (2)

A

A: Depending on the size and location of the damage you can get adverse left ventricular remodelling

This remodelling involves an expansion of the heart muscle, thinning of the scar and impairment of heart function (can lead to heart failure)

It is accompanied with an increased risk of heart failure and arrhythmias

You want to try and attenuate this process as much as possible in the management of MI

This can be done by treating people early to reduce the extent of the ischaemic damage and by treating with therapies that intervene with the mechanism of remodelling

43
Q

Q: What are the mechanisms underlying LV remodelling?

A

A: Left Ventricular Dilation

  • INCREASED wall tension
  • Dilation allows maintenance of cardiac output

Non-infarcted myocardium

  • Left ventricular hypertrophy and myofilament dysfunction
  • Altered eletromechanical coupling
  • Myocardial fibrosis
  • Apoptosis
  • Inflammation
44
Q

Q: What are the consequences of adverse LV remodelling?

A

A: o Altered mechanics → pump failure
– Increased systolic wall tension/stress
– Increased diastolic wall tension/stress
– Increased myocardial oxygen demand
– Reduced myocyte shortening
– Dysynchronous depolarization/contraction
– Reduced subendocardial perfusion
– Mitral regurgitation
o Malignant ventricular arrhythmia → sudden
cardiac death

45
Q

Q: How do you manage acute thrombotic risk? (4) Recurrent? (2)

A

A: 1. Oral antiplatelets:
• Aspirin
• Thienopyridines: clopidogrel, prasugrel, ticagrelor
2. IV anticaogulants: UFH, Bivalirudin, LMWH
3. IV antiplatelets: GpIIb/IIIa inhibitors
4. Thrombectomy

ensure doesn't come back
1. Oral antiplatelet drugs
– Aspirin
– Thienopyridines: clopidogrel, prasugrel, ticagrelor
2. Anticoagulants
– Factor Xa inhibitors
46
Q

Q: Hoe do you stabilise the plaque? (3)

A

A: Mechanical
o Stent

Drugs
o Statins (high dose)
o ACE inhibitors
-> partly to reduce inflammation

47
Q

Q: How do you manage LV remodelling? (6)

A

A: Non-Drug
o CRT-P/D
o Progenitor cells

Drugs
o beta blockers
o ACE inhibitors
o Angiotensin receptor blockers
o Aldosterone receptor antagonists

=> prevent dilation of ventricle and development of heart failure

48
Q

Q: What is an embolism? 2 types. Most common?

A

A: An obstruction in a blood vessel due to a thrombus or other foreign matter that gets stuck while travelling
through the bloodstream

o Arterial (thrombus [ACS, TIA, stroke], air, fat, amniotic, foreign body/material)
o Venous (thrombus [DVT, PE])

the one associated with TIA/ stroke

49
Q

Q: What are the 2 types of TIA/stroke? Causes? (3,5)

A

A: A: Embolic:

  • plaque instability in carotid artery (not coronary) -> clot can go off into cerebral circulation
  • Intracardiac where remodelled heart has area of scar -> break off and go to brain
  • intracardiac communication clot from venous side can go across into arterial side and go to brain
Haemorrhagic
- occur as a result of bleeding
– Vascular malformation
– Hypertension
– Tumour
– Iatrogenic (mainly due to usage of blood thinners)
50
Q

Q: How do you treat an embolic TIA/stroke?

A

A: – Fibrinolysis
– Clot extraction
– Antiplatelet drugs
– Modify atherosclerotic risk factors
– Endarterectomy, stent for internal carotid artery stenosis
– Hole closure if it was intracardiac communication

51
Q

Q: How do you treat a haemorrhagic TIA/stroke?

A

A: – Coil/clip aneurysm
– Withdraw pro-haemorrhagic medication
– Control hypertension
(treatment depends on cause)

52
Q

Q: What are the causes of venous thromboembolism?

A

A: – Trauma (associated with immobility)
– Orthopaedic surgery
– Malignancy (associated with increased thrombosis risk)
– Autoimmune disease (associated with increased thrombosis risk)
– Thrombophilia (primary disorders of clotting system)
– Immobility

53
Q

Q: How can venous thromboembolism be diagnosed? Treatment? (3) Why is it important to treat?

A

A: number of clinical scoring mechanisms
Clinical (Wells Score), D-Dimer, Duplex ultrasound, CT, MRI, Venography

Treatment- Anticoagulation, Fibrinolysis, thrombectomy

Important to treat as it can result in lower limb venous hypertension and reduced mobility in legs or even cause pulmonary embolism -> up venous side-> into R side of heart -> lungs -> if it blocks artery in lung= pulmonary embolism

54
Q

Q: Pulmonary Embolism. Symptoms? (5) Diagnosis? (2) Complications? (3) Treatment? (3)

A

A: Dyspnoea, chest pain,

MRI, pulmonary arteriogram

death, shock, pulmonary hypertension

anticoagulation, fibrinolysis, IVC filter

55
Q

Q: What are other forms of embolism? (4)

A

A: air, fat, amniotic fluid, cholesterol

56
Q

Q: What can cause an air embolism? (3) Fat embolism?

A

A:– Iatrogenic: due to hospital treatment eg leaving drip in with no liquid left= get air in
– Decompression sickness = nitrogen bubbles coming out of solution from blood
– Trauma

trauma= if you have a long bone fracture-> bone marrow lipid can embolise

57
Q

Q: What can an amniotic fluid embolism cause?

A

A: Sudden CV collapse: Pulmonary HTN + RV failure -> LV failure

58
Q

Q: What can cause a cholesterol embolism? Worst case? Treatment?

A

A: – Showers of microemboli from within plaque of large calibre artery
– Plaque rupture (spontaneous, traumatic, iatrogenic)

– End-organ damage due to microvascular plugging and inflammation

depends on which organs become effected

LSS Cardiovascular System (17 decks)

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