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LSS 1 - Thorax anatomy, Respiratory and Circulatory system > CVS Lecture 18 - Coronary heart disease (CHD), Angina, Myocardial infarction (MI) and Embolism > Flashcards

CVS Lecture 18 - Coronary heart disease (CHD), Angina, Myocardial infarction (MI) and Embolism Flashcards

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1
Q

How is coronary artery disease presented?

A

Sudden cardiac death, heart failure, arrhythmia, acute coronary syndrome (acute MI and unstable angina)

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2
Q

What happens to patients who present with sudden onset of chest pain?

A

They are classified into 2 groups: Unstable angina or MI

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3
Q

What are the risk factors for CAD?

A

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

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4
Q

What is the problem with risk factors for CAD?

A

Although one risk factor can cause it, if many together, then risk is multiplicative

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5
Q

What happens if you have CAD?

A

Damage of the heart muscle, can lead to HF, scar tissue formation in myocardium > can lead to arrhythmia and then sudden cardiac death

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6
Q

Epidemiology of CVD:

A

No. 1 cause of death worldwide, leading cause of death in women, accounts for 17M deaths per year

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7
Q

How does CHD burden the UK?

A

Commonest cause of premature death, 88,000 deaths/year

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8
Q

MI statistics for UK

A

190,000 MI/year, 33,000 deaths/year - 6% of all deaths in UK, £3.6b/year

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9
Q

Epidemiology of stable angina

A

^ incidence and prevalence, 2M cases in UK, 67,000 PCIs/year, 45K admission to hospital and 65K bed days

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10
Q

What are PCIs?

A

Percutaneous coronary intervention which is the same as a coronary angioplasty which is a catheter moves up the coronary artery and a stent is placed to open that artery

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11
Q

What is myocardial ischemia?

A

Mismatch between oxygen demand and supply in the myocardium

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12
Q

What is MI caused by?

A

A primary reduction in blood flow (blockage) or inability to increase blood flow to match ^ metabolic demand

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13
Q

What are the main roles of epicardial coronary arteries?

A

Conductance vessels which are dependent on arterial blood pressure

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14
Q

How are nutrients and O2 delivered to the myocardium?

A

Big conduit arteries are divided into smaller arterioles, which divide into the myocardium

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15
Q

What happens when BP changes?

A

Arterioles dilate/constrict depending on BP - subject to vasoconstriction/dilation from autonomic nervous system

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16
Q

What causes the changes in capillary resistance?

A

Myocardial metabolic stimuli

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17
Q

What is the job of the coronary circulation?

A

Autoregulation - to make sure that flow remains constant over wide range of perfusion pressures To match coronary blood flow to myocardial demands

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18
Q

What is the usual resistance between arteries and the intramyocardial arterioles/capillaries?

A

Usually they are equal pressure

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19
Q

What happens when the artery is blocked by a atherosclerotic plaque - stenosis?

A

The pressure in the epicardial part is higher than that in the intramyocardial part

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20
Q

What effect can the pressure difference between the intramyocardial and epicardial have?

A

There is a compensation by increasing the diameter of the intramyocardial resistance vessels up to around 70% blockage. As stenosis ^, blood flow remains unchanged because the intramyocardial vessels can’t dilate further, so coronary blood flow decreases rapidly

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21
Q

What is the coronary flow reserve ratio?

A

Resting blood flow: blood flow achieved under maximal stress

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22
Q

What is coronary flow reserve?

A

The ability of the coronary circulation to adapt to increasing demand due to ^ epicardial coronary stenosis

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23
Q

Around what % stenosis is there an impairment of ability to maintain blood flow needed under stressful conditions?

A

50% stenosis

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24
Q

What is flow response equation?

A

Peak stress/normal resting blood flow

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25
What is angina pectoris?
Clinical diagnosis based on symptoms: tight feeling in the chest, jaw, shoulder, arm or back provoked by stress/exertion
26
How can angina pectoris be relieved?
By rest or Inorganic nitrate vasodilator (reduces coronary resistance and ^ blood flow, reversing the supply/demand imbalance)
27
How do you confirm stable CHD diagnosis?
Determine myocardial ischemia
28
How do you assess future adverse cardiovascular events risk?
The burden of MI, autonomic severity of CAD, Left ventrical function
29
What are the functional tests for CAD?
Demonstrate imbalance between supply and demand
30
What are the anatomical tests for CAD?
Look at severity of narrowing of the artery and make inference about how flow is compromised
31
What are the functional tests for CHD? \*anything after means exposure to ionising radiation
Non-invasive: Exercise ECG, Stress echo, Stress cardiac MRI, \*CT, Stress nuclear MPS, FFRct Invasive: \*CFR, FFR (pressure wire), iFR, IVUS, OCT
32
What are the anatomical tests for CHD (everything uses ionising radiation)?
Non-invasive: CT of coronary Ca store OR coronary angiogram Invasive: Coronary angiogram
33
What can anatomical tests be used for?
To see if there are any narrowings in the artery - catheter inserted into radial/femoral artery and used to identify the stenosis
34
What can computational fluid dynamics be use for?
To determine the extent to which flow is impaired
35
What stressing agents can be used in the non-invasive methods?
Beta antagonists (inotropic agents), vasodilators, or patient exercises
36
What imaging techniques can be used to diagnose CHD?
MRI, echocardiography, nuclear perfusion imaging
37
What are the treatment strategies for preventing atherosclerosis progression and risk of death/MI?
Educating the public, lifestyle modifications and medications: aspirin, statins and ACE inhibitors
38
What are the treatment strategies for reducing myocardial oxygen demand?
Reducing heart rate using beta blockers, Ca antagonists; reducing wall stress (ACE inhibitors, Ca antagonists); metabolic modifiers
39
How can you improve symptoms (CHD) so chest discomfort doesn't develop?
Attend to mismatch in supply and demand by DECREASING HEART RATE
40
How can you decrease heart rate to improve symptoms of CHD?
^ time spent in diastole, improving cardiac perfusion (beta blockers), decrease work that myocardium has to do (ACE inhibitors), improve coronary blood supply (vasodilators/relieve coronary obstruction)
41
How does acute coronary syndromes occur - 3 steps?
Inflammation (systemic/local), plaque rupture/erosion and thrombosis
42
What are the mechanisms of how heart cells die from interrupted blood flow?
Coronary: plaque rupture, plaque erosion or dissection
43
What are the mechanisms of myocardial death?
Oncosis (passive cell death often considered a lethal injury) or apoptosis
44
What is the main cause of acute coronary syndrome?
Plaque rupture
45
What is Virchow's Triad?
Abnormal vessel wall, abnormal blood flow, abnormal blood constituents - with endothelial dysfunction causing all 3
46
What are the types of thrombus?
White - mainly in acute myocardial infarction, Red - DVT
47
What is a white thrombus?
Platelet rich, common in arterial thrombosis with high pressure and turbulent circulation
48
What does a white thrombus benefit from?
Anti-platelet therapy
49
What is a red thrombus?
Fibrin rich with TRAPPED RBC, common in venous/low pressure situations/stasis
50
What does a red thrombus benefit from?
Anti-coagulation/anti-fibrinolytic therapy
51
What is the effect of coronary stenosis on haemodynamics?
Area of high shear before stenosis and low/oscillatory shear stress in distal areas
52
Why are the areas of low/oscillatory shear stress important in areas distal to high shear?
They help mediate endothelial dysfunction and accelerate endothelial dysfunction
53
Why is tissue factor important?
Key factor triggering coagulation cascade, produced from cell parts of atherosclerotic plaque/ischemic heart muscle/circulating inflammatory cells (humoural source)
54
What is the universal definition of acute MI?
Detection of a rise/fall in a biomarker (troponin) with at least one value \>99th percentile limit AND at least one of: symptoms, new/presumed new ST-T changes/LBBB on ECG, development of Q waves, imaging evidence of new loss of viable myocardium, intracoronary thrombus/angiography/autopsy
55
What diagnostic test is used for acute MI?
Troponin test - accurate enough to detect 1hr after infarction BUT insufficient to diagnose as need symptoms
56
What is the troponin test? How does it work?
Troponin exists in 3 isoforms I, T, C w/I, T being specific to cardiac muscle and it's released due to proteolytic cleavage during MI, so detection is synonymous with cell death
57
What types of Acute Coronary syndrome are there?
1) ST elevation - complete occlusion of coronary artery due to thrombus 2)No ST elevation - partial occlusion, embolising distally into microcirculation resulting in myocardial cell death and troponin elevation
58
How can no ST elevation present?
As ST depression or T wave inversion or even normal ECG
59
How do we treat ST elevation acute coronary syndrome?
Primary percutaneous coronary intervention: Guide wire passed through occlusion (thrombus) and a balloon is passed, a stent deployed allowing recanalisation of the vessel
60
How does an infarct develop?
The necrosis zone develops from the innermost layers - subendocardium which is where most work of the heart occurs - and then moves outwards, becoming a transmural myocardial infarction
61
What is a reperfusion injury?
The act of opening an artery causing damage to the heart - however not reperfusing can cause 70% heart muscle death, whereas reperfusion can cause
62
What is Post-MI remodelling?
When an infarct occurs, adverse LVentricular remodelling can occur - expansion of heart muscle, thinning of scar and impairment of heart function
63
How do you prevent/treat post MI remodelling?
Treating people early, reducing the extent of ischemic damage and by treating with therapies that intervene with remodelling
64
What are the mechanisms underlying LV remodelling?
Infarct causes thinning, elongation and expansion - dilation due to ^ wall tension and to maintain cardiac output
65
Why does LV remodelling occur in non-infarcted myocardium?
LV hypertophy, myofilament dysfunction, altered electromechanical coupling, myocardial fibrosis, apoptosis, inflammation
66
What are 3 consequences of adverse LV remodelling?
^: systolic wall tension/stress, MVO2, diastolic wall tension/stress; decreased: myocyte shortening, subendocardial perfusion; dysynchronous depolarisation/contraction; mitral regurgitation; ventricular arrhythmia/fibrillation
67
How can you manage thrombotic burden/risk of acute?
Thrombectomy, drugs (oral/IV anti-platelets, SC/IV anticoagulants
68
How can you manage the thrombotic burden/risk of recurrent?
Oral antiplatelet drugs, anticoagulants
69
How do you stabilise a plaque?
Stent (mechanical), Statins/ACE inhibitors (drugs)
70
How do you manage LV remodelling?
Cardiac resynchronisation therapy (defibs, pacemakers), progenitor cells OR beta-blockers, ACE inhibitors, Ang receptor blockers, Aldosterone receptor antagonists
71
Whais an embolus?
Obstruction in a vessel due to throbus/other foreign material stuck in vessel
72
What kind of embolic ICA/strokes are there?
ICA plaque rupture, intracardiac communication
73
What are the treatments for embolic ICA/stroke?
Fibrinolysis, clot extraction, antiplatelet drugs, stent
74
What kind of haemorrhagic ICA/stroke?
Vascular malformation, hypertension tumour, iatrogenic
75
What are the treatments for haemorrhagic ICA/stroke?
Coli/clip aneurysm, withdraw pro-haemorrhagic medication, control hypertension
76
What are the types of venous thromboembolisms?
DVT (compli: PE, post-thrombotic syndrome, venous ulcer, preve/treat: anti-coagulants) and pulmonary embolism (compl: death, shock, pulm hypertension, RV failure, treat: anticoagulants, fibrinolysis)
77
What other kinds of embolisms exist?
Air embolism (iatrogenic), fat embolism (trauma), amniotic fluid embolism, cholesterol embolism (plaque rupture)
78
What are the determinants of myocardial O2 demand?
Heart rate, BP, myocardial wall tension
79
What is the recognised mechanism of coronary plaque instability in acute coronary syndrome?
Plaque erosion and rupture

LSS 1 - Thorax anatomy, Respiratory and Circulatory system (27 decks)

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