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CVS > 20. Coronary Heart Disease, Myocardial Infarction and Embolism > Flashcards

20. Coronary Heart Disease, Myocardial Infarction and Embolism Flashcards

1
Q

What can Coronary Heart Disease lead to?

A 
• Sudden cardiac death
• Acute coronary syndrome (sudden onset of chest pain)
- acute MI
- unstable angina
• Stable angina pectoris
• Heart failure
• Arrhythmia

(all count as coronary artery disease)

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2
Q

What 2 categories do patients that present with sudden onset chest pain (in the emergency room) fall into?

A
  • Myocardial Infarction

* Progressive (Unstable) Angina

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3
Q

What is the link between myocardial damage, arrhythmia and sudden cardiac death?

A
  • Damage to heart muscle leads to scar tissue formation
  • Substrate for arrhythmia
  • Substrate for sudden cardiac death
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4
Q

Summarise the epidemiology of CVD

A
  • Number 1 cause of death
  • Mortality has decreased
  • 17m deaths per year worldwide
  • 88,000 death per year in the UK
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5
Q

Summarise the epidemiology of Stable Angina

A
  • Incidence increases with age

* 2m cases in the UK

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6
Q

What is PCI (percutaneous coronary intervention)?

A
  • Same as coronary angioplasty

* Widen narrowed/blocked arteries

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7
Q

What type of vessels are epicardial coronary arteries?

A
  • Mainly conductance vessels
  • Elastic arteries
  • Dilate in response to changes in BP
  • Also subject to vasoconstriction/dilation due to the autonomic nervous system
  • Changes in capillary resistance is responsive to myocardial metabolic stimuli
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8
Q

What is the function of the coronary circulation?

A
  • Supply the myocardium
  • Make sure flow remains constant over a wide range of perfusion pressures - autoregulation
  • Make sure coronary blood flow matches myocardial demand
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9
Q

What 2 components are the coronary arteries made up of?

A

Epicardial (large arteries out of the myocardium) and Intramyocardial (small arteries in the myocardium)

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10
Q

What is the difference in resistance between the epicardial and intracardial arteries?

A

Resistance is usually equal

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11
Q

What happens to the resistance in the epicardial component if you have stenosis and how is it compensated for?

A

• Resistance increases
• Compensated to a degree by:
- increase in diameter of intramyocardial resistance vessels
- decreases the resistance in the intramyocardial component to maintain flow

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12
Q

How does the resting coronary blood flow change with increasing stenosis?

A
  • Blood flow generally remains unchanged due to response of intramyocardial arterioles
  • After around 70% stenosis, blood flow decreases rapidly
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13
Q

What is the coronary flow reserve?

A
  • Ability of the coronary circulation to adapt to an increasing demand in the face of an increasing epicardial coronary stenosis
  • Ratio of: resting blood flow : blood flow achieved under maximal stress
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14
Q

Describe a graph of ‘Coronary Flow Reserve’ against ‘Percent Stenosis’ (including the axes)

A
  • CFR decreases at a decreasing rate, with increasing stenosis
  • Coronary Flow Reserve - y axis
  • Percent Stenosis - x axis
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15
Q

How does the threshold of stenosis change under stressful conditions?

A

Resting coronary blood flow drops at 50% instead of 70%

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16
Q

Describe the ischaemic cascade?

A
  • Myocardial oxygen demand increases with a decrease in coronary blood flow
  • Perfusion abnormality => regional diastolic dysfunction => regional systolic dysfunction => ischaemic ECG changes => ANGINA pectoris
  • Worse with increased exercise load
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17
Q

How is angina pectoris felt?

A
  • Tight feeling in the chest

* Diffuses across the jaw, shoulders, back or arms

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18
Q

What provokes angina, and how can it be relieved?

A 
• Provocations 
- physical exertion
- emotional stress
- anxiety
• Relief 
- inorganic nitrate vasodilator (reduces coronary resistance and increases blood flow)
- rest
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19
Q

How is stable CHD investigated?

A
  • Confirm clinical diagnosis - demonstrate myocardial ischaemia
  • Assess risk of future adverse cardiovascular events
  • Tests for coronary artery disease - functional (demonstrate imbalance between supply and demand) & anatomical (show how anatomical severity of narrowing within the artery compromises flow)
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20
Q

Give examples of functional & anatomical tests

A

Functional
• Non-invasive: exercise ECG, stress echo, stress MRI, PET/CT
• Invasive - CFR, pressure wire, iFR

Anatomical
• Non-invasive: CT coronary calcium score, CT coronary angiogram
• Invasive - Coronary angiogram

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21
Q

Which artery is a catheter inserted into to identify stenoses?

A
  • Radial or femoral artery

* Moved along to the left main coronary artery

22
Q

What can be used to determine the degree to which flow is impaired?

A

Computational fluid dynamics

23
Q

Which do non-invasive tests involve giving stressing agents?

A
  • Create situations of increased oxygen demand

* Can be done with iontropic agents or vasodilators as well as exercise

24
Q

How can angina be treated?

A
  • Prevention - education, lifestyle modification, aspirin, statins, ACE inhibitors
  • Reduce myocardial oxygen demand - blockers, metabolic modifiers
  • Improve blood supply - vasodilators e.g. nitrates, revascularisation e.g. stents
25
What medication can be used to: - increase the time in diastole to improve coronary perfusion - decrease the amount of work that the myocardium has to do
* Beta blockers | * ACE inhibitors
26
What is oncosis?
* A form of accidental or passive cell death that is often considered a lethal injury * Mechanism of myocardial death
27
What is a calcific nodule?
* Spikey piece of calcium that sticks out into the lumen * Initation site for the thrombus * Rare
28
What is the difference between a white and red thrombus?
White • platelet rich • common in arterial thrombosis (high pressure/turbulent circulation) • benefit from anti-platelet therapy Red • fibrin rich with trapped erythrocytes • common in venous or low pressure situations (stasis) • benefit from anticoagulant or anti-fibrinolytic therapy
29
What is the effect of coronary stenosis on haemodynamics?
``` • Narrowing - area of high shear - blood accelerates • Energy dissipates - pressure drop • Areas of low and oscillatory shear stress - mediate endothelial dysfunctioning and accelerate atherogenesis ```
30
Where is tissue factor made?
* Cellular constituents of the atherosclerotic plaque * Ischaemic heart muscle * Circulating inflammatory cells - humoral source
31
How is Acute MI determined (following a test)?
Detection of a rise or fall in a biomarker (troponin) with at least one value >99th percentile reference limit and at least one of: • Symptoms suggestive of ischaemia • New or presumed ST-T changes or Left Bundle Branch Block (LBBB) on ECG • Development of pathological Q waves on ECG • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality • Identification of intracoronary thrombus/angiography/autopsy
32
Where is cardiac troponin normally found?
Part of the thin filament of the sarcomere
33
What are the 3 isoforms of troponin and which of those are specific to the cardiac muscle?
* I, T and C | * I and T are highly specific to cardiac muscle
34
When is troponin released from the cell?
Proteolytic cleavage during myocardial ischaemia
35
How long can troponin be detected after a MI?
2 weeks
36
What are the 2 types of Acute Coronary Syndrome?
* ST elevation - complete occlusion of coronary artery * No ST elevation - partial occlusion which embolises distally into the microcirculation => myocardial cell death and troponin elevation
37
Where does the myocardial necrosis zone start during an infarction?
Inner layers of the myocardium
38
Which layer of the heart gets hit first and worst during an infarction?
Subendocardium
39
What is the difference between the subepicardial and intramyocardial pressures?
* Subepicardial < Intramyocardial | * Threatens to increase the difference between supply and demand
40
What does an infarction become when it has spread from the endocardium (through the myocardium) to the epicardium?
Transmural myocardial infarction
41
What percentage of the heart muscle dies if we: • occlude an artery and don't recanalise it • reperfuse a blocked artery (and what are the problems with this)
* Not recanalised - 70% muscle dies * Reperfused - 40% muscle death * Some of the reperfusion causes part of the 40% injury e.g. inflammation and microinfarctions, but this can be reduced using various strategies * Opening an infarction can lead to cardiac arrest
42
What does the remodelling of the left ventricles following MI involve?
``` • Left ventricular dilation - increased wall tension - allows maintenance of CO • Thinning of the scar • Impairment of heart function • Increases the risk of heart failure and arrhythmias ```
43
What does the remodelling of the left ventricles in a non-infarcted myocardium involve?
* Left ventricular hypertrophy and myofilament dysfunction * Altered electromechanical coupling * Myocardial fibrosis * Apoptosis * Inflammation * Abnormal blood flow
44
What are the consequences of adverse Left Ventricular Remodelling?
* Increased systolic & diastolic wall tension * Increased myocardial oxygen demand * Reduced myocyte shortening * Dysynchronous depolarisation * Reduced subendocardial perfusion * Mitral regurgitation * Malignant ventricular arrhythmia => sudden cardiac death
45
How is acute and recurrent thrombosis treated similarly and differently?
• Both treated with - oral antiplatelets (aspirin, thienopyridines etc.) • Acute - IV anticoagulants and antiplatelets, thrombectomy • Reccurent - Factor Xa inhibitors (anticoagulant)
46
How are plaques stabilised (mechanically vs drugs)?
* Mechanical - stent | * Drugs - statins and ACE inhibitors
47
How is Left Ventricular Remodelling treated (non-drug vs drug)?
``` • Non-drug - Cardiac Resynchronisation Therapy (pacemakers or defibrillators) - Progenitor cells • Drugs - Beta blockers - ACE inhibitors - Angiotensin receptor blockers - Aldosterone receptor antagonists (prevents dilation of ventricle => heart failure) ```
48
What is a transient ischaemic attack (TIA)?
* Like a stroke * Symptoms only last a few minutes * No permanent damage
49
How can a deep vein thrombosis be treated?
* Anticoagulation * Fibrinolysis * Thrombectomy
50
What leads to air, fat, amniotic and cholesterol embolisms?
* Air - iatrogenic, decompression sickness, trauma * Fat - trauma * Amniotic - pulmonary vasconstriction, inflammation * Cholesterol - many of microemboli from within plaque, foreign body inflammatory response

CVS (21 decks)

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