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

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

Flashcards in CVS Lecture 18 - Coronary heart disease (CHD), Angina, Myocardial infarction (MI) and Embolism Deck (79)
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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)

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

3
Q

What are the risk factors for CAD?

A

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

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

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

6
Q

Epidemiology of CVD:

A

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

7
Q

How does CHD burden the UK?

A

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

8
Q

MI statistics for UK

A

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

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

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

11
Q

What is myocardial ischemia?

A

Mismatch between oxygen demand and supply in the myocardium

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

13
Q

What are the main roles of epicardial coronary arteries?

A

Conductance vessels which are dependent on arterial blood pressure

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

15
Q

What happens when BP changes?

A

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

16
Q

What causes the changes in capillary resistance?

A

Myocardial metabolic stimuli

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

18
Q

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

A

Usually they are equal pressure

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

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

21
Q

What is the coronary flow reserve ratio?

A

Resting blood flow: blood flow achieved under maximal stress

22
Q

What is coronary flow reserve?

A

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

23
Q

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

A

50% stenosis

24
Q

What is flow response equation?

A

Peak stress/normal resting blood flow

25
Q

What is angina pectoris?

A

Clinical diagnosis based on symptoms: tight feeling in the chest, jaw, shoulder, arm or back provoked by stress/exertion

26
Q

How can angina pectoris be relieved?

A

By rest or Inorganic nitrate vasodilator (reduces coronary resistance and ^ blood flow, reversing the supply/demand imbalance)

27
Q

How do you confirm stable CHD diagnosis?

A

Determine myocardial ischemia

28
Q

How do you assess future adverse cardiovascular events risk?

A

The burden of MI, autonomic severity of CAD, Left ventrical function

29
Q

What are the functional tests for CAD?

A

Demonstrate imbalance between supply and demand

30
Q

What are the anatomical tests for CAD?

A

Look at severity of narrowing of the artery and make inference about how flow is compromised

31
Q

What are the functional tests for CHD? *anything after means exposure to ionising radiation

A

Non-invasive: Exercise ECG, Stress echo, Stress cardiac MRI, *CT, Stress nuclear MPS, FFRct Invasive: *CFR, FFR (pressure wire), iFR, IVUS, OCT

32
Q

What are the anatomical tests for CHD (everything uses ionising radiation)?

A

Non-invasive: CT of coronary Ca store OR coronary angiogram Invasive: Coronary angiogram

33
Q

What can anatomical tests be used for?

A

To see if there are any narrowings in the artery - catheter inserted into radial/femoral artery and used to identify the stenosis

34
Q

What can computational fluid dynamics be use for?

A

To determine the extent to which flow is impaired

35
Q

What stressing agents can be used in the non-invasive methods?

A

Beta antagonists (inotropic agents), vasodilators, or patient exercises

36
Q

What imaging techniques can be used to diagnose CHD?

A

MRI, echocardiography, nuclear perfusion imaging

37
Q

What are the treatment strategies for preventing atherosclerosis progression and risk of death/MI?

A

Educating the public, lifestyle modifications and medications: aspirin, statins and ACE inhibitors

38
Q

What are the treatment strategies for reducing myocardial oxygen demand?

A

Reducing heart rate using beta blockers, Ca antagonists; reducing wall stress (ACE inhibitors, Ca antagonists); metabolic modifiers

39
Q

How can you improve symptoms (CHD) so chest discomfort doesn’t develop?

A

Attend to mismatch in supply and demand by DECREASING HEART RATE

40
Q

How can you decrease heart rate to improve symptoms of CHD?

A

^ 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
Q

How does acute coronary syndromes occur - 3 steps?

A

Inflammation (systemic/local), plaque rupture/erosion and thrombosis

42
Q

What are the mechanisms of how heart cells die from interrupted blood flow?

A

Coronary: plaque rupture, plaque erosion or dissection

43
Q

What are the mechanisms of myocardial death?

A

Oncosis (passive cell death often considered a lethal injury) or apoptosis

44
Q

What is the main cause of acute coronary syndrome?

A

Plaque rupture

45
Q

What is Virchow’s Triad?

A

Abnormal vessel wall, abnormal blood flow, abnormal blood constituents - with endothelial dysfunction causing all 3

46
Q

What are the types of thrombus?

A

White - mainly in acute myocardial infarction, Red - DVT

47
Q

What is a white thrombus?

A

Platelet rich, common in arterial thrombosis with high pressure and turbulent circulation

48
Q

What does a white thrombus benefit from?

A

Anti-platelet therapy

49
Q

What is a red thrombus?

A

Fibrin rich with TRAPPED RBC, common in venous/low pressure situations/stasis

50
Q

What does a red thrombus benefit from?

A

Anti-coagulation/anti-fibrinolytic therapy

51
Q

What is the effect of coronary stenosis on haemodynamics?

A

Area of high shear before stenosis and low/oscillatory shear stress in distal areas

52
Q

Why are the areas of low/oscillatory shear stress important in areas distal to high shear?

A

They help mediate endothelial dysfunction and accelerate endothelial dysfunction

53
Q

Why is tissue factor important?

A

Key factor triggering coagulation cascade, produced from cell parts of atherosclerotic plaque/ischemic heart muscle/circulating inflammatory cells (humoural source)

54
Q

What is the universal definition of acute MI?

A

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
Q

What diagnostic test is used for acute MI?

A

Troponin test - accurate enough to detect 1hr after infarction BUT insufficient to diagnose as need symptoms

56
Q

What is the troponin test? How does it work?

A

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
Q

What types of Acute Coronary syndrome are there?

A

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
Q

How can no ST elevation present?

A

As ST depression or T wave inversion or even normal ECG

59
Q

How do we treat ST elevation acute coronary syndrome?

A

Primary percutaneous coronary intervention: Guide wire passed through occlusion (thrombus) and a balloon is passed, a stent deployed allowing recanalisation of the vessel

60
Q

How does an infarct develop?

A

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
Q

What is a reperfusion injury?

A

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
Q

What is Post-MI remodelling?

A

When an infarct occurs, adverse LVentricular remodelling can occur - expansion of heart muscle, thinning of scar and impairment of heart function

63
Q

How do you prevent/treat post MI remodelling?

A

Treating people early, reducing the extent of ischemic damage and by treating with therapies that intervene with remodelling

64
Q

What are the mechanisms underlying LV remodelling?

A

Infarct causes thinning, elongation and expansion - dilation due to ^ wall tension and to maintain cardiac output

65
Q

Why does LV remodelling occur in non-infarcted myocardium?

A

LV hypertophy, myofilament dysfunction, altered electromechanical coupling, myocardial fibrosis, apoptosis, inflammation

66
Q

What are 3 consequences of adverse LV remodelling?

A

^: systolic wall tension/stress, MVO2, diastolic wall tension/stress; decreased: myocyte shortening, subendocardial perfusion; dysynchronous depolarisation/contraction; mitral regurgitation; ventricular arrhythmia/fibrillation

67
Q

How can you manage thrombotic burden/risk of acute?

A

Thrombectomy, drugs (oral/IV anti-platelets, SC/IV anticoagulants

68
Q

How can you manage the thrombotic burden/risk of recurrent?

A

Oral antiplatelet drugs, anticoagulants

69
Q

How do you stabilise a plaque?

A

Stent (mechanical), Statins/ACE inhibitors (drugs)

70
Q

How do you manage LV remodelling?

A

Cardiac resynchronisation therapy (defibs, pacemakers), progenitor cells OR beta-blockers, ACE inhibitors, Ang receptor blockers, Aldosterone receptor antagonists

71
Q

Whais an embolus?

A

Obstruction in a vessel due to throbus/other foreign material stuck in vessel

72
Q

What kind of embolic ICA/strokes are there?

A

ICA plaque rupture, intracardiac communication

73
Q

What are the treatments for embolic ICA/stroke?

A

Fibrinolysis, clot extraction, antiplatelet drugs, stent

74
Q

What kind of haemorrhagic ICA/stroke?

A

Vascular malformation, hypertension tumour, iatrogenic

75
Q

What are the treatments for haemorrhagic ICA/stroke?

A

Coli/clip aneurysm, withdraw pro-haemorrhagic medication, control hypertension

76
Q

What are the types of venous thromboembolisms?

A

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
Q

What other kinds of embolisms exist?

A

Air embolism (iatrogenic), fat embolism (trauma), amniotic fluid embolism, cholesterol embolism (plaque rupture)

78
Q

What are the determinants of myocardial O2 demand?

A

Heart rate, BP, myocardial wall tension

79
Q

What is the recognised mechanism of coronary plaque instability in acute coronary syndrome?

A

Plaque erosion and rupture

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