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Medicine - Year 2 > The cardiovascular system - Coronary artery disease 1 > Flashcards

The cardiovascular system - Coronary artery disease 1 Flashcards

1
Q

Define the term ‘arteriosclerosis’

A

A generic term reflecting arterial wall thickening and loss of elasticity

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2
Q

Name 5 major consequences of atherosclerosis

A
  • Sudden death
  • MI
  • Stroke
  • Aortic aneurysm
  • Acute ischaemia of the legs and abdominal organs
  • Peripheral vascular disease
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3
Q

List the non-modifiable and modifiable risk factors of atherosclerosis

A

Non-modifiable risk factors
- Increasing age
- Male gender
- Genetic abnormalities
- Family history

Modifiable
- Hyperlipidaemia
- Hypertension
- Cigarette smoking
- Diabetes mellitus
- Inflammation (C-reactive protein)

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4
Q

Describe the pathophysiology of atherosclerosis using the “response to injury” hypothesis

A
  1. Endothelial injury
    - causes increased vascular permeability
    - Causes enhanced leukocyte adhesion/alterred gene expression
    - Causes thrombosis
  2. Accumulation of lipoproteins in the vessel wall
  3. Adhesion of monocytes and platelets
  4. Factors release
    - By activated platelets
  5. Smooth muscle cell proliferation
    - causes extra cellular matrix production
  6. Lipid accumulation
    - extracellularly and within the cells
  7. Atheroma
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5
Q

Describe the flow pattern in straight regions of arteries and regions of arteries that divide or curve sharply

A

In straight regions of arteries blood flow is always in the same direction during the cardiac cycle, known as laminar flow pattern

In regions where arteries divide or curve sharply, flow in these regions is slower and can reverse direction during there cardiac cycle, known as oscillatory flow pattern

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6
Q

Describe how endothelial cells in regions of high, laminar shear are protected from athereosclerosis

A

The endothelial cells have. quiescent, anti-inflammatory phenotype

They are characterised by:
- alignment in the direction flow
- expression of anti-inflammatory genes
- low levels of oxidative cell turn over and permeability

This leads to protection from atherosclerosis

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7
Q

Describe how endothelial cells in regions of disturbed shear are associated with high susceptibility to atherosclerosis

A

Have an activated, pro-inflammatory phenotype

Characterised by poor alignment, high turnover, oxidative stress and expression of inflammatory genes

This is associated with high susceptibility to atherosclerosis

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8
Q

a) What are fatty streaks?

b) Describe the morphology of fatty streaks

A

a) Earliest lesions in atherosclerosis

b) Composed of lipid filled macrophages. Not significantly raised and does not cause flow disturbance

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9
Q

Name the 5 most extensively involved vessels in atherosclerosis in descending order

A
  1. Lower abdominal aorta
  2. Coronary arteries
  3. Popliteal arteries
  4. Internal carotid arteries
  5. The vessels of the circle of willis
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10
Q

Describe the morphology of a typical atherosclerotic lesion (from superficial to deep)

A
  1. Superficial cap - smooth muscle cells and relatively dense collagen
  2. Cellular area beneath and to the side of the cap (shoulder) - macrophages, T cells, smooth muscle cells
  3. Necrotic core deep to the fibres cap - lipid, debris from dead cells, foam cells, fibrin, organised thrombus, and other plasma proteins; the cholesterol crystals “clefts”
  4. Neovascularization - periphery of the lesions show proliferating small blood vessels
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11
Q

Atherosclerotic plaques are susceptible to several clinically important changes. Name 5 of these changes

A
  1. Calcification
  2. Rupture, ulceration, or erosion
  3. Haemorrhage into plaque
  4. Atheroembolism
  5. Aneurysm formation
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12
Q

Damaged area of MI undergoes progressive sequence of morphologic changes. This can be split into two phases, known as the inflammatory phase and the repetitive & proliferative phase. Describe these two phases

A
  1. Inflammatory phase
    - 6-12hours : Myocardial infarction - changes of coagulative necrosis
  • 1-3 days: acute inflammation (elicited by the necrotic muscle fibres)
  • 3 to 7 days : Phagocytosis (Macrophages remove necrotic muscle fibres)
  1. Reparative & proliferative ophase
    - 1-2 weeks: Inflammation resolution, neovascularisation of damaged zone
  • By end of week 6: Scar formation, wound healing
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13
Q

a) What is coronary artery disease?

A

Narrowing of coronary arteries due to atherosclerosis (lipid deposition, inflammation, and thrombosis)

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14
Q

a) List 6 modifiable risk factors of coronary artery disease

b) List 4 non-modifiable risk factors of coronary artery disease

A

a)
- Smoking
- Hypertension
- Increased cholesterol
- Diabetes
- Obesity
- Poor diet
- Physical inactivity

b)

  • Age
  • Gender
  • Family history
  • Ethnicitiy
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15
Q

a) What tool can be used to assess the absolute risk of having an adverse reaction of CVD

b) Where is it commonly used

A

a) QRISK2

b) Primary care

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16
Q

What are the possible differential diagnosis of recurrent chest pain

A

Cardiac
- Angina
- Acute coronary syndrome
- Aortic dissection
- Pericarditis
- Valve disease
- Arrythmias

Respiratory
- Pulmonary embolism
- Pneumothorax
- Haemothroax
- Pneumonia

Gastrointestinal
- Oseophagitis
- Oesophageal spasm
- Peptic ulcer disease
- Reflux (GORD)
- Biliary Colic

Musculoskeletal
- Costochondritis
- Cervical radiculitis
- Rib fracture

Neuro
- Herpes zoster
- Depression/anxiety
- Radiculopathy/Myopathy
- MS

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17
Q

What is stable angina?

A

Angina refers to classic cardiac pain that is felt when there is a reduction in blood flow (ischaemia) through the coronary arteries

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18
Q

Describe the difference between stable and unstable angina

A

Stable angina
- Refers to pain that occurs predictably with physical or emotional exertion and lasts longer than 10 minutes. It should be relieved within minutes of rest or with medication (e.g., GTN spray)

Unstable angina
- Refers to a sudden new onset of angina or a significant, and abrupt , deterioration in engine that he been stable. Typically relates to pain that increases with frequency or pain that is experienced at rest

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19
Q

What is the aetiology of stable angina?

A

Primary related to atherosclerosis

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20
Q

Describe the pathophysiology of stable angina

A

Ischaemia due to a combination of fixed vessel narrowing due to plaque and abnormal vascular tone due to inappropriate vasoconstriction of coronary artery

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21
Q

Describe the presentation of stable angina

A

3 classic features of angina

  1. Retrosternal/central chest pain +/- radiation that may involve both chest sides (L.R), arms, neck, lower jaw, upper abdomen
    - character: pressure, tightness, or heavy weight. Sometimes “burning”. In neck - “choking”. in the lower jaw - “toothache”
    - Last a few minutes
  2. Provoked by physical exertion (especially walking uphill), more easily provoked after heavy meal/cold weather
  3. Rapid relief (2 mins) by rest or with GTN
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22
Q

What symptoms are non-anginal chest pain?

A
  • Continuous or very prolong pain
  • Unrelated to activity
  • Bought on by breathing
  • Associated with dizziness, palpitations, paraesthesia
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23
Q

What features of a chest pain make it concerning?

A
  • Chest pain lass > 10 minutes
  • Chest pain not relieved by two doses of GTN taken 5 minutes apart
  • Significant worsening/deterioration in angina (e.g., increased frequency, severity or occurring at rest)
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24
Q

Describe the 5 grades of angina by the Canadian cardiovascular society

A

Grade I - angina with strenuous activity

Grade II - angina with moderate activity

Grade III - angina with mild exertion

Grade IV - angina at rest

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25
Q

Describe the investigations for stable angina

A

Basic investigations
- Blood tests
- Resting ECG
- Echocardiography

Diagnostic tests
- 1st line: CT coronary angiogram
- 2nd line: functional test e.g., exercise ECG, myocardial perfusion imaging with SPECT, Dobutamine stress echo, stress MRI
- 3rd line: coronary angiogram (invasive)

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26
Q

a) When should you offer anatomical non-invasive testing (e.g.,CT coronary angiography)

b) When should non-invasive function testing be offered (e.g., stress echo)

c) When should you offer anatomical invasive testing (coronary angiography)

A

a)
- Low clinical likelihood of CAD
- No history of CAD

b)
- High clinical likelihood of CAD
- Revascularisation therapy likely needed
- Established CAD

c)
- High clinical likelihood of CAD and symptoms unresponsive to medical therapy
- Typical angina at low activity level and high risk of cardiac event
- Left ventricle dysfunction on ECHO suspected secondary to CAD

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27
Q

What is obstructive cardiovascular disease defined as?

A

≥ 70% stenosis of ≥ 1 coronary artery segment

OR

≥ 50% stenosis in the left main coronary artery

28
Q

Stable angina

a) Conservative management

b) Pharmacological primary ad secondary management

c) Invasive management

A

a)

  • Balanced diet
  • Alcohol reduction
  • Smoking cessation
  • Exercise
  • Weight reduction
  • Glycemic control

b)

PRN control
- All patients offered a short-acting nitrate (e.g., GTN) to relieve episodes of angina

1st line treatment
- beta-blocker (e.g., bisoprolol) or rate-limiting

OR

  • Non-dihydropryidine calcium channel blocker (e.g., verapamil or diltiazem) –> they are contraindicated with beta-blocker
  • if patients cannot tolerate beta-blockers or CCB, then mono therapy with one of the following medications may be offered:
    1. Long-acting nitrate (e.g., isorbide mononitrate)
    2. Ivabradine
    3. Nicorandil
    4. Ranolazine

2nd line treatment
- if symptoms ongoing then combine a beta blocker with a long-acting dihydropyridine CCB e.g., amlodipine/felodipine

3rd line treatment
- added if the patient is symptomatic despite 2 anti-anginal drugs e.g., isorbide mononitrate
- coronary angiography should be arranged unless contraindicated as PCI/CABG may be required
- ACEi for patients with diabetes and HTN should be considered

Secondary management
- Statins, aspiring, +/- beta blockers, +/- ACEi

c) Revascularisation
- Percutaneous coronary intervention (PCI)
- Coronary artery bypass graft (CABG)

29
Q

Describe the process of a percutaneous primary intervention (PCI)

A

A catheter is inserted in the patient’s brachial or femoral artery, feeding that up to the coronary arteries under x-ray guidance (fluoroscopy)

Contrast is injected so that the coronary arteries and any areas of stenosis are highlighted on the x-ray images

The catheter delivers a ballon with a stent

The balloon is inflated, compressing the plaque

The ballon is deflated and withdrawn with the stent in place, holding the artery open

30
Q

Following a stent insertion for ‘stable angina’ what must be offered?

A

Dual-antiplatelet therapy should be offered for a minimum of 6 months

31
Q

What are the indications for a PCI in stable angina?

A
  • Limiting symptoms despite 2 antianginals
  • 1,2,3 vessel or leimyosarcoma (LMS) disease
  • Less complex disease (SYNTAX </= 22)
32
Q

Describe the process of coronary artery bypass graft (CABG)

A

“Surgical disease”
- > 50% stenosis of left main STEM
- > 70% stenos of proximal left anterior descending and circumflex arteries
- Triple-vessel disease (asymptomatic or symptomatic)
- Triple-vessel disease with proximal LAD stenos and poor ventricular function

Especially if:
- left ventricular dysfunction
- Diabetes
- Complex coronary disease (high SYNTAX risk score > 22)

33
Q

a) Suitable coronary artery for PCI vs CABG

b) PCI or CABG in complex disease (SYNTAX > 22)

c) Higher percentage for rrepeat revascularisation at 5 years, PCI or CABG?

A

a)

PCI
- 1,2,3 vessel or LMS disease may be suitable

CABG
- Usually LMS/3VD
- Adjunct to other cardiac surgery (e.g., valve surgery)

b) Less advisable in PCI and preferred option in CABG

c) PCI - 25% and CABG- 13%

34
Q

ACS is classified into one of three conditions according to clinical features, ECG findings and cardiac enzymes (troponin)

Name the 3 conditions and how they are differentiated in terms of: extent of occlusion, ECG findings and troponin

A

STEMI - total occlusion, ST elevation and new LBBB, troponin raised

NSTEMI - Incomplete occlusion, other ischaemic changes (ST depression/T wave inversion), troponin raised

Unstable angina - incomplete occlusion, ther ischaemic changes (ST depression/T wave inversion), troponin normal

35
Q

What is a myocardial infarction?

A

Myocardial necrosis, seen as a rise in troponin with evidence of acute myocardial ischaemia

36
Q

What is myocardial injury? and provide 3 examples

A

Myocardial necrosis, seen as a rise in troponin without evidence of acute myocardial ischaemia e.g., myocarditis, damage following cardioversion/ablation, cytokine/mediated injury

37
Q

There are two types of atherosclerotic plaques: Stable and vulnerable.

Describe the features and and an example of where this would occur in a:

a) Stable plaque

b) Vulnerable plaque

A

a) Thick fibrous cap, small lipid content e.g., Stable angina

b) Thin fibrous cap, large lipid content e.g., ACS

38
Q

Describe the pathophysiology of a STEMI

A

An atherosclerotic plaque ruptures which forms a thrombus. The thrombus causes the complete occlusion of a coronary vessel. This blocks blood flow and so oxygen to the myocardium. This leads to necrosis.

39
Q

Describe the pathophysiology of an unstable angina and NSTEMI and the difference between the two

A

An atherosclerotic plaque ruptures which forms a thrombus. If the thrombus does not fully occlude the coronary vessel, blood supply to the myocardium is not fully compromised and varying levels of ischaemia may occur.

In unstable angina there is no myocardial necrosis and troponin is not raised

In NSTEMI there is a rise in troponin, indicating underlying injury has taken place

40
Q

a) Describe the symptoms of an ACS

b) Describe the signs of an ACS

A

a)
- Retrosternal and centre/left-sided chest pain > 15 mins: central crushing or pressing pain +/- radiation to neck or arm (usually the left) –> sudden onset and severe
- Occurs at rest
- Dyspnoea (Shortness of breath)
- Collapse
- Sweating
- Cause and vomiting
- Palpitations

b)
- Levine’s sign: a clenched fist on the chest
- Pallor
- Diaphoresis (clammy)
- Low-grade pyrexia
- Tachycardia
- Cardiac failure (e.g., pulmonary oedema, hypotension)

41
Q

Describe the difference in clinical features between stable angina ACS

A

Unlike stable angina, ACS:

  • commences at rest
  • Is new in onset and severe
  • Crescendo or worsening in nature
42
Q

Describe the initial investigation for ACS

A

Brief clinical assessment - ABCDE (if acutely unwell) followed by a brief history and examination

ECG - look for ST elevation or new LBBB

Blood tests - FBC, U&Es, glucose, lipid profile, LFTs and serial cardiac troponin (at least 3 hours after pain starts

43
Q

Describe the imaging for ACS and what to look for

A

CXR - may demonstrate signs of heart failure

Echocardiogram - may demonstrate reduce ejection fraction / or valve;ar pathology

CT pulmonary angiography- if PE is suspected or needs to be excluded

CT angiography - if aortic dissection is suspected or needs to be excluded

44
Q

Name the three main features of ischaemia

A
  • ST elevation
  • ST depression
  • T wave inversion
45
Q

What is the ECG criteria for a diagnosis of a STEMI

A
  • ST segment elevation > 2mm in adjacent chest leads
  • ST segment elevation > 1 mm in adjacent limb leads
  • New LBBB with chest pain or suspicion of MI
46
Q

Describe the evolution of A STEMI on ECG split into: normal, acute, hours, days 1-2 days later and weeks later

A

Normal
- no changes

Acute
- ST elevation

Hours
- ST elevation
- Decrease R wave
- Q wave begins

Days 1-2
- T wave inversion
- Q wave deeper

Days later
- ST normalizes
- T wave inverted

Weeks later
- ST & T normal
- Q wave persists

47
Q

Describe the evolution of an unstable angina split into: normal, acute, weeks later

A

Normal

Acute
- T wave inversion or ST depression

Weeks later
- ST & T normal
- no Q waves

48
Q

ST elevation usually occurs alongside Q waves and will occur in the leads that represent a coronary artery vessel territory. For the following area of myocardium give 1. the location of ST elevation and 2. the coronary artery

a) Inferior STEMI

b) Anteroseptal STEMI

c) Lateral

d) Posterior

A
49
Q

ST elevation usually occurs alongside Q waves and will occur in the leads that represent a coronary artery vessel territory. For the following area of myocardium give

  1. the location of ST elevation and
  2. the coronary artery

a) Inferior STEMI

b) Anteroseptal STEMI

c) Lateral

d) Posterior

A

a)
1. II, III, aVF

  1. Right coronary artery (RCA)

b)

  1. V1-V4
    - V1-V2: septal
    - V3-V4 Anterior
  2. V1-V2 = proximal left anterior descending artery (LAD) & V3-V4 = LAD
    Main = LAD

c)
1. V5-V6,I, aVL

  1. V5-V6 = distal LAD/ Lcx/RCA & I,aVL = Lcx
    Main = Left circumflex artery (LCx)

d)
1. V7-V9

  1. RCA/LCx
50
Q

During a STEMI, there are usually reciprocal changes. This refers to ST depression in the leads opposite those with ST elevation. For the following STEMIs, state the reciprocal changes that’ll be seen

a) Anterolateral STEMI

b) Lateral STEMI

c) Inferior STEMI

d) Posterior STEMI

A

a) Inferior ST depression (II, III, aVF)

b) Inferior ST depression (II, III, aVF)

c) Inferior STEMI: lateral ST depression (I, aVL)

d) Anterior ST depression (V1-V3)

51
Q

Describe the role of troponin in a heart attack

A
  • Troponin is released when there is myocardial cell death.
  • This aids in diagnosing ACS
  • It has a high negative predictive value (>95%) and so useful in ruling out ACS in patients with possible NSTEMI/UA
52
Q

Evaluate the results of troponin levels if it is:

a) Low

b) Mildy raised

c) Raised

A

a) No myocardial cells deaths. The patient is not having an MI although they may be experiencing unstable angina

b) This is an equivocal result and may be due to other non-MI related factors. These patients usually need a 6-12 hour repeat test
1. If repeat troponin is raised on the repeat, they are having an MI.
2. If repeat troponin is stable or falling, then they are unlikely to be having an MI.

c) MI confirmed

53
Q

List 8 other causes of troponin elevation

A
  • Tachyarrhythmias
  • Heart failure
  • Hypertensive emergencies
  • Critical illness (e.g., sepsis, burns)
  • Myocarditis
  • Cardiomyopathy (e.g., Takotsubo)
  • Structural heart disease (e.g., aortic stenosis)
  • Pulmonary embolism
  • Renal dysfunction
  • Coronary spasm
  • Acute neurological event
54
Q

Describe the immediate management of a STEMI/NSTEMI/Unstable angina

A

MONA

Morphine - pain, anxiety, or pulmonary oedema

Oxygen - indicated if SpO2 < 94% using a nasal cannula to give low-flow

gtN - sublingual spray, should be avoided if systolic blood pressure < 90mmHg

Aspirin - 300mg PO

Antiplatelet - Clopidogrel 300mg (600mg in pPCI) given in addition to aspirin

Blood glucose control

Early risk stratification - helps to identify those at high risk that may benefit from early revascularisation

Continuous cardiac monitoring

55
Q

Describe the advanced management of a STEMI

A
  1. Primary percutaneous coronary intervention (pPCI) + anti-platelet (initiated on aspirin and a second anti-platelet drug prior to PCI e.g., clopidogrel) + Antithrombotic therapy using UFH/LMWH +/- Glycoprotein IIb/IIIa inhibitors (e.g., tirofiban)
  • Indicated if symptom onset of chest pain is within 12 hours
  • Should occur within 120 minutes of being diagnosed with ST elevation

2.Thrombolysis/fibrinolysis + clopidogrel + Antithrombotic therapy using UFH/LMWH + PCI
- if a pPCI is unable to performed within 120 minutes then thrombolysis/fibrinolysis should considered (e.g., alteplase)
- Coronary angiography +/- PCI should be performed in the following 2-24 hours

56
Q

a) Within what time frame must chest pain occur for a pPCI to take place?

b) What is the time frame of a diagnosis of a STEMI for a pPCI to take place?

A

a) Indicated if symptom onset of chest pain is within 12 hours

b) This should occur within 120 minutes of diagnosis

57
Q

Describe the advanced management of an NSTEMI/UA

A
  1. Risk stratification
    - GRACE (Global Registry of Acute Coronary Events): estimates six-month mortality risk in patients with NSTEMI / UA. Divides patients from lowest (≤1.5%) to highest >9.0%).
    - HEART (History, ECG, Age, Risk factors and Troponin): estimates six-week risk of major cardiac event (AMI, PCI, CABG, death) in patients with NSTEMI / UA.
    - TIMI (Thrombolysis in Myocardial Infarction): estimated 14-day all-cause mortality in patients with NSTEMI / UA.
  2. Pharmacological management
    - Additional anti-platelet agent (e.g., clopidogrel, ticagrelor)
    - Antithrombotic agent (e.g., fondaparinux if no contraindications or UFH if patients are planned for coronary angiography within the next 24hrs)
    - Patients deemed low risk can be initiated on aspirin only (as part of initial management. Patients should be initiated on dual antiplatelet therapy (DAPT) and fondaparinux if: significant delta change in troponin, worsening/recurrent ischaemic pain, deterioration
  3. Invasive coronary angiography - patients very high risk
58
Q

a) Invasive coronary angiography is indicated in patients with a NSTEMI/UA that are very high risk. List 5 types of high risk patients included

b) When must the coronary angiography for patients who are intermediate-to-high risk

A

a)
- Cardiogenic shock
- Pain refractory to medial therapy
- Life-threatening arrhythmia or cardiac arrest
- Mechanical complication (e.g., valve rupture)
- Acute heart failure with refractory angina
- Recurrent dynamic ECG changes (esp. brief ST elevation)

b) Within 96 hours

59
Q

Discuss the long-term management of ACS

A

Lifestyle
- Smoking cessation
- Dietary changes
- Excercise
- Reduce alcohol consumption

Pharmacological - all patients put on first 4
- Dual anti-platelet therapy (normally aspirin 75mg OM and clopidogrel 75g OD)
- Beta-blockers (normally bisoprolol)
- High-dose statin (normally atorvastatin 80mg)
- ACE inhibitor (normally ramipril) / ARB if intolerant to side-effects
- Consider mineralocorticoid antagonist: reserved for patients with LV dysfunction (i.e., heart failure) following MI.

60
Q

Describe the acute management of an ACS

A

MONA

Morphine
Oxygen
GTN
Aspirin

61
Q

List 10 complications of an MI

A
  • Ventricular arrhythmia
  • Recurrent ischaemia/infarction/angina
  • Acute mitral regurgitation
  • Congestive heart failure
  • 2nd, 3rd degree heart block
  • Cardiogenic shock
  • Cardiac tamponade
  • Ventricular septal defects
  • Left ventricular thrombus/aneurysm
  • Left/right ventricular free wall rupture
  • Dressler’s syndrome
  • Acute pericarditis
62
Q

Intraventricular septal rupture is a short-term complication of myocardial infarction. Without reperfusion septal rupture typically occurs within the first week after the infarction

a) What are the clinical features?

b) How is it diagnosed?

c) What is the management?

A

a)

  • Shortness of breath
  • Chest pain
  • Heart failure
  • Hypotension
  • Harsh, loud pan-systolic murmur along the left sternal border
  • Palpable parasternal thrill

b) Diagnosis with echocardiogram

c) Emergency cardiac surgery

63
Q

a) What is Dressler’s syndrome?

b) What are the clinical features

c) What is the management

A

a) Post-infarction pericarditis

b) Persistent fever and pleuritic chest pain 2-3 weeks or up to. a few months after an MI

(Note that patients can get pericarditis immediately following MI which is NOT considered Dressler’s syndrome)

c)
- Symptoms usually resolve after several days
- High dose aspirin given

64
Q

a) What is the biomarker to establish the diagnosis of a reinfarct?

b) What is the one advantage of this over troponin

c) What is indicative of a reinfarct?

A

a) Creatinine kinase (CK-MB)

b) The one advantage of CK-MB over the troponins is the early clearance that helps in the detection of reinfarct. Tropinin levels can be elevated for up to 2 weeks after the initial infarct episode, whilst CK-MB usually clears by 72 hours

c) A CK-MB level of more than 3 times the upper limit of normal is generally considered to be indicative of one

65
Q

What are the two functional components of the circulatory system?

A
  1. Blood vascular system (circulation of blood)
  2. Lymph vascular system (circulation of lymph)

Medicine - Year 2 (27 decks)

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