Coronary heart disease Flashcards

1
Q

What are the 2 main forms thromboembolic diseases?

A
  • Arterial Thrombosis
  • Venous Thrombosis
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2
Q

What are the examples of arterial thrombosis?

A
  • Acute myocardial infarction (AMI)
  • Transient ischaemic attacks (TIAs)
  • Cerebral vascular infarcts/accidents (CVAs)
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3
Q

What are the examples of venous thrombosis?

A
  • Deep vein thrombosis (DVT)
  • Pulmonary embolism (PE)
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4
Q

What is the 3rd group of thromboembolic diseases?

A

Inherited/Acquired thrombosis
- Thrombophilia

This is a series of genetic diseases, so where theres an increased susceptibility to clotting, which can cause both arterial or venous thrombi.

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5
Q

What is arterial thrombosis?

A
  • Occurs as a result of rupture of atherosclerotic plaques
  • It results in platelet deposition and vessel occlusion
  • Often known as “White thrombi”, relating to the colour of its platelet rich core.
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6
Q

What is venous thrombosis

A
  • Often occurs in normal vessels
  • Majority start In the deep vein of the leg
  • Often known as “Red thrombi”, relating to the colour of its platelet rich core.
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7
Q

What is coronary heart disease?

A

Coronary heart disease is a condition in which the vascular supply to the heart is impeded/obstructed by atheroma (fatty plaques formed on the inside of the blood vessel walls), thrombosis or spasm.

  • Ultimately reduction of blood flow to the blood.
  • If the reduction of blood flow is severe enough, it will cause symptoms of ischemia or lack of oxygen secondary to lack of blood supply.
  • Has the potential to damage the cardiac muscle
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8
Q

What are the series of events that happens after inadequate blood supply?

A

Inadequate blood supply causes an inadequate reduction in oxygen supply to the heart. As a consequence the patient will develop ischaemic chest pain. Chest pain the the main symptom of Ischaemic Heart Disease (IHD).

Depending of the extent of that reduction in blood supply, can cause various clinical issues:

  • Stable angina (sometimes called ‘Exercise induced angina’)
  • Acute Coronary Syndrome (ACS) (Includes Myocardial infection, heart attack and unstable angina)
  • Sudden death
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9
Q

What is the main cause of coronary heart disease?

A

The main cause is Atherosclerosis of the coronary artieries.

  • Atherosclerosis is a complex inflammatory process initiated due to ‘injury’ or dysfunction of the endothelium.
  • This then results in increased permeability to oxidised lipoproteins. These oxidised lipoproteins are taken up by macrophages in cell walls which will then produce lipid-laden foam cells.
  • This results in the production of fatty-streaks, which can be seen on the surface of the endothelium under microscopic view.
  • This is then followed by migration and proliferation of smooth muscle cells into the intimate of the blood vessels.
  • These smooth muscles cells secrete fibrous and protein material like collagen, proteoglycans, elastin and glycoproteins.
  • These proteins eventually form a fibrous cap, known as these fatty plaques associated with coronary heart disease.
  • As these plaques develop and enlarge, it results in the narrowing of the blood vessels within the heart and reduction in blood flow.
  • These fatty plaques can then rupture and a clot will form causing complete blockage.
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10
Q

The development of coronary heart disease is influenced by what risk factors?

A

Main risk factors:
- Age (non-modifiable)
- Gender (non-modifiable)
- Family history (non-modifiable)
- Smoking
- Diet
- Obesity
- Hypertension
- Hyperlipideamia

Other risk factors:
- Diabetes Mellitus
- Sedentary lifestyle
- Ethnicity
- Excess Alcohol
- Excess Stress

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11
Q

What is the assessment of CV risk used for?

A
  • For primary prevention
  • Treat if >10% in there next 10 years
  • If already have CVD then assessment not needed, assume high risk and treat
  • CV risk assessment is an online tool called QRISK3
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12
Q

What is the pathophysiology of the underlying disease coronary heart disease?

A
  • The chest pain occurs when theres an imbalance between oxygen demand and supply.
  • The oxygen demand depends on your heart rate, contractility and systolic wall tension/pressure
  • Your oxygen supply depends on your coronary blood flow and oxygen carrying capacity of your blood.
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13
Q

What is stable angina?

A

Plaques of the atherosclerosis fats have build up on the wall of the blood vessels, which causes narrowing of the diameter and hence reduction in blood supply.

In stable angina the narrowing becomes critical at a certain level of demand from the heart.

=> Ischeamic Chest pain typically provoked by exercise, stress, heavy meals or extremes of temperature, where there is excess demand on the heart and the blood supply is not enough to meet that demand.

=> Stable angina will be relived by rest (hence reducing the demand on the heart) or s/l GTN

Often known as exercise induced angina

  • “demand ischaemia”
  • Definition: Narrowed coronary arteries unable to meet increased oxygen demand during exercise, stress etc.
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14
Q

What are the clinical symptoms & diagnosis of stable angina?

A
  • Central crushing chest pain
  • May radiate to jaw, neck, back or arms
  • “Constricting”, “Choking”, “Heavy weight”, or “stabbing”, “burning” or “like a knife”
  • Induced by exercise etc & relieved by rest or GTN
  • Lack of ECG or cardiac enzymes changes
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15
Q

How can you manage symptom control in stable angina?

A

Ischaemic chest pain control

  1. S/L (sublingual) GTN for acute angina
    - Where they’ll place a tablet or spray under the tongue which is used to treat attacks of angina.
  2. Antianginal therapy
    - Used to prevent attacks in the first place
    - 1st line treatment: Beta-blockers, Calcium channel blockers or combination of both
    - 2nd line add-ons include: Long acting nitrate, ivabradine, ranolazine or nicorandil
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16
Q

What can you do as secondary prevention in terms of management in stable angina?

A
  1. Lifestyle changes
    - Smoking
    - Weight loss
    - Diet
    - Exercise
  2. Antiplatelet (aspirin 75mg)
  3. Statins (Atorvastatin 20mg/80mg)
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17
Q

What is Acute Coronary Syndrome?

A

Includes:

  1. Myocardial infarction (MI)
    - ST elevated MI (STEMI)
    - Non-ST elevated MI (NSTEMI)
  2. Unstable Angina (Troponin Positive ACS)
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18
Q

What are the 3 aspects considered in differential diagnosis of acute coronary syndrome?

A
  • History of ischaemic chest pain
  • ECG changes
  • Increased release of cardiac enzymes
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20
Q

What is the first assessment that is done when a patient presents with history of ischaemic chest pain?

A

12 lead ECG
- This may well of already been done at the GP surgery or by the ambulance crew

  • These are placed in different positions to pick up electrical signals from different parts of the heart and this allows identification of what has happened and where in the heart this has occurred.
  • Can result in a diagnosis of myocardial infarction depending on which lead is affected and pinpoint where the myocardial infarction is happening.
20
Q

Name some there causes of increased Troponin levels?

A
  • Pulmonary embolism
  • Heart failure
  • Myocarditis
  • CKD
  • Sepsis
20
Q

What is the main enzymes released when the cardiac muscles are damaged? (cardiac enzymes)

A

Main one is Troponin (Troponin T & Troponin I (Trop I):
- Highly specific

  • Released after 2-4 hrs, peaks at 12 hrs & can persist up to 7 days
  • Measured on admission
  • Standard Troponin assay - repeated 10-12hrs
  • High sensitivity Troponin assays- repeated after 3hrs (enables early rule out of NSTEMI)
  • STEMI/NSTEMI => Increased Troponin >99th percentile cut-off / upper reference limit (varies according to specific assay used)
  • Unstable angina => Some change in Troponin level but does not meet criteria for MI
  • <0.4ng/ml => ACS unlikely
  • Size of increased = size of infarct
20
Q

What are the ECG changes that occur in a STEMI (ST elevated MI)?

A
  • There is an elevation in the ST segment - diagnostic of STEMI

This ST elevation is not seen in NSTEMI and Unstable or stable angina

21
Q

What other cardiac enzymes rise in STEMI/NSTEMI?

A
  1. Creatine Kinase (CK):
    - Peaks within 24hrs
    - Normal within 48hrs
    - Also in skeletal muscle and brain
    - CK-MB- cardiac specific isoform
  2. Aspartate Transaminase (AST) and Lactate dehydrogenase (LDH):
    - Non-specific
    - Released from other parts of body
    - Not used routinely
    - LDH peaks at 3-4 days and remains increased for up to 10 days => can be useful in late presentations
21
Q

How is myocardial infarction and unstable angina linked?

A
  • “Stable ischaemia” (vs “demand ischaemia” of stable angina)
  • Decreased coronary blood flow and decreased oxygen supply due to thrombus formation
  • => Partial blockage (UA) & complete blockage (STEMI/NSTEMI)
  • Thrombus forms as a result of plaque rupture => activation & aggregation of platelets
21
Q

What is myocardial infarction?

A

Thrombosis forms at site of rupture of atheromatous plaque.

  • => Severe & prolonged ischaemia
  • => Death of cardiac muscle cells
    (=> release of enzymes from cells)
  • STEMI => Damage to full thickness of cardiac muscle
  • NSTEMI => Damage to partial thickness of cardiac muscle
22
Q

What are the clinical features of STEMI and NSTEMI?

A
  • Severe chest pain, sudden onset, often at rest and constant
  • 20% of AMI => no symptoms
  • “Silent” MIs - more common in elderly & DM

Additional symptoms:
- Sweating
- Breathlessness
- Nausea & vomiting
- Restless
- Pale
- Grey

23
Q

What are the clinical features of unstable angina?

A
  • Sudden deterioration in angina symptoms
  • Often at rest, not relieved by rest of s/l GTN
24
Q

What can be done for the management of STEMI?

A
  1. Acute/immediate care
    - Pain relief, thrombolysis/ reperfusion & minimisation of infarct size
  2. Management of complications
    - E.g. LVF, arrhythmia
  3. Secondary prevention
    - Drug therapy and lifestyle changes
25
Q

What can be done for the immediate care of STEMI?

A
  1. Oxygen (if indicated)
    - Relieves ischaemia
  2. Diamorphine
    - Pain relief
    - Anxiolytic
    - Vasodilatation
    - + antiemetic (eg. cyclising, metoclopramide)
  3. Aspirin
    - 300mg stat ASAP
  4. Clopidrogel (or Ticagrelor* or Prasugrel**)
    - 300mg stat (or 180mg or 60mg)
26
Q

What are the complications of STEMI?

A
  • Arrhythmias
  • Heart failure
  • Treat if they occur
27
Q

What can be done for the secondary prevention of STEMI?

A

Drug therapy:
1. Antiplatelets (aspirin + clopidogrel/tiacgrelor/prasugrel*)
- Dual anti platelet therapy (DAPT) for 12months then aspirin for life

  1. Beta-blockers (review at 12 months - continue is also heart failure)
  2. ACE inhibitors
  3. Statins - Atorvastatin 80mg OD

Lifestyle changes:
- Smoking
- Weight loss
- Diet
- Exercise

28
Q

What can be done for the management of NSTEMI and Unstable Angina?

A

Give immediate:
- Aspirin
- Diamorphine
- Aspirin
- Clopidrogrel (or Ticagrelor or Prasugrel)

Also
- Fondaparinux => until stable

29
Q

What can be done for the secondary prevention of NSTEMI and Unstable angina?

A

Drug therapy:
1. Antiplatelets (aspirin + clopidogrel/tiacgrelor/prasugrel*)
- Dual anti platelet therapy (DAPT) for 12months then aspirin for life

  1. Beta-blockers (review at 12 months - continue is also heart failure)
  2. ACE inhibitors
  3. Statins - Atorvastatin 80mg OD

Lifestyle changes:
- Smoking
- Weight loss
- Diet
- Exercise

30
Q

What is angiography

A
  • It is a thin radiopaque tube (catheter) introduced into coronary circulation
  • X-Ray contrast material injected into coronary artery via catheter
  • Allows observation of severity of narrowing (stenosis) due to atherosclerotic plaque.
31
Q

What surgical interventions can be done for coronary heart diseases?

A
  1. Percutaneous Coronary Intervention (PCI):
    - Angioplasty
    - Stenting
  2. Coronary Artery By-pass Graft (CABG)
32
Q

What is angioplasty?

A
  • The process of a balloon mounted on tip of very thin catheter inserted through obstruction and inflated
  • Restenosis common (the reduction in the diameter of the vessel lumen after angioplasty)
33
Q

What Is stenting?

A

Wire mesh inserted with balloon to keep stenosis open.

Bare metal stent (BMS) or drug eluting stent (DES)

  • Elutes anti-proliferative drug (E.g. Tacrolimus, Paclitaxel)
  • Stops overgrowth of stent by wall tissue
34
Q

How can angioplasty and stents damage the vessel wall?

A

They both can damage vessel wall by increasing clotting in stent thrombosis.

  • Hence need to be on long term aspirin and 12 months Clopidogrel/Ticagrelor/Prasugrel
35
Q

What is drug eluting balloon?

A
  • Balloon covered with anti-proliferative drug (e.g. Paclitaxel)
  • Released into vessel wall during inflation
  • Very lipophilic hence absorbed into the vessel wall
  • Reduces restenosis
  • No problem of in-stent thrombosis
36
Q

What is Primary Percutaneous Coronary Intervention (PPCI)?

A
  • An alternative treatment for STEMI instead of using thrombolysis
  • Better outcomes and less people contraindicated compared to thrombolysis
  • Patients taken straight to to angio suite for angio then angioplasty (with or without stenting)
  • Clot is removed during the procedure
  • “Call to balloon” time 120min
  • “Door to balloon” time 30min
37
Q

What is coronary artery by-pass grafting (CABG)?

A

Veins grafted to by-pass stenosis in coronary artery.