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Personalised Medicine - Cardiovascular > L11 - Ischaemic Heart Disease > Flashcards

L11 - Ischaemic Heart Disease Flashcards

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1
Q

What is the path-biology of IHD?

A

Disease of coronary arteries that progresses gradually culminating in heart attack, heart failure and dysrhythmia

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2
Q

When does IHD occur?

A

Occurs when a fatty/fibrotic plaque (atherosclerosis) blocks the coronary artery
Blood flow to tissues is restricted –> less nutrients to tissue –> ischaemia
Oxygen demand of the myocardium exceeds supply

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3
Q

What does IHD present itself as?

A

Chest pain (angina)

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4
Q

What potentially causes angina?

A

Release of K+, H+ and adenosine can sensitise or stimulate nociceptors
Typically central in the chest and can radiate to arms neck and jaw

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5
Q

How many cases of IHD are they a year in the UK?

A

21,000

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6
Q

What is the prevalence of IHD in the UK?

A

> 55yrs
12% men
5% for women

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7
Q

Death rates from IHD have halved in the last 10 years mainly due to efforts to reduce which two types of risk factors?

A

Non-modifiable

Modifiable

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8
Q

What are non-modifiable risk factors?

A

Advanced age
Male
Personal history of ischaemic heart disease
Positive family history of heart disease

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9
Q

What are modifiable risk factors?

A 
High BP 
Diabetes/obesity 
Smoking 
High cholesterol 
Poor diet
Chronic kidney disease
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10
Q

What are the 3 acute coronary syndromes IHD patients are susceptible to?

A

Unstable angina
NSTEMI - non ST elevation
STEMI - ST elevation

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11
Q

What is unstable angina?

A

Pre MI condition

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12
Q

What is NSTEMI?

A

Type of MI

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13
Q

What is STEMI?

A

Caused by a complete blockage of one of the main coronary arteries

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14
Q

When do the acute coronary syndromes present themselves in IHD patients?

A

Syndrome presents when the plaque ruptures –> platelet clots and blockage of coronary artery –> ACS –> ischaemia

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15
Q

What is the prevalence of ACS?

A
  1. 6% in 35-74

2. 3% in age >74

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16
Q

How many new causes of ACS are there a year in the UK?

A

233,600

75% of these are NSTEMI or unstable angina

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17
Q

How many people does STEMI affect in the UK a year?

A

5 in 1000

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18
Q

Is the prevalence of STEMI or NSTEMi rising?

A

NSTEMI

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19
Q

What is angina characterised by?

A

Characterised by heavy or central crushing pain on exertion

Relieved by rest

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20
Q

What are the two types of angina?

A

Stable - if pain occurs under exertion

Unstable - if pain with little exertion

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21
Q

How do you treat stable angina?

A 
Reduce cardiac work
- Nitrates
- Ca antagonists
Treat the underlying condition
- Statin 
Prophylaxis	
- An anti-platelet drug like aspirin
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22
Q

How do you treat unstable angina?

A

Treat as for a heart attack using DAPT and nitrates

- Dual anti-platelet therapy

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23
Q

What 3 things do you look at to help distinguish between different acute coronary syndromes?

A

If glycerol trinitrates give relief
If ECG trace is normal
If troponin concentration increases

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24
Q

What is troponin?

A

A cardiac muscle specific protein

Released when myocytes in ventricles die

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25
Which form of angina is an acute coronary syndrome?
Unstable angina - can progress to STEMI and NSTEMI | Stable is different in terms of pathology, risk and treatment
26
Which forms of ACS give GTN relief?
Stable angina | Unstable angina
27
Which forms of ACS have a normal ECG?
Stable angina | Unstable angina
28
In which forms of ACS are troponin concentrations raised?
NSTEMI | STEMI
29
What is the main treatment for ischaemia?
Restore blood flow – and quickly
30
Why do you need to restore blood flow so quickly in ischaemia?
Need treatments within 2 hours of chest pain | If blood flow is not restored --> necrosis of the heart muscle --> myocardial infarction --> can lead to heart failure
31
What are the 4 aims of ischaemia treatment?
``` Reopen blocked arteries - Done by cardiologist – use a stent Reduce the coagulability of blood - Anti-platelts, heparins, aspirin Control risk factors - Statins Reduce myocardial oxygen demand ```
32
What are the two ways you can restore blood flow in ischaemia?
Nitrates | PCI - for patients with uncontrolled angina
33
What is PCI?
Percutaneous Coronary Intervention
34
How does PCI work?
Non-surgical technique - aim to widen the artery using dilation from within Insertion of metallic stent via brachial or radial artery into heart - Track a catheter under fluoroscopic guidance into the coronaries
35
What drugs are stents coated in?
Popular drugs inhibit cell re-growth e.g. rapamycin or taxol | Rapamycin – inhibits cells in G1/S
36
What is the door balloon time for STEMI?
2 hours
37
How does stenting work?
Underneath the stent is a balloon which is inflated – 8 atmospheres - Helps keep the stent up against the vessel wall Then remove balloon leaving behind stent
38
What treatments do patients have after stenting?
DAPT
39
What is DAPT therapy?
Aspirin plus an anti-platelet or anti-clotting drug | E.g. PLAVIX (clopidogrel) or Brilinta (ticagrelor)
40
What are the adverse effects of DAPT?
Must be continued for up to a year after stenting | Excess bleeding
41
What are the benefits of DAPT?
Stent doesn’t block | Positive effects upon neutrophils and therefore reduction in pulmonary infections
42
What is the main aim of pharmacological treatments of IHD?
To keep the coronary plaques as stable as possible to avoid an acute clot blockage (occlusion) which can be partial or full and to reduce pain
43
What are the symptomatic pharmacological treatments for IHD?
``` Reduce strain on the heart Increase vasodilation of arteries and veins Nitrates - Glyceryl trinitrate (short acting) - Isosorbide mononitrate (long acting) Aspirin and antiplatelet drugs Ca channel blockers e.g. amlodipine K channel activators e.g. Nicorandil Analgesia e.g. morphine ```
44
What are the prognostic pharmacological treatments for IHD?
Aspirin Statins/PCSK9 inhibitors Beta blockers oACE inhibitor Anti-inflammation approaches are being developed - Inhibit IL-1 – can use microtubule inhibitor
45
How are nitrates administered?
First line agent - GTN as a short acting spray given sublingually
46
What are the primary effects of nitrates?
Relax smooth muscle and veins --> reduces central venous pressure --> reduces preload --> reduces cardiac work Mainly impacts larger muscular arteries --> coronary vasodilation --> increases coronary flow
47
What are the secondary effects of nitrates?
Reduces cardiac work Redirection of flow towards ischemic areas of heart muscle - Evidence from animals that GTN diverts blood from normal to ischemic areas through dilatation of collaterals in the heart Improves coronary artery spasm
48
What is the mechanism of action of nitrates?
GTN metabolism releases NO NO --> guanylyl cyclase --> GTP converted to cGMP --> PKG --> relaxation of smooth muscle via dephosphorylation of myosin chains and sequestration of intracellular Ca
49
What are the adverse effects of nitrates?
Possible hypotension - administer sitting down Headaches Tolerance - possibly because of depletion of –SH groups - More common with longer acting agents
50
What is GTN inactivated by?
Hepatic/liver metabolism
51
How long do nitrates take to act?
Sublingual delivery effective in 1-2 minutes - Conversion from TN to di and mononitrates in minutes - Length of effect 30 min - Transdermal patches or lung acting forms also available
52
What do nitrates reduce?
Ishaemia - not mortality
53
What is the mechanism of action of Ca channel blockers?
Block receptor response --> prevent channel opening --> prevent influx of calcium This non-selectively blocks the contraction of smooth muscle Dilate coronary vessels
54
What 3 types of drugs act on L-type Ca channels?
Phenylalkylamines (e.g.verapamil) Dihydropyridines (e.g. amlodipine) Benzothiazepines (e.g. diltiazem)
55
Where does verapamil act?
More active on the heart
56
Where does nifedipine act?
On smooth muscle
57
What are the side effects of Ca channel blockers?
Flushing and headache due to vasodilator action | Verapamil - constipation due to effects on gastrointestinal nerves or smooth muscle
58
What does aspirin reduce?
Reduces mortality and risk of a future heart attack
59
When/how is Aspirin administered?
Given immediately on presentation and daily thereafter 75mg/day suppresses platelet function Given orally
60
What is the mechanism of action of aspirin?
Inhibits COX-1 receptor on platelets --> irreversibly acetylates COX enzymes --> prevents conversion of arachadonic acid to thromboxane A2  reduces platelet aggregation Effects last for the lifetime of the platelet - 10 days - Platelets do not have a nucleus so cannot replace enzymes - Have to be made in bone marrow
61
Where is aspirin hydrolysed/protonated?
A weak acid so protonated in the stomach and able to pass across the mucosa Rapidly hydrolysed to salicylate by esterases in the liver (75%) and plasma
62
How does aspirin cause its anti-inflammatory actions?
Through inhibition of nFkB
63
What are the side effects of aspirin?
Gastric bleeding Deafness/tinnitus (with larger doses/overdoses) Risk of self poisoning Resistance to aspirin is known - no genetic tests available Interacts with warfarin increasing warfarin concentration
64
What do anticoagulants do?
Anticoagulants prevents blood clotting and inhibit clotting factors in clotting cascade
65
What are heparins?
Glycosaminoglycans found in mast cells and basophils
66
What do heparins do?
Activate antithrombin IIIa --> inactivates thrombin and factor Xa --> prevents formation of a stable clot/thrombus
67
What are the side effects of anti-coagulants/heparins?
Bleeding
68
What is a second anti-platelet approach?
Second antiplatelet approach alongside aspirin use thienopyridines – Clopidogrel and Tiagrelor
69
What can be used to treat analgesia?
Opiates and antiemetics
70
Where does morphine bind?
Binds to opioid receptors (Gi/G0 coupled to ion channels) in the brain as a partial agonist - Binds the mu receptor
71
What are the side effects of morphine?
Respiratory depression – modulated by mu receptors as well Nausea and vomiting (40%) - Because opioids have their effects in the postrema in the medulla where chemical stimuli act and cause vomiting Reduced tone and motility in the gut Histamine release Tolerance
72
Overall what are the 5 steps to treat unstable angina?
1. DAPT - aspirin plus clopidogrel or ticagrelor 2. Heparin 3. Analgesics 4. Secondary prevention - statin, ACE inhibitor or beta blocker 5. Once stabilised - elective (planned) PCI
73
Overall what are the 5 steps to treat NSTEMI?
1. Antiplatelet and anti-thrombotic therapy a. Antiplatelets only active in the arterial circulation not the venous circulation i. Anticoagulants active in both 2. Additional platelet inhibitor if ECG changes are rapid 3. Analgesics 4. PCI within 72 hours to determine lesion severity and suitability for stenting or bypass surgery. 5. Persistent pain plus markers
74
What are the key markers of STEMI?
Most severe presentation - must have clear ST elevation on ECG and chest pain of less than 12h duration
75
Overall what are the 4 steps to treat STEMI?
1. First - primary PCI at heart attack centre 2. If heart attack centre is too far - clot buster drug used intravenously a. Clot buster drugs stimulate the breakdown of stable fibrin clots b. Not to be used with anti-platelets 3. Antiplatelet medications – aspirin and ticagrelor 4. Lifelong medications after STEMI - Aspirin 75mg/day - Antiplatelet agent for 1 year - Statins - ACE inhibitors - Beta blockers to aid myocardial recovery
76
What is the mortality for STEMI patients who reach hospital?
4.4% | 30% die before reaching hospital
77
What are 3 ways to personalise treatments for STEMI?
1 - Bedside device at the time of PCI after STEMI to measure individual platelet reactivity 2 - Individualised maps of a patient’s coronary arteries help decide which lesions 3 - Inflammation

Personalised Medicine - Cardiovascular (11 decks)

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