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Medicine 2 - 05 Heart Failure > 8 Cardiovascular (Ischaemic Heart Disease) Therapeutics > Flashcards

8 Cardiovascular (Ischaemic Heart Disease) Therapeutics Flashcards

1
Q

Define and describe Ischaemic Heart Disease

A

Vascular supply of Heart to the heart is impeded by atheroma, thrombosis or spasm of the coronary arteries

The resultant myocardial infarction occurs when oxygen demand exceeds myocardial oxygen supply

  • Pain can be induced, but sometimes the ischaemia is ‘silent’
    (e. g. in people with diabetes mellitus)
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2
Q

List some risk factors of Ischaemic Heart Disease

A
  • Smoking
  • Raised Serum Cholesterol
  • Hypertension
  • Diabetes
  • Stress
  • Obesity
  • Male
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3
Q

Describe the prevalence of Ischaemic Heart Disease

A
  • CHD levels lower in groups with higher incomes
  • CHD deaths have fallen in this group since the 1970s (linked to a reduction in fat consumption/smoking)
  1. 3 million people in the Uk have had a myocardial infarction
    - and 2 million have Ischaemic Heart Disease
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4
Q

Describe atherosclerosis, and the relation with CVD

A

IHD occurs when atherosclerosis occurs in the coronary arteries (starts to occur before adulthood)

  • Atherosclerosis occurs in coronary arteries
  • Fatty streaks contain LDL cholesterol, macrophages, T cells

The proliferation of smooth muscle cells into the inner coating of artery and build-up of collagen, glycoproteins leads to the formation of a fibrous cap surrounding cells leading to plaque formation

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5
Q

Describe plaque attack, and how this plaque can lead to ACS

A

Plaques reduce blood flow

  • Coronary arteries get stiffer and have less dilation - less blood flow (ischaemia)
  • The plaque can rupture, leading to a loss of endothelium
  • This leads to a formation of a thrombus

Formation of ACS
(acute coronary syndrome)

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6
Q

Describe chest pain, and how it can present, and be caused

A

Chest pain can present in similar ways, and maybe caused by different things:

  • Angina pectoris
  • Variant angina (prinzmetals)
  • GORD/oesophageal spasm
  • Hypertrophic cardiomyopathy
  • Pulmonary embolus
  • Costochondritis
  • Myocardial infarction
  • Mitral valve prolapse
  • Pneumonia/Lung cancer
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7
Q

Give the relation between chest pain and angina

and how it can be a concern for angina, ACS, and MIs

A

NICE guidelines:
- NICE considers those patients who present with acute, new-onset chest pain and those who present with intermittent, stable chest pain (develops chest pain after exercise)

There is a major concern that the pain may be due to Acute Coronary Syndrome (ACS), which includes conditions such as:

  • Unstable Angina
  • ST-segment-elevation MI (STEMI)
  • Non-STEMI (NSTEMI)
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8
Q

Describe some symptoms of Acute Coronary Syndrome

A
  • New-onset chest pain
  • OR abrupt deterioration in previously stable angina, with recurrent chest pain occurring with little or no exertion. Episodes last > 15mins
  • Pain in chest and other areas such as arms, back and jaw lasting longer than 15 mins
  • Chest pain is associated with nausea and vomiting, breathlessness, marked sweating
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9
Q

Describe when/how to refer to the hospital if suspected of ACS

A

Send to hospital for suspected ACS

  • currently have chest pain
  • currently pain-free, but had chest pain in the last 12 hours, and a resting 12-lead ECG is abnormal

A normal ECG DOES NOT EXCLUDE ACS if other clinical features are present

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10
Q

Describe what to be aware of when taking a clinical history of a patient suspected of ACS/IHD

A

PMH - e.g. history of angina, MI, CVD and PCI (percutaneous coronary intervention)

  • Risk factors for cardiac disease
  • Pain history e.g. longer than 15mins
  • Chest pain may not be the main presenting symptom (e.g. may present with mainly breathlessness)
    > Diabetes can have damaged cardiac nerve endings
    > Do not use response to GTN (glycerol Trinitrate) to diagnose whether pain is cardiac or not
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11
Q

Describe what to do if ACS is suspected (emergency)

A

ACS ASAP!

  • Emergency admission
  • Relieve pain with GTN (glycerol trinitrate) and/or opioid
  • Aspirin 300mg unless allergic (then give clopidogrel)
  • Carry out an ECG, and send to the hospital
  • Measure O2 sats (give O2 if Sats <94%)
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12
Q

Describe a stable angina

and what is done to manage it

A

Some having a current angina
- they can undergo a PCI, where a stent is inserted

If it is an ongoing/chronic angina (MI)
- CABG (coronary artery bypass graft)

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13
Q

Describe factors affecting stable angina

(what can relieve it)

(imaging that can be used)

A
  • Stable angina can be provoked by numerous factors including cold weather, exertion, eating a heavy meal, or stress

Angina attack can be relieved by Glyceryl Trinitrate (GTN)

Coronary Angiography is a procedure that uses contrast dye and X-ray pictures to detect blockages in the coronary arteries that are caused by plaque build-up

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14
Q

Describe Prinzmetal’s (Variant) Angina

A
  • Achy, dull, tight, pressy pain
  • Can occur at rest or at night
  • Mainly in younger women
  • Spasm of coronary artery
  • Relieved by GTN
  • ECG during attack must be done
  • CCB’s first line (calcium channel blockers)
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15
Q

Describe the treatment for an angina attack

A

GTN - glycerol trinitrate - treatment for angina
- Relieves load on the heart

It is sprayed on the tongue
- as GTN has high 1st pass metabolism, so this way it can bypass the liver and enters the bloodstream directly

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16
Q

Describe the use of short-acting nitrates

A

Offer a short-acting nitrate, for use immediately before planned exertion or when the pain occurs
- Warn patients about SIDE EFFECTS:
> flushing, headache, and light-headedness
- If the patient is having to use it regularly, then it indicates poor control of symptoms

17
Q

Describe what advice is given to GTN spray

A

British Heart Foundation advice:

  • Carry GTN at all times
  • IF you get pain, stop what you are doing, sit down + rest. Take a puff of GTN
  • If the pain doesn’t ease within 5 mins, take the 2nd puff of GN
  • If the pain doesn’t ease within 5 mins, take the 3rd puff of GTN and DIAL 999

Whilst waiting for the ambulance, take 300mg of aspirin
(if allergic, then just sit and wait for the ambulance)

18
Q

Describe the management of stable angina

A

If a patient’s symptoms:
- are not satisfactorily controlled on a B-blocker or CCB, consider switching to the other option, or combination of the two
(BUT, do not give B-blocker + rate-limiting agents)

Do not routinely offer anti-angina drugs other than B-blockers as 1st line for stable angina

If a patient cannot tolerate B-blockers and CCBs, consider monotherapy with a:

  • Long-acting nitrate
  • Ivabradine
  • Nicorandil
  • Ranolazine
19
Q

Describe the use of B-blockers in the treatment of ischaemic heart disease

AND give MOA

A

Beta-blockers (1st line) e.g. Bisoprolol

  • Negative inotropic (slows heart rate)
    > allows more efficient work
  • Negative chronotropic
    > (reduce heart contraction - reduce load)

These effects reduce cardiac work + prevent symptoms
- Anti-arrhythmic effects and reduce the risk of Myocardial Infarction
- Provides symptomatic relief
Aim for a heart rate of 60bpm

Use more cardio-selective B1-blockers like:
- Bisoprolol, atenolol, and metoprolol

20
Q

Describe some contraindications fo B-beta-blockers

A
  • Asthmatic patients

- Patients who have bradycardia (can’t reduce heart rate anymore - not good!)

21
Q

Describe the use of Calcium Channel Blockers in the treatment of IHD

give MOA

and SE, contraindications etc.

A

Calcium channel blocks (CCGs)
- These work by inhibiting Ca2+ channels, leading to depolarisation

CCGs can be used where B blockers are contra-indicated (another 1st line)

e. g. Asthmatics, bradycardia
- Useful in patients with underlying blood pressure issues
- Consider in patients who are diabetics, peripheral vascular disease

2 types:

Dihydropyridine type (long-acting)

  • e.g. Amlodipine, felodipine, nifedipine
  • work by relaxing smooth muscles
  • they decrease afterload and improve coronary perfusion
  • NO EFFECT ON RATE

Rate-limiting agents

  • e.g. verapamil, diltiazem
  • also have myocardial and bradycardic actions - Reducing cardiac work
  • AVOID with B-blockers + patients with heart failure
22
Q

Describe the use of Nitrates in the treatment of IHD

give MOA

A

Nitrates
e.g. GTN (glycerol trinitrate)

They work by causing vasodilation of veins - reducing preload
- They relax the smooth muscle by causing endothelium to produce Nitric Oxide (NO), which relaxes vascular smooth muscle

SO, it improves coronary blood flow

Nitrates are rapidly broken down by a liver enzyme

  • SO, can be given orally,
  • transdermally (RARE) and
  • sublingually (under tongue - GTN)
23
Q

Give some important prescribing points to keep in mind when giving Nitrates as a treatment

(SE, contraindications, uses etc.)

A

SE of nitrates:
- Dizziness, flushing, headache, postural hypertension, tachycardia, GI disturbances

Tolerance is a major issue

  • need to have a nitrate-free period 6-10 hours a day
  • Modified release tablets tend to be given in the morning
  • They release nitrates during the daytime, but evening washout period when the patient is less active
24
Q

Describe the MOA of Potassium Channel Activators in the treatment of IHD

A

K+ channel activators
- e.g. Nicorandil

MOA:
Nicorandil is a combined NO donor and activator of ATP-sensitive K+ channels:
- Once these ATP-sensitive K+ channels are activated
- It causes hyperpolarisation
- and relaxation of cardiac muscle cells

25
Q

Describe the use of Potassium Channel Activators in the treatment of IHD

A

Potassium Channel Activators
- e.g. Nicorandil

Nicorandil is now a second-line treatment for Angina
- use Nicorandil for treatment of stable angina only in patients:
> whose angina is inadequately controlled by 1st line anti-anginal therapies
> or who have a contraindication/intolerance to 1st line anti-anginal therapies
i.e. B-blockers or CCB

26
Q

Give some side effects/contraindications of Potassium Channel Activators like Nicorandil

A

SE:
- Can cause serious skin, mucosal, and eye ulceration:
> including GI ulcers, which may progress to perforation, haemorrhage, fistula or abscess

STOP NICORANDIL TREATMENT

  • if ulceration occurs
  • consider the need for alternative treatment, or specialist advice if angina symptoms worsen
27
Q

Describe the use of Ivabradine in the treatment of IHD

And any SE’s/contraindications

A

Ivabradine inhibits If channels
- pacemaker Na+/K+ currents in the SAN

Ivabradine:
- reduces heart rate
- BUT NOT the force of contraction (heart failure use)
> those with symptomatic angina had increased CV death

STOP Ivabradine treatment if:

  • the resting heart rate remains below 50bpm
  • or symptoms of bradycardia persist

AVOID in:
- patients on Diltiazem/Verpamil (rate-limiting CCB’s)

28
Q

Describe the use of Antiplatelet drugs in the treatment of IHD

A

Antiplatelet treatment is drug treatment that:
- decreases platelet aggregation + inhibits thrombus formation in the arterial circulation

e. g. Aspirin
- irreversibly inhibits COX + blocks the production of thromboxane

In angina, use
- Aspirin 75mg
- Clopidogrel 75mg daily
(should be considered for px who are unable to take aspirin)

29
Q

Describe the principle behind how statins work

HMG-CoA reductase inhibitors

A

HMG-CoA reductase inhibitors

  • in the pathway for cholesterol synthesis
  • 3-hydroxy-3-methylglutaryl coenzyme A reductase catalyses the first step of cholesterol synthesis
30
Q

Describe the use of statins in the treatment of IHD

give the MOA

SE, interactions etc.

A

Statins reduce plasma cholesterol

e. g. Atorvastatin and simvastatin
- The receptors in hepatic cholesterol synthesis leads to an upregulation of hepatic LDL receptors, promoting LDL uptake

Side effects:
- Muscle damage
(simvastatin must be taken at night)

Drug-Drug interactions:

  • with macrolides (e.g. clarithromycin)
  • with CCB’s (simvastatin and amlodipine)

Drug-food interactions:
- with grapefruit juice

31
Q

Describe why patients with IHD need to be on a statin

A 
Primary prevention
- treat patients with >10% risk of CV or over in the 10 years
(balancing risks vs benefits vs cost)
- assess this via QRIS3
[20mg atorvastatin) - low intensity]

Secondary Prevention

  • or patients with CVD
  • 80mg atorvastatin [high intensity]
32
Q

Describe the Quad treatment policy post-ACS

A

Dual antiplatelet therapy
- e.g. aspirin + clopidogrel required after PCI (stents)

ACE inhibitor
- ramipril

Beta-blocker

  • e.g. Bisoprolol
  • OR CCB like amlodipine (reduced load)
  • or verapamil (reduced load + reduced heart rate as well)

Statins
- atorvastatin

Medicine 2 - 05 Heart Failure (8 decks)

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