Ischaemic Heart Disease

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Ischaemic Heart Disease

• Khalid Husain Sachak
• Warwick Cardiology Society

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• These ESA style questions are made by myself,
  they are not necessarily representative of the
  style/content of examinations used by WMS but I
  hope you find them useful.
• Good luck with exams.

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Q. Define ischaemic heart disease (1)
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• IHD is characterized by
• reduced blood supply
• i.e ischaemia of the heart muscle
• The majority of which is caused by
• coronary artery atherosclerosis

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Q. Atherosclerosis is the main cause of IHD. Name
4 other causes of IHD (4)
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• Emobolism
• Coronary spasm
• Congenital arterial disease
• Arteritis

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IHD presents as

1. Stable angina
2. Acute coronary syndrome

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Q. Describe what is meant by stable angina (2)
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• Stable Angina
• Ischaemic chest pain occuring when myocardial
  oxygen demand exceeds oxygen supply
• Must be bought on by exertion and relieved at
  rest

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Q. What are the 3 components of Acute Coronary
Syndrome (1.5)
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• Acute coronary syndrome
• Unstable angina
• Myocardial infarction
• NSTEMI
• STEMI

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Q1. Define unstable angina (1)
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• Unstable angina is defined as recurrent episodes
  of angina on minimal effort or at rest.
• It may be the initial presentation of ischaemic
  heart disease, or it may represent the abrupt
  deterioration of a previously stable anginal
  syndrome

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Q2. Define STEMI AND NSTEMI (2)
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• STEMI
• (ST Elevation Myocardial Infarction)
• One sole criteria
• ST elevation on ECG

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• NON STEMI
• (Non ST Elevation Myocardial Infarction)
• Atleast two of the following criteria
• Symptoms at rest
• Raised serum Troponin
• ECG changes

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Q3. Pathologically, what does a STEMI indicate?
(1)
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• That the infarction is transmural

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Atherosclerosis- The cause of ischaemia
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Q. Describe the key steps in atheroma formation
(5)
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• LDL cholesterol crosses damaged epithelium and is
  oxidised
• Monocytes enter, differentiating into macrophages
• Oxidised LDL is taken up by macrophages
• Lipid laden macrophages form fatty streak
• Endothelium is exposed to LDLs causing
• Angiotensin II release
• Stimulates vasoconstriction, platelet
  aggregation, and vascular smooth muscle cell
  proliferation

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• Macrophages
• They express cytokines, triggering the
  inflammatory response
• Lymphocytes enter

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• MMPs and ECM secreted by smooth muscle cells
• Formation of the fibrous cap

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Q. State 3 mechanisms by which the atheroma can
lead to ischaemia
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• Plaque rupture and overlying thrombosis
• Emboli
• Progressive stenosis

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Q. Risk Factors for IHD? (4)
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• Fixed
• Age
• Male sex
• Menopause
• Family history
• Diabetes

• Modifiable
• Smoking
• Hypertension
• Hyperlipidaemia
• Obesity
• Alcohol
• Sedentary lifestyle

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HistoryChest pain (gripping,
crushing)Radiation to neck, jaw,
epigastriumAssociations Breathlessness, NV
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List some findings on examination of a patient
with ACS?
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• Pallor
• Restless
• Sweating
• Pyrexial
• Arrythmia
• New murmur from septal rupture

• Signs of shock
• Hypotension
• Tachycardia
• Cold peripheries

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Q. Investigations in a patient presenting with
symptoms of IHD? (3)
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• ECG
• Initially hyperacute T waves, then ST elevation,
  then T wave inversion then Q waves
• Bloods
• FBC, UEs, LFTs, Glucose, Cardiac enzymes e.g. CK
  MB and Troponins.
• ? Echo Chest x-ray?

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END
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Q. How would you manage a patient with stable
angina? (4)
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• Lifestyle modification
• Stop smoking
• Good diabetic control
• Cut down alcohol
• Lose weight reduces myocardial work
• Symptom control
• Nitrates dilate coronary arteries
• Rest

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Stable angina Management

• Drug therapy
• Antihypertensives
• Statins help prevent plaque rupture, ? LDL
• Aspirin antiplatelet
• Beta blockers
• Antagonists of adrenaline noradrenaline
• Reduced contractility and heart rate
• Calcium antagonist
• Vasodilation (especially dihydropyidines)
• Prolongation of action potential, antidysrrythmic
  

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Stable angina Management

• Coronary revascularisation
• PCI (angioplasty/stenting)
• Angina post myocardial infarction
• Unstable angina
• Severe IHD
• Stable angina uncontrolled by medication

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Q. Management of a patient with unstable
angina/NSTEMI?
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• Admit to CCU
• Oxygen, IV access, monitor vital signs
• Analgesia (e.g. morphine)
• Aspirin and clopidogrel (loading)
• Beta blocker
• Look for improvement
• If no improvement angiography and consider
  revascularisation.

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Immediate Management

• Airway
• Breathing oxygen, RR, sats, creps
• Circulation BP, HR, cannula, bloods, monitoring
  if unstable, CRT
• Disability GCS, BM
• Exposure Other causes for chest pain, abdomen,
  calves

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Immediate Management

• MONA
• Morphine analgesia and reduced preload
• Metoclopramide (avoid cyclizine)
• Oxygen
• Nitrates vasodilator
• Aspirin 300mg, Clopidogrel 300mg

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Reperfusion Therapy

• Percutaneous Coronary Intervention
• Used for STEMI as these suggest full thickness
  infarction
• Should be done in lt90mins
• Method Occluded vessel identified, guidewire
  passed, balloon inserted, stent inserted
• Advantages
• Culprit artery re-opened to normal calibre
• Lower risk of major bleeding

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Reperfusion Therapy

• Thrombolysis
• Advantages easy to perform, can be done quickly
  
• Disadvantages
• Inability to achieve reperfusion in all cases
• Risk of inducing bleeding
• Cannot detect success of reperfusion
• Contraindications
• Recent CVA or previous haemorrhagic stroke
• Recent surgery
• Active bleeding

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Secondary prevention

• Low Molecular Weight Heparin 1mg/kg OD
• Aspirin
• Clopidogrel
• Beta blocker usually Bisoprolol
• ACE inhibitor usually Ramipril
• Glycoprotein IIb/IIIa inhibitor
• Statin
• Omacor
• Cardiac rehabilitation

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CABG

• Usually reserved for severe triple vessel disease
  not amenable to PCI
• Two forms
• Vein grafts leg saphenous veins, quick to
  apply, annual failure 8
• Arterial grafts more technically difficult,
  better long term survival, uses internal mammary
  artery
• 1 mortality if elective
• Prior to surgery optimise diabetes, do
  pulmonary function tests and vein mapping

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Early Complications of MI (24-72 hrs)

• Cardiogenic shock
• Arrythmia
• Heart block
• Pericarditis
• Myocardial rupture
• Thromboembolism

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Late complications of MI (72 hours)

• Ventricular rupture
• Septal rupture
• Ventricular aneurysm
• Tamponade
• Dresslers Syndrome (pericarditis 2-10 weeks post
  MI)

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Post MI counselling

• Explain medications and their use
• 2 months off work and avoid heavy labour
• Avoid sex for one month
• Build up exercise gently
• Stop smoking
• Reduce alcohol
• Avoid driving for 4-6 weeks
• Avoid flying for 2 months

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Cardiac sounding chest pain
ECG ST elevation
Normal ECG
ECG non specific changes (T wave inversion, ST
depression, Q waves, AF)
STEMI
12 hour troponin I
Positive Trop I
Negative Trop I
Reperfusion
NSTEMI
Unstable angina
PCI
Thrombolysis
Medical Management
Medical management