Ischaemic Heart Disease and its Consequences Flashcards

(38 cards)

1
Q

Epicardial

A

outer surface of heart

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2
Q

Endocardial

A

inner surface of heart

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3
Q

Subendocardial region

A

water-shed area of perfusion and first to become ischaemic

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4
Q

Coronary Artery Imaging in humans in life

A
  • Coronary Angiography • CT

* MR imaging

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5
Q

Causes:

A

Chronic coronary insufficiency:
Angina

Unstable coronary disease:
Myocardial infarction
Sudden ischaemic coronary death

Heart Failure

Arrhythmia:
acute Ischaemia
Scar related

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6
Q

Atherosclerotic Coronary Artery Disease risk factors

A
Age
Hypertension Hypercholesterolaemia Smoking
Diabetes
Obesity
Physical inactivity
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7
Q

Atherosclerotic Coronary Artery Disease

Pathology- the three components

A
  • fatty streak
  • fibro-fatty plaque
  • plaque disruption (plaque rupture or erosion)
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8
Q

symptoms of angina

A

– Gripping central chest pain
– Radiation to arm and jaw
– Clear and precise relationship to exercise
– Goes off in 2-10 mins after discontinuation of exercise – Worse after food. Worse in cold
– No autonomic features
– Flat of hand/fist to describe pain

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9
Q

cause of angina

A

– Sub-Endocardial ischaemia

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10
Q

how does angina present on an ECG

A

ST depression

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11
Q

angina mechanism

A

MISMATCH OF BLOOD SUPPLY TO DEMAND BECAUSE OF EPICARDIAL STENOSIS:
Supply = Coronary Blood Flow
Demand = Myocardial Oxygen Consumption
(MVO2 )

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12
Q

• Two regulatory systems with two control mechanisms

A

– Autoregulation (myogenic control)

– Metabolic regulation

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13
Q

determinants of myocardial oxygen consumption

A
- variable per unit mass of tissue:
tension development – LV pressure and LV volume Contractility
Heart rate
- fixed per unit mass of tissue:
basal activity (10-20%)
- Mass of tissue
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14
Q

Identification of Coronary Disease as the cause: anatomical assessment

A

– CT coronary angiography

– Invasive angiography

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15
Q

Identification of Coronary Disease as the cause: Test of Inducible ischaemia

A

– Exercise stress test
– Dobutamine stress echo
– Myocardial perfusion imaging with either exercise or phamacological stress
– Cardiac magnetic resonance imaging (cMR)

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16
Q

Identification of Coronary Disease as the cause: anatomic and functional

A

– Invasive angiography and fractional flow reserve (FFR)
– cMR
– Novel CT

17
Q

Angina Treatment - Reduce Myocardial Oxygen consumption.

18
Q

Angina Treatment - improve coronary flow reserve

A

– Percutaneous Coronary Intervention (stents and balloons)

– Coronary Artery Bypass Grafting (CABG) – Drugs - Vasodilators

19
Q

Drug treatment and Angina

A
  1. Reduction in myocardial oxygen consumption

2. Reduction in the variability of coronary flow reserve

20
Q

Beta Adrenoceptor Blockers

A

– Reduce Heart Rate, Reduce Blood Pressure

– i.e. Reduce work of heart

21
Q

• Nitrates(GTN)

A

– Venodilation → Reduced LV size → Wall tension. (reduces work) Small effect on epicardial stenosis dilation (improved supply)

22
Q

• Calcium Channel blockers

A

– Reduce HR, some reduce Heart rate, small effect on from epicardial dilatation (mixed)

23
Q

• Ikf Channel Inhibitors

A

– Selective heart rate reduction by inhibiting channels in SA node - Ivabridine

24
Q

MYOCARDIAL INFARCTION – Clinical Presentation

A
  • chest pain, severe, crushing radiating to jaw and arm
  • associated ‘autonomic’ symptoms (nausea, sweating, terror)
  • breathlessness
25
events modifying presentation of AMI
- time of day - inflammatory activity - infection esp. respiratory - elevation of BP - catecholamines
26
Classifications of Myocardial Infarction - by site of infarction, pathology
– Full thickness, transmural | – Sub endocardial
27
Classifications of Myocardial Infarction - By ECG - Clinical
– ST Elevation myocardial infarction (STEMI) | – Non-ST elevation myocardial infarction (non- STEMI)
28
Classifications of Myocardial Infarction - By cause
– Type 1-4
29
Relation between anatomy and ECG
* STEMI implies transmural myocardial infraction | * NSTEMI will include subendocardial infraction but does not exclude transmural infraction in regions remote from ECG
30
• A Clinical History with: | – ECGChanges,definingsub-classificationof:
* STEMI | * NSTEMI
31
ECG Changes, defining sub-classification of: And raised cardiomyocyte markers in blood
* Troponin T or I * Creatine kinase MB isoform (CKMB) * Creatine Phosphokinase (CPK) * AST * Myoglobin
32
STEMI Management
Antiplatelet agents: Aspirin + Clopidogrel or other antiplatelet (P2Y12 inbibitor) Immediate revascularisation: Primary PCI (Thrombolysis – clot busting)
33
Adjunctive Therapy for STEMI: • After anti-platelets agents and revascularisation
– Statin drugs (reduce cholesterol – plaque passivation) – ACE inhibitors (usually a couple of days later to inhibit dilation of the left ventricle) – Beta blockers (reduce myocardial infarction)
34
Complications of STEMI - immediate
– Ventricular Arrhythmia and death | – Acute Left Heart Failure
35
Complications of STEMI - Early (Day 2-7)
– Myocardial Rupture – Mitral valve insufficiency – Ventricular Septal defect – Mural thrombus and emobolisation
36
Complications of STEMI Late (beyond day 7)
– LV dilatation and heart failure – Arrhythmia – Recurrent myocardial infarction
37
NSTEMI
• Getting more frequent (STEMI less common) • More common in elderly • Implies sub-endocardial ischaemia • Caused by: – Threatened STEMI – Small branch occlusion – Occlusion of well collateralised vessel – Lateral STEMI in territory not well seen by ECG
38
Treatment of non-STEMI
• Anti platelet therapy (Aspirin and clopidogrel) • Anti-ischaemics(beta blockers and nitrates) • Statin drugs • ACE inhibitors • Coronary angiography and revascularisation – Early if symptoms continue – Early if Troponin raised – Risk score (eg GRACE)