18- Coronary Heart Disease, Mi And Embolism Flashcards

1
Q

How does coronary heart disease present

A

Sudden cardiac death
o Acute coronary syndrome – Acute myocardial infarction – Unstable angina
o Stable angina pectoris o Heart failure
o Arrhythmia

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2
Q

What increases your risk of CHD

A

Tobacco use, physical inactivity, harmful use of alcohol, unhealthy diet accounts results in:
– Hypertension
– Obesity
– Diabetes mellitus – Hyperlipdaemia

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3
Q

What is myocardial ischaemia

A

Mismatch between myocardial oxygen supply and demand

• Primary reduction in blood flow

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4
Q

What are the 2 components of coronary arteries

A

the coronary arteries have an epicardial component and an intramyocardial component

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5
Q

What happens in epicardial stenosis

A

If you have stenosis in the epicardial compartment - the resistance in the epicardial component INCREASES
• This can be compensated to a degree by an increase in the diameter of the intramyocardial resistance vessels - thus decreasing the resistance in the intramyocardial component to maintain flow

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6
Q

What is coronary flow reserve

A

ability of the coronary circulation to adapt to

an increasing demand in the face of an increasing epicardial coronary stenosis

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7
Q

What is angina pectoris

A

It is a tight feeling in the chest which can diffuse across the jaw, shoulders,
back or arms
• It can be provoked by physical exertion, emotional stress or anxiety
• Use of an inorganic nitrate vasodilator (e.g. glyceryl trinitrate) - the nitrates act
as a vasodilator leading to reduced coronary resistance and increasing blood
flow thus reversing the supply and demand imbalance
• It can be relieved by rest

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8
Q

What are the 2 types of test for CHD

A

Functional - demonstrate that there is an imbalance between supply and demand
Anatomical - look at anatomical severity of the narrowing within the artery then make an inference about how it is compromising flow - some of these tests are invasive and others are not

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9
Q

Which imaging techniques can be used to diagnose CHD

A

Imaging techniques include: echocardiography, MRI or nuclear perfusion imaging

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10
Q

What are the 3 types of treatment strategy for CHD

A

Prevent atherosclerosis progression and risk of death/MI
– Education
– Lifestyle modification
– Aspirin, statins, ACE inhibitors
o Reduce myocardial oxygen demand
– HR (b blockers, Ca antagonists, If blockers) – wall stress (ACE inhibitors, Ca antagonists) – Metabolic modifiers
o Improve blood supply
– Vasodilators (nitrates, nicorandil, Ca antagonists) – Revascularisation (PCI, CABG)

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11
Q

What 3 ways can coronary arteries become blocked

A

Coronary plaque rupture
Coronary plaque erosion
Coronary dissection

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12
Q

What is Virchow’s triad

A

Abnormal Vessel Wall
• Abnormal Blood Flow
• Abnormal Blood Constituents (hypercoagulability)

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13
Q

What is the difference between a white and red thrombus

A

WHITE thrombus
Platelet rich
Common in arterial thrombosis (high pressure/turbulent circulation) Benefit from anti-platelet therapy
• RED thrombus
Fibrin rich with trapped erythrocytes
Common in venous or low pressure situations (stasis) Benefit from anti-coagulant or anti-fibrinolytic therapy

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14
Q

Where does tissue factor come from

A

Tissue factor can be made from the cellular constituents of the atherosclerotic plaque or by the ischaemic heart muscle itself
• Circulating inflammatory cells can also act as a humoural source of tissue factor that can promote the atherosclerotic process
• Tissue factors triggers a cascade of factor activation leading to coronary thrombosis
• Factor 10a and Factor 2a are important molecular targets

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15
Q

Was is acute MI

A

DEFINITION: Detection of a rise or fall in a biomarker (TROPONIN) with at least one value >99th percentile reference limit AND at least one of:
Symptoms suggestive of ischaemia
New or presumed new ST-T changes or LBBB on ECG
Development of pathological Q waves on ECG
Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
Identification of intracoronary thrombus or angiography or autopsy

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16
Q

What is cardiac troponin

A

There are THREE isoforms: I, T and C
• Troponin I and T are highly specific to cardiac muscle
• This troponin is released as a result of proteolytic cleavage during myocardial ischaemia
• So, troponin I and T can be related to cardiac cell death
• After the onset of symptoms, cardiac troponin levels rise and then fall after a period of time

17
Q

What are the 2 types of acute coronary syndrome

A

Those who present with ST elevation have complete blockage of a coronary artery due to an occlusive thrombus
No ST elevation - partial occlusion which embolises distally into the microcirculation resulting in myocardial cell death and troponin elevation

18
Q
What is Primary Percutaneous Coronary Intervention (PPCI) for ST Elevation Acute
Coronary Syndrome (STEACS)
A

A guide wire is passed through the coronary thrombus and over the wire a balloon is passed and a stent is deployed which allows recanalisation of the vessel

19
Q

How does an infarction develop

A

The myocardial necrosis zone will start at the inner layers of the myocardium and progress as a wave front to spread through the entire extent of the myocardium if the coronary artery wasn’t quickly recanalised

20
Q

What is a reperfusion injury

A

The act of opening an artery can be associated with damage to the heart muscle - reperfusion injury

21
Q

How much does reperfusion reduce infarction by and how can it be reduced further

A

By 40%

Cardio protection reduces by a further 25%

22
Q

Describe post MI left ventricular remodelling

A

expansion of the heat muscle, thinning of the scar and impairment of heart function
• It is accompanied with an increased risk of heart failure and arrhythmias

23
Q

How can left ventricular modelling be managed

A
Non-Drug
Cardiac Resynchronisation Therapy (Pacemakers (P) or Defibrillators (D)) • Often written as CRT-P and CRT-D
Progenitor cells • Drugs
Beta blockers
ACE inhibitors
Angiotensin receptor blockers