Acute Coronary Syndromes

Question 1

2nd most common cause of death in Scotland

Answer 1

Heart disease

Question 2

What is ACS

Answer 2

A sudden collection of symptoms suspected or proven to be related to a problem with the coronary arteries which supply the myocardium, causes myocardial ischemia

Question 3

What is MI

Answer 3

Cell death in heart muscle due to prolonged ischemia

Question 4

What is cardiac arrest

Answer 4

Abnormal heart rhythm not compatible with life eg ventricular fibrillation, ventricular tachycardia, asystole

Can occur during acute MI or after due to scar

Or be unrelated

Question 5

What is a heart attack

Answer 5

Doctors usually mean MI

Question 6

Chronic ischemic heart disease

Answer 6

Stable angina

Question 7

Acute coronary syndromes

Answer 7

Unstable angina (MI stemi or non-stemi)

Question 8

ECG of complete coronary occlusion MI

Answer 8

Initial ST elevation then Q waves after 3 days

STEMI (full thickness damage)
Transmural

Question 9

ECG of partial coronary occlusion MI

Answer 9

No st initially and no q wave after 3 days

Non STEMI
Subendocardial

Question 10

Diagnosis of MI

Answer 10

Detection cardiac cell death/injury with positive cardiac biomarkers
And one of
Ischaemia symptoms
New ECG changes
Evidence of coronary problem on angiogram or autopsy
Evidence of new cardiac damage on another test

Question 11

Cardiac biomarkers

Answer 11

Troponin-B1 large infarction eg STEMI B2 Small infarction but could be from arrythmias, PR, cardiac contusion, sepsis, renal failure

Myoglobin
CK-MB

Question 12

Types of MI

Answer 12

1-spontaneous and due to primary coronary event eg rupture

2- due to imbalance in oxygen supply/demand

3- sudden cardiac death with new ST elevation or LBBB. Coronary thrombus but death

4a- from percutaneous coronary intervention, increased biomarkers

4b- from verified stent thrombosis via angiography or autopsy

5- associated with CABG, new Q waves

Question 13

Coronary causes of MI other than atherosclerosis

Answer 13

Coronary vasospasm from drugs
Coronary dissection often in young healthy females
Embolism
Inflammation (vasculitis)

Question 14

Symptoms of acs

Answer 14

Chest pain, may radiate
A discomfort
Not agony
Maybe nausea, sweating, breathlessness

Question 15

Things to examine and investigations

Answer 15

HR and BP
Murmurs and crackles
ECG
Full bloods

Question 16

ECG at 3 days for stemi and non-stemi

Answer 16

Stemi- full occlusion and Q waves

Non-stemi- partial occlusion and no Q waves
May have st depression, t wave inversion or be normal

Question 17

Which artery is the problem

Answer 17

Inferior MI- right coronary artery

Anterior MI- left anterior descending coronary artery

Posterior MI- circumflex coronary artery (may be little ECG change like ST elevation, put leads on back of chest)

Question 18

Treatments of STEMI

Answer 18

Reperfusion therapy
Mechanical in cath lab for primary PCI
Or pharmacological eg tenecteplase for thrombus if no time, risk of bleeding

Question 19

Non-stemi patients

Answer 19

Older, more likely to have history, may not be as clear

Question 20

Unstable angina

Answer 20

Convincing anginal symptoms, rapidly worsening. No cell deaths so no raised troponin

Question 21

Risks of PCI and angiography

Answer 21

Bleeding
Damage
mI
Coronary perforation
Stroke
Dye affecting kidney

Question 22

When CABG instead of pci

Answer 22

Three vessels

Left main stem

Question 23

Goal of Pharmacotherapy

Answer 23

Goal of therapy is to:
Increase myocardial oxygen supply
through coronary vasodilation.
Decrease myocardial oxygen demand
Decrease in heart rate, 
Decrease blood pressure, 
Decrease preload or myocardial contractility

Question 24

Thrombolysis indication

Answer 24

STEMI usually occurs as a result of coronary artery occlusion due to formation of thrombus overlying an atheromatous plaque.
If no PCI within 2 hours then thrombolysis is indicated.

Question 25

how thrombolytic agents work

Answer 25

Thrombolytic agents available today are serine proteases that work by converting plasminogen to the natural fibrinolytic agent plasmin.

Plasmin lyses clot by breaking down the fibrinogen and fibrin contained in a clot

Question 26

types of thrombolytic agents

Answer 26

Fibrinolytics are divided into two categories.
1: Fibrin-specific agents such as
alteplase,
reteplase,
tenecteplase
All catalyse conversion of plasminogen to plasmin in the absence of fibrin.

2: Non–fibrin-specific agents such as streptokinase catalyse systemic fibrinolysis.

Question 27

contraindications for thrombolysis

Answer 27

Prior intracranial hemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischaemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed-head trauma or facial trauma within 3 months

Question 28

benefits of thromolysis

Answer 28

Timely thrombolysis associated with:
23% reduction in mortality
39% when used with aspirin

Question 29

If no evidence of a STEMI ACS Medical Treatment Protocol

Answer 29

Aspirin
Tigagrelor/Clopidogrel (blood thinners)
Fondaparinux/LMW heparin
Intravenous nitrate ( like GTN for lowering bp)
Analgesia
Beta Blockers

Question 30

Management to reduce risk from NSTEMI

Answer 30

PCI or CABG
Aspirin
Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
Heparin (LMWH)
Fondaparinux
GIIb/IIIa receptor blockers
Statins
B blockers

Question 31

Antiplatelet Agents

Answer 31

Low dose ASPIRIN (75-150 mg)
The formation of platelet aggregates are important in the pathogenesis of angina, unstable angina and acute MI
Aspirin is a potent inhibitor of platelet thromboxane A2 production
Thromboxane stimulates platelet aggregation and vasoconstriction

The regular daily use of aspirin can
In acute MI 
reduce mortality by 23%
in combination with thrombolysis reduce mortality by 42% and reinfarction by 52%
In unstable angina
reduce MI and death by 50%
In secondary prevention 
reduce reinfarction by 32% and combined vascular events by 25%

but no difference between high and low dose

Question 32

Clopidogrel and issues with it

Answer 32

Clopidogrel is a prodrug
Inhibits ADP receptor activated platelet aggregation.
Specifically and irreversibly inhibits the P2Y12 ADP receptor which is important in aggregation of platelets and cross-linking by fibrin

The blockade of this receptor inhibits platelet aggregation by blocking activation of the GP IIb/IIIa pathway.

The IIb/IIIa complex is a receptor for fibrinogen, fibronectin and von WF. Activation of this receptor complex is the “final common pathway” for platelet aggregation and cross-linking of platelets by fibrin.

Always used in combination with aspirin
Relative risk reduction of 21% when used together with aspirin.
Claimed lower incidence of GI bleeding.
However GI bleeding very common
Possible interaction with PPI with a reduction in effect
Evidence for clinical importance of this interaction very poor

Clopidogrel activated by Cyp 2C19
14% of population have low CYP2C19 levels and demonstrate resistance to clopidogrel

Question 33

Prasugrel

Answer 33

Member of the thienopyridine class of ADP receptor inhibitors, like clopidogrel 
Compared to clopidogrel prasugrel inhibits ADP–induced platelet aggregation more rapidly, more consistently,

Question 34

Low Molecular Weight Heparin

Answer 34

Low molecular weight heparin is an integral component of the ACS protocol
Several different products, probably all similar in effect:
Enoxaparin
Dalteparin
Tinzeparin
Fondaparinux

Question 35

Fondaparinux

Answer 35

A Selective Inhibitor of Factor Xa
Single chemical entity
Synthetic pentasaccaride
Highly selective for antithrombin 
Once-daily administration
No need for platelet monitoring

Question 36

Glycoprotein IIb/IIIa Receptor Inhibitors

Answer 36

GPIIb/IIIa is an integrin complex found on platelets
receptor for fibrinogen aids in platelet activation.
Platelet activation by ADP(blocked by clopidogrel) leads to a conformational change in platelet GPIIb/IIIa receptor that induces binding to fibrinogen.
The GPIIb/IIIa receptor is a target of several drugs including abciximab, tirofiban
Intravenous GPIIb/IIIa inhibitors block platelet aggregation by inhibiting fibrinogen binding to a conformationally activated form of the GPIIb/IIIa receptor on two adjacent platelets.

A meta-analysis involving 29570 showed a 9% RRR in death or non-fatal MI with GPIIb/IIIa inhibitors

Question 37

major adverse effect in GPIIb/IIIa inhibitors

Answer 37

The major adverse effect is bleeding:
major bleeding occurrs in 1.4% of patients
minor bleeding in 10.5%.
Blood transfusion required to terminate bleeding and to improve bleeding-related anaemia in 4.0% of all patients.

Question 38

Beta blockers post MI

Answer 38

for secondary prevention in the survivors of an acute MI.
I.V.atenolol or metoprolol reduce mortality following an acute MI
Oral beta blockade started weeks or months post MI reduce cardiac death
Beta-blockers competitively inhibit the myocardial effects of circulating catecholamines (stress hormones adrenaline and noradrenaline) and reduce myocardial oxygen consumption by lowering heart rate, blood pressure and myocardial contractility.
Evidence for benefitshowing that beta-blocker was associated with a significant (RRR) of mortality
In patients at risk of developing cardiogenic shock (i.e. age >70 years, heart rate >110 beats/min, systolic blood pressure < 120 mmHg) the observed shock or death rate was significantly increased in patients receiving beta-blockers within 24 h of hospital admission.
Avoid in these and patients with symptoms possibly related to coronary vasospasm or cocaine use.