Acute Coronary Syndrome

Question 1

What is acute coronary syndrome?

Answer 1

 This is usually due to rupture of atheromatous plaque in coronary artery leading
to thrombus formation and vessel occlusion locally or elsewhere in the heart.

Question 2

Types of acute coronary syndromes

Answer 2

 There are 3 acute coronary syndromes:
 ST segment elevation myocardial infarction (STEMI): increased troponin and
ST elevation on ECG. In practice ST elevation alone is sufficient to treat as
troponins take time to rise.
 Non-ST segment elevation myocardial infarction
(NSTEMI): increased troponin and ischemic symptoms
or ECG changes
 Unstable angina: prolonged, severe angina, usually at
rest, possibly with ECG changes.
 NSTEMI and unstable angina are often grouped together as
non-ST elevation ACS (NSTEACS)

Question 3

CF of acute coronary syndrome

Answer 3

 Chest pain. It must be evaluated using SOCRATES
 Site: central
 Onset: usually sudden but can be more gradual.
 Character: tight, crushing, but not sharp.
 Radiation: left arm, neck, jaw. Less commonly right arm,
epigastrium, back
 Associated symptoms: sweating, clamminess, SOB,
dizziness, faint, angor animi (an impending sense of doom)
 Timing: duration >15 minutes
 Exacerbating factor: Exertion, Emotion, Eating. Relieving factors: ACS less
likely if relieved by glyceryl trinitrate <5 mins.
 Severity: high but can atypically be low.
 Atypical presentations, more commonly seen in elderly or diabetic patients:
 Little or no chest pain
 SOB
 Sweating
 Nausea and vomiting
 Signs:
 Heart rate and blood pressure may be increased or decreased
 Pallor
 S3or S4 heart sounds (especially in STEMI)

Question 4

Investigations in acute coronary syndrome

Answer 4

 ECG: do immediately and if negative
repeat after 20 minutes if pain continues or
suspicion is high.
 ECG is diagnostic in 85% of cases.
 Transmural MI: ST segment elevation
in those leads reflecting the area of
myocardial infarction. As ST segments
fall, Q waves appear and T waves
become inverted
 Subendocardial infarction: ECG
findings are less certain and ST
segment depression may be the only
finding.
 Cardiac enzymes:
 Troponin T and I are cardiac specific.
Test on admission and at 3-6 hours.
Troponin peaks at 12-24 hours then
declines over 10 days. Troponin I is the
most sensitive and specific marker for
MI, levels rise 2-4 hours.
 Creatinine phosphokinase elevation appears 6 hours after infarction
 AST elevates 12 hours after infarction
 Lactate dehydrogenase starts elevation 24 hour after infarction
 Cardiac imaging:
 Chest X-ray: rule out other causes and check for heart failure.
 Blood investigations:
 Full blood count: decrease hemoglobin may exacerbate heart strain and
baseline Hb and PLT needed before anticoagulation
 U and Es: baseline before anticoagulants and ACEi, and screens for co-morbid
renal disease from hypertension.
 Glucose: tight control improves outcomes.
 Lipids: check on admission, as cholesterol can dip 24 hours post-MI
 Exercise tolerance test: consider in decreased risk patients.

Question 5

Causes of raised troponin

Answer 5

 Causes of raised troponin: “HEART
DIES”
o H-heart failure
o E-embolus (pulmonary)
o A-Atrial fibrillation
o R- Renal failure (due to
decreased clearance)
o T-Thrombus
o D- dissection of the aorta
o I- Inflammation (myo/pericarditis)
o E-Exercise (very strenuous)
o S-Sepsis

Question 6

Management of acute coronary syndrome

Answer 6

 General measures:
 Reassure and make the patient comfortable
 Supply oxygen by mask
 Secure IV line
 Give aspirin 160-325mg tablets- helps to prevent further
platelet aggregation. Also give P2Y12 inhibitor
(Clopidogrel, Ticagrlor or prasugrel) loading dose
 If patient is tachycardic/hypertensive beta-blockers IV
can be given (but not if unstable)
 Treatment of pain:
 Give morphine sulphate PRN: it is very effect analgesic for pain associated
with ACS. It is administered in small doses of 2-4mg IV every 5 minutes.
 Nitrates (Oral spray, sublingual tablets or IV infusion) can be added to
refractory cases. Nitroglycerin sublingual up to 3 times doses of 0.4mg should
be administered at about 5 minutes intervals for up to 3 doses.
 Anticoagulation:
 Unfractioned heparin or bivalirudin IV in those going for immediate or early
angiography. GP IIb/IIIa inhibitor IV (eptifibatide, tirofiban or abciximab) is
sometimes added as adjunctive antiplatelet but not routinely.
 Enoxaparin or fondaparinux SC for those without angiography planned
 Reperfusion with:
 Percutaneous coronary intervention (PCI) i.e. dilation of artery with balloon
catheter +/- stent placement for STEMI presenting within 12 hours of onset.
o If PCI not available within 120 minutes, consider thrombolysis
(alteplase, reteplase, or tenecteplase) and transfer to PCI center.
 Thrombolytic agents: such as Streptokinase, t-plasminogen
activator, urokinase: these drugs are given to dissolve the
occlusive thrombus and promote reperfusion of the infarct
related artery reduces mortality from MI when administered
within 6 hours of the onset of chest pain
 Contraindication: history of cerebrovascular hemorrhage,
marked hypertension, bleeding disorder
o Patients persisting beyond 12 hours are essentially managed like
NSTEMI.
 Angiography +/- revascularization within 48 hours (‘early invasive strategy).
Revascularization is usually PCI but sometimes coronary artery bypass graft
(CABG) if left main or triple vessel disease can be done for NSTEACS.
o Immediate PCI if unstable, refractory chest pain, or acute severe heart
failure
o Conservative management otherwise

Question 7

Prognosis of acute coronary syndrome

Answer 7

 Depends on 2 factors:
 Extent of coronary artery disease in terms of the number of vessels affected.
 The extent of ventricular damage: left ventricular ejection faction (especially
<40% doubles yearly mortality)

Question 8

List the complications of acute coronary syndrome

Answer 8

SHORT TERM COMPLICATIONS
ELECTRICAL
STRUCTURAL
INFLAMMATORY
LONG TERM COMPLICATIONS

Question 9

Electrical complications of acute coronary syndrome

Answer 9

 Heart block or sinus bradycardia following inferior MI (right coronary artery) as
supply to the AV and SA node is disrupted.
 Bundle branch block (Right or left bundle branch) following anterior MI (left
anterior descending artery)
 Ventricular fibrillation

Question 10

Structural complications of acute coronary syndrome

Answer 10

 Acute mitral regurgitation: may occur if the papillary muscles are affected by
infarction.
 Papillary muscle rupture
 Ventricular aneurysm: blood pools under dyskinetic, thin area of the left ventricle
walls. Causes persistent (>6 weeks) ST elevation. The infarcted myocardium may
evaginate and heal with fibrous connective tissue. It may be a source of cardiac
emboli
 Ventricular free wall rupture leading to hemopericardium
 Ventricular septal rupture. Causes pan-systolic murmur. May lead to cardiogenic
shock later

Question 11

Inflammatory complications of acute coronary syndrome

Answer 11

 Peri-infarction pericarditis
 Dressler’s syndrome: post AMI pericarditis which is believed to be autoimmune
in origin

Question 12

Management of complications of acute coronary syndrome

Answer 12

 Malignant arrhythmias:
 Cardiac defibrillation
 Prophylactic defibrillation
 Prophylactic lidocaine
 Other antiarrhythmic agent: bertyluim tosylate and procainamide
 Conduction disturbances:
 Sinus bradycardia: Atropine 2mg IV may restore conduction and restore heart
rate
 AV block: transcutaneous cardiac pacemakers
 Heart failure:
 Diuretics, salt restriction, ACE inhibitors, vasodilators. Use of digoxin is
controversial.
 Cardiogenic shock: do echocardiography to assess the ventricular function
 IV infusion of fluids to maximize left ventricular filling
 Use of vasopressors: Dobutamine, dopamine in IV infusion
 Intra-aortic balloon pumping
 Percutaneous transluminal angioplasty

Question 13

secondary prevention of acute coronary syndrome

Answer 13

 Secondary prevention
 ASA 75-150mg PO OD
 Beta blockers have short term and long term benefits for patients with AMI
o Short term benefit is they relieve pain and decrease the risk of
malignant arrhythmias
o Long term benefits: improved myocardial performance and facilitate
the healing process in post MI patients
o Metoprolol-25-200mg BD
o Atenolol 50-150mg PO OD
o Contraindications: Severe CHF, AV block
 ACE inhibitors: reduces mortality and improves long term survival post MI
by preventing cardiac remodeling which may have led to progressive heart
failure. They should be prescribed with 24 hours and maximum benefit is
achieved when they are given at higher doses than are recommended. In
patients with CHF ACE inhibitors are given indefinitely.
o Captopril: start with smaller dose 12.5mg PO day to gradually escalate
to 75mg PO BD
o Enalapril: start with 2.5mg PO daily and escalate gradually to 40mg PO
OD
 Statins. Evidence of short-term benefit is unclear, but it will be needed for
secondary prevention anyway.

Question 14

long term complication of acute coronary syndrome

Answer 14

 Myocyte death and decreased stroke volume leads to decreased heart rate and
blood pressure.
 The decreased in BP results in a sympathetic neurohumoral response and left
ventricular changes that result in heart failure.