CARDIOLOGY

Acute Coronary Syndrome

Classification
Acute coronary syndrome (ACS) describes a group of clinical conditions, all of which usually present with
chest pain or discomfort resulting from myocardial ischemia:

 ST- segment elevation myocardial infarction (STEMI)

o ST-segment elevation or new left bundle branch block (LBBB) present on ECG
 Non-ST segment elevation acute coronary syndrome
o Non-ST segment elevation myocardial infraction (NSTEMI)
 Other ECG changes (e.g.: ST-segment depression, T wave inversion) or normal
ECG with troponin release present.
o unstable angina (UA)
 Other ECG changes or normal ECG with troponin consistently negative

Pathophysiology
In most cases this results from coronary artery disease and is initiated by the rapture or erosion of an
atherosclerotic plaque within a coronary artery causing:

 Acute thrombosis within the vessel lumen, often with hemorrhagic extension in the
atherosclerotic plaque
 Construction of smooth muscle cells within the artery wall resulting in veso construction that
reduces the lumen of the artery.
 Associated partial complete obstruction of the lumen, often with embolism of thrombus into the
distal part of the vessel.

This process results in a sudden and critical reduction in blood flow to the myocardium.

Risk factors
 Family history of atherosclerosis  Hypertension
 Old age  Hyperlipidemia
 Male gender  Sedentary Lifestyle
 Smoking  Obesity
 Diabetes mellitus

Clinical features
Determine whether chest pain is likely to be cardiac in origin by considering:

 the history of the chest pain

 the presence of cardiovascular factors
 any history of ischemic heart disease and any previous treatment
  any previous investigations for chest pain

Initial assess people for any of the following symptoms, which may indicate and acute coronary
syndrome:

 pain in the chest or other areas (for example the arms, back, or Jaw) lasting longer than 15
minutes.
 chest pains in associated with nausea and vomiting, market sweating, breathlessness or
combination of these
 chests pain associated with hemodynamic instability.
 new onset chest pain or abrupt deterioration in previously stable angina; with recurrent chest
pain occurring frequently and with little no exertion, and with episodes lasting longer than 15
minutes.
 do not use people response to GTN to make diagnosis.

N.B some patient groups (e.g.: elderly people, people with diabetes, females, people with renal disease,
and people during perioperative period) are more likely to develop ACS with little or no chest
discomfort; In such people, the dominant symptoms maybe breathlessness.

History Likelihood History Likelihood

Ratio Ratio

Increased Likelihood Decreased Likelihood

Radiation to right arm/shoulder 4.7 Described as pleuritic 0.2

Radiation to both arm/shoulder 4.1 Described as positional 0.3

Associated with exertion 2.4 Described as sharp 0.3

Radiation to left arm 2.3 Reproducible with palpation 0.3

Associated with diaphoresis 2 Inframammary location 0.8

Associated with nausea/vomiting 1.9 Not associated with exertion 0.8

Worse than previous angina 1.8

Describes as pressure 1.3

Investigations
 12-lead ECG
o Do not exclude and acute coronary syndrome when people have a normal resting 12-
lead ECG
o Ischemic ECG findings:
 Regional ST-segment elevation (2mm ST-elevation in two contagious chest leads
or 1mm ST-elevation in two contiguous limb leads)
 New onset left bundle branch block (LBBB)
 Regional ST-segment depression (>0.5mm) or deep T wave inversion (>2mm
deep)
 Pathological Q waves
  Serum troponin (I or T)
o Use validated tool to risk stratified patients at initial assessment for likelihood of acute
Myocardial Infarction (AMI)
o For people at high or moderate risk of AMI: 8
 Perform high sensitivity troponin test as recommended
 When interpreting high sensitivity troponin measurements take in to account:
 the clinical presentation
 the time from onset of symptoms
 the resting 12-lead ECG findings
 the pre-test probability of NSTEMI
 the length of time since the suspected acute coronary syndrome
 the probability of chronically elevated troponin levels in some people
 the 99th percentile threshold troponin I and T may differ between sexes
o For people at low risk of AMI:
 Perform a second high-sensitivity troponin test as recommended if the first
troponin test at presentation is positive.
 Consider performing a single high sensitivity troponin test only at presentation
to rule out NASTEMI if the first troponin test is below the lower limit of
detection (negative)
o N. B. Older standard troponin assays were taken at initial assessment and 10 to 12 hours
after onset of symptoms.
 Chest radiograph
o May diagnose complications of myocardial infarction such as pulmonary oedema, or
exclude alternative diagnosis such as pneumothorax or pneumonia
 Echocardiography
o Lift ventricular (LV) systolic function is directly related to prognosis, and in a person with
acute chest pain, regional wall abnormalities increase the likely hood ASC.
o May allow prompt diagnosis of other conditions e.g.: cardiomyopathies, valve disease,
pericardial disease, aortic dissection and pulmonary embolism
o Can confirm or exclude right ventricular (RV) dilatation and impairment when extensive
right ventricular infection is suspected
o Can be used to diagnose complications of AMI such as ventricular septal defect and
severe mitral regurgitation which may require urgent surgical correction.

Diagnosis
A diagnosis of acute Myocardial Infarction is defined as the detection of the rise and/or fall of cardiac
biomarkers (preferably troponin) with at least 1 value about the 99th percentile of the upper reference
limit, together with evidence of myocardial ischemia with at least one of the following:

 Symptoms of ischemia
 ECG changes indicative of ischemia (new ST-segment or T wave changes or new LBBB)
 Development of pathological Q waves in the ECG
 Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
 Identification of an intracoronary thrombus by angiography
When a raised troponin level is detected in people with a suspected acute coronary syndrome, reassess
to exclude other causes for raised troponin (for example myocarditis, aortic dissection, or pulmonary
embolism) before confirming the diagnosis of acute coronary syndrome.

Localization of lesion in STEMI

The ECG provides some information about the site and extent of myocardial damage in acute
Myocardial infraction, particularly in STEMI, The ECG changes that may occur in NSTEMI are less clearly
related to the site of myocardial damage than the changes in STEMI.

 A septal infarct show changes in the V1-V2 leads, and typically involves the left anterior
descending artery.
 An anterior infarct shows changes in the V3 - V4 leads, and typically involves the left anterior
descending artery.
 A lateral infarct shows changes in leads V5 - V6, I, aVL and typically involves left circumflex
artery or diagonal branch of the left anterior descending artery.
 An anteroseptal infarct shows changes in leads the V1 - V4 and typically involves the left anterior
descending artery
 An anterolateral infarct shows changes in lead I, aVL, V3 -V6 (and reciprocal changes in leads II,
III, aVF) and typically involves the left anterior descending or the left circumflex artery.
 And inferior infarct show changes in leads II, III, aVF (and reciprocal changes in leads I, aVL) and
typically involves the right coronary artery.
 A posterior infarct shows reciprocal changes in lead V1-V3 and requires placement of posterior
leads (V7 - V9) to identify ST-elevation - it typically involves the right coronary artery or the left
circumflex artery.

Affected myocardia area Leads with ST-segment Occluded coronary artery

elevation

Septal V1 - V2 Proximal LAD

Anterior V3 - V4 LAD

Lateral V5 - V6, I, aVL LCX

Anteroseptal V1 - V4 LAD

Anterolateral V3 - V6, I, aVL (R: II, III, aVF) LAD or LCX

inferior II, III, aVF (R: I, aVL) RCA

Posterior/Posterolateral R: V1 - V3 (P: V7- V9) RCA or LCX

* RCA = right coronary artery, LAD = lift anterior descending coronary artery, LCX = left circumflex
coronary artery, R = reciprocal ST-depression, P = posterior leads

Immediate management of ACS

Immediate treatment for ACS comprises:

 Aspirin 300mg orally, crushed or chewed (unless there is clear evidence of allergy)
  Sublingual glyceryl trinitrate, spray or Tablet (unless the patient is hypotensive)
 Oxygen is the patient is hypoxic (sats < 94%), AIMS for saturation of 94 - 98% (unless COPD)
 Analgesia with IV opioid, titrated to control symptoms while avoiding sedation or respiratory
depression, and given with an antiemetic

Management of STEMI
 Coronary reperfusion therapy
o Immediately assess eligibility (irrespective of age, ethnicity or sex) for coronary
reperfusion therapy and eligible, deliver coronary reperfusion therapy as quickly as
possible
o Presentation within 12 hours:
 offer coronary angiography, with follow on primary percutaneous intervention
(PCI) if indicated, as the preferred coronary reperfusion strategy for people with
acute STEMI if presentation is within 12 hours of onset of symptoms and
primary PCI can be delivered within 120 minutes of the time when fibrinolysis
could have been given.
 offer fibrinolysis to people with acute STEMI presenting within 12 hrs of onset of
symptoms if primary PCI cannot be delivered within 120 min of the time when
fibrinolysis could have been given.
o Presentation beyond 12 hours:
 Consider coronary angiography, with follow on primary PCI if indicated, for
people with acute STEMI presenting more than 12 hours after the onset of
symptoms, if there is evidence of continuing myocardial ischemia or of
cardiogenic shock

Primary percutaneous coronary intervention

 In addition to aspirin, all patient should be given one of the platelet ADP receptor blockers prior
to PCI using a loading dose (clopidogrel, presugrel, ticagrelor)
 Anticoagulation with unaffectionate low molecular weight heparin is given in the catheter
laboratory and in high-risk cases a glycoprotein IIb/IIIa inhibitor may also be given. Bivalirudin, a
direct thrombin inhibitor may be chosen as an alternative to heparin therapy.

Fibrinolytic therapy

 Additional antithrombin therapy must be given to minimize the risk of further thrombotic
occlusion. In addition to aspirin, all patient should be given a loading dose of clopidogrel and
antithrombin therapy using unfractionated low molecular weight heparin.
 An ECG should be recorded 60 - 90 minutes after administration of fibrinolysis. For those who
have residual ST-segment elevation suggesting failed coronary reperfusion offer immediate
coronary angiography, with follow-on PCI if indicated and do not repeat fibrinolytic therapy.
 If a person has recurrent myocardial ischemia after fibrinolysis, seek immediate specialist
cardiological advice and, if appropriate, offer coronary angiography, with follow on PCI if
indicated.
 Consider coronary angiography during the same Hospital admission for people who are clinical
stable after successful fibrinolysis.

Management of NSTEMI/UA
  Initial drug treatment
o Aspirin
 Offer aspirin as soon as possible to all patients (initial loading dose 300mg) and
continue indefinitely (75mg daily) unless contraindicated by bleeding risk or
aspirin hypersensitivity.
o Antithrombin therapy
 Offer fondaparinux to patients who do not have high bleeding risk, unless
coronary angiography is planned within 24 hours of admission.
 Offer unfractionated heparin as an alternative to fondaparinux to patients who
are likely to undergo coronary angiography within 24 hours of admission or in
renal impairment.
 Further drug treatment
o As soon as the diagnosis of unstable angina or NSTEMI is made, and aspirin and
antithrombin therapy have been offered, formally assess individual risk of future
adverse cardiovascular events using an established risk scoring system that predicts 6
months mortality. (For example, GRACE).
o Clopidogrel
 Offer a loading dose of 300mg clopidogrel in addition to Aspirin to patients with
a predicted 6 months mortality of more than 1.5% and no contraindications (for
example, an excessive bleeding risk).
 Offer a 300mg loading dose of clopidogrel all patients with no contraindications
who may undergo PCI within 24 hours of admission to hospital.
 Offer clopidogrel as a treatment option for up to 12 months to people who have
had an NSTEMI, regardless of treatment.
 ADP receptor blocker alternative to clopidogrel include presugrel or ticagrelor.
o Glycoprotein inhibitors
 Consider intravenous eptifibatide or tirofiban as part of the early management
for patient who have and intermediate higher risk of adverse cardiovascular
events (predicted 6 months mortality above 3%, and who are scheduled to
undergo angiography within 96 hours of hospital admission.
 Coronary angiography
o Offer conservative management without early coronary angiography to patients with a
low risk of adverse cardiovascular events (predicted 6-months mortality 3.0% or less)
o Offer coronary angiography (with follow-on PCI if indicated) to patients initially assessed
to be at low risk of adverse cardiovascular events (predicted 6-months mortality 3% or
less) if ischemia is subsequently experienced or is demonstrated by ischemia testing.
o Offer coronary angiography (with follow-on PCI if indicated) within 96 hours of first
admission to hospital to patients who have an intermediate or higher risk of adverse
cardiovascular events (predicted 6-month mortality above 3%) if they have no
contraindications to angiography (such as active bleeding or comorbidity). Perform
angiography as soon as possible for patients who are clinically unstable or at high
ischemic risk.

Secondary Prevention
 Antithrombotic therapy
o Low dose (75mg) aspirin daily for life
 o Clopidogrel 75mg daily/presugrel 10mg daily/ticagrelor 90 mg daily for 1 yr for patients
with high-risk ACS and all those undergo PCI.
 Preservation of left ventricular function
o Treatment after AMI with ACS inhibitor can reduce the remodeling that contribute to
left ventricular dilatation and impairment; the use of ACEI therapy in adequate dose can
reduce the risk and severity of subsequent heart failure and the risk of future MI.
 Beta-adrenoceptor blockade
o Treatment with a beta-blocker, started early after AMI and continued, has been shown
to reduce mortality
 Reduction of cholesterol
o Statins reduce future coronary events by at least 30%: a low-fat fiber diet and regular
exercise will complement cholesterol suppression by drugs.
 Antihypertensive therapy
o Effective control of raised blood pressure reduces the risk of stroke, heart failure and
future coronary events.
 Smoking cessation