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Acute Coronary Syndrome

 Definition: a spectrum of clinical presentations:


o Unstable angina: angina of recent onset (<2 months), worsening or angina at rest.
o Non ST elevation myocardial infarction: incomplete occlusion of coronary vessels
leading to ischemia and mild necrosis of myocardium (Troponin-I raised only)
o ST elevation myocardial infarction: complete occlusion of coronary vessels leading to
necrosis of the myocardium
 Epidemiology: Leading cause of death in Ireland, 1,200,000 cases / year in the US, more
common in males, age of onset 50-60.
 Aetiology:
o Atherosclerosis of the coronary vessels
 Risk factors:
o Non-modifiable: male, family history, age, ACE gene polymorphism
o Modifiable: smoking, hypertension, hyperlipidemia, diabetes mellitus, obesity,
sedentary lifestyle, high F-VII & fibrin, cocaine use, alcoholism, COX-2 inhibitors,
hyperinsulinism, lipoprotein(A), OCP
 Pathology
o Formation of atheroma in the coronary vessels:
 Following insult to the vascular endothelium platelets aggragate and lipids,
scavenger cells (macrophages) move to the injured site and start ingesting
the lipid until they become foam cells.
 There is also migration of muscle cells to the endothelium and hyperplasia
 A fibrous cap is formed by fibroblasts at the endothelium
o The major trigger for coronary thrombosis is considered to be plaque rupture caused
by the dissolution of the fibrous cap due to the release of metalloproteinases
(collagenases) from activated inflammatory cells. This event is followed by platelet
activation and aggregation, activation of the coagulation pathway, and
vasoconstriction. This process culminates in coronary intraluminal thrombosis and
variable degrees of vascular occlusion
 History & Exam
o Central crushing chest pain, that may radiate to the arm, neck or jaw, brought on by
exercise, cold weather, following a big meal, or stress.
o The pain is associated with nausea +/- vomiting, diaphoresis, pallor, syncope or pre-
syncope, palpitations and dyspnoea.
o On examination:
 Tachycardia, tachypnoea, hypo/hypertension, pallor, anxiety, signs of left or
right heart failure, a 4th heart sound, pansystolic murmur.
 Investigations: the diagnosis is clinical
o Bloods:
 FBC  haemoglobin (anaemia?), leucocytosis (infection?)
 U&E  electrolyte disturbances establish a baseline for the patient and
assess their renal function.
 LFTs  deranged in case of right heart failure.
 Coags  bleeding disorder, this patient may undergo thrombolysis.
 Glucose  Diabetes mellitus, hypoglycaemia/hyperglycaemia
 Fasting serum lipids  hyperlipidemia
 BNP  heart failure??
 Cardiac enzymes:
 Troponin-I: highly sensitive and specific for myocardial muscle
injury, elevated in STEMI and non-STEMI. Rises 8 hours after the MI
and peaks at 2-3 days, disappears from serum after 10 days.
 CK-MB: cardiac creatine kinase, rises after 6 hours of MI, peaks after
1-2 days.
 LDH: rises after 2 days of MI, returns to normal after 10 days
 AST: rises after 1 day of MI, peaks after 2 days of MI, and normalises
at the 3rd day.



Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level after
infarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set at
the myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic

o ECG:
 Unstable angina: Normal, there may be ST Depression/T wave inversion
 Non-STEMI: ST depression/T wave inversion
 STEMI:
 ST elevation for >1mm in 2 contiguous chest leads
 New onset LBBB
o Imaging:
 CXR: Cardiomegaly?
 ECHO: assessment of valves and EF? (heart failure)
 Cardiac perfusion scintiography(assessment of a perfusion of the
myocardium looking at areas that are under perfused
o Invasive:
 Angiogram: the gold standard to diagnose coronary artery disease, can be
therapeutic as well.
 Management
o Advice patient regarding losing weight, stopping smoking, low fat diet, exercise (30
minutes every day), good control of DM,
o Acute management: (MONA BAH)
 Oxygen (2-4L) as 70% of ACS patients is hypoxemic.
 Morphine 2.5-5 mg IV + Metoclopramide 10mg IV (analgesia and antiemetic)
 GTN spray sublingual 2 puffs (vasodilator)
 Aspirin 300mg PO chewable (anti-platelet) + Clopidogrel 300mg PO (inhibits
platelet aggregation)
 Atenolol 5mg IV for 15 minutes (beta blocker)
 Ramipril 2.5-10 mg PO (ACEI for thrombus remodelling)
 Atorvastatin 80mg PO (HMG-CoA inhibitor for thrombus remodelling and
hyperlipidemia)
o If the patient has non-STEMI [Add] (since there is a thrombus that is incompletely
occluding; want to prevent further formation of thrombus):
 Enoxaparin (antithrombin; LMWH) 1mg/kg SC BD
 Tirofiban (GP IIIa/IIb antagonist, prevents aggragation) 0.4mg/kg/min IV for
30 mins then 0.1mg/kg/min IV for 48-108 hours
o If the patient has STEMI [treatment as above +] thrombolyse the patient
 Indicated in:
 Symptoms of ischemia
 Symptoms are within the last 12 hours
 New LBBB
 ST elevation in 2 contiguous chest leads >1mm
 Contraindications
 History of intracranial haemorrhage
 Known structural cerebral vascular lesion (AV Malformation)
 Intracranial malignancy
 Ischemic stroke within the last 3 months (but not within 3 hours)
 Suspected aortic dissection
 Active bleeding or bleeding diathesis
 Significant head trauma within the last 3 months.
 Relative contraindications:
 Poorly controlled chronic severe hypertension
 Severely uncontrolled hypertension on presentation (>180 SBP,
>110 DBP)
 Recent internal bleeding (2-4 weeks)
 Pregnancy
 Active peptic ulcer
 Use of anticoagulants (high INR  high risk of bleed)
 Major surgery within the last 3 weeks or trauma
 Ischemic stroke more than 3 months ago/ dementia
 Noncompressible vascular punctures
 Allergy (more than 5 days ago) to altepase/streptokinase.
 Altepase (tissue-Plasminogen activator) 15mg IV stat, then 50mg IV for 30
minutes, then 35mg IV for 1 hour
o PCI or Fibrinolysis:
 Fibrinolysis preferred if:
 <3 hours from onset
 PCI not available/delayed
 door to balloon > 90min
 door to balloon minus door to needle > 1hr
 Door to needle goal <30min
 No contraindications
 PCI preferred if:
 PCI available
 Door to balloon < 90min
 Door to balloon minus door to needle < 1hr
 Fibrinolysis contraindications
 Late Presentation > 3 hr
 High risk STEMI
 Killup 3 or higher
 STEMI dx in doubt
o Percutaneous intervention (PCI) (AKA cardiac catheterisation)
 Indicated in:
 Identification of the extent and severity of coronary artery disease
 Assessment of valvular or cardiomyopathies
 Confirming the diagnosis of ACS
 Contraindicated:
 Severe uncontrolled hypertension
 Ventricular arrhythmias
 Acute stroke
 Severe anemia
 Active gastrointestinal bleeding
 Allergy to radiographic contrast
 Acute renal failure
 Uncompensated congestive failure (patient cannot lie flat)
 Unexplained febrile illness and/or untreated active infection
 Electrolyte abnormalities (eg, hypokalemia)
 Severe coagulopathy
 Method: done under local anaesthesia
 Arterial access from the upper extremity (modified Sones method)
using sones catheter from the brachial, radial or axillary arteries
 Lower extremity (femoral artery) using Judkins technique:
o Advantages: ease of access and safety of procedure
o Disadvantages: Vascular injury if puncture was done higher
or lower than the common femoral artery and the need for
extended bed rest after the procedure (2-6 hours)
 Complications:
 Intra-procedural: hypotension, heart failure, chest pain and
arrhythmias
 Major complications: death 0.08%, MI less than 0.03%, stroke
0.06%, infection (0.06%, 0.6% in upper extremity approach), Renal
dysfunction (due to contrast; 5%  1% long term dialysis),
arrhythmias
 Bleeding from vessels at puncture site, most common complication:
bleeding into the retroperitoneal space (unexplained hypotension
and decreasing haematocrit) do Abdominal USS and then CT to
confirm. Also pseudoaneurysm (connection between haematoma
and the lumen  pulsatile mass with systolic bruit). AV formation.
o In summary:

o
o

o
 Complications:
o Arrhythmias, Heart failure, papillary muscle rupture, valvular dysfunction,
myocardial rupture, mural thrombi, PE, Stroke, death
 Prognosis:
o 38% die within a year of presentation