Acute Coronary Syndrome

I remember when I was a little first year wannabe doctor and I would stumble trying to say myocardial infarction, and once I learnt it, I always said myocardial infarction in full, just to sound smart, and now I have to consciously make an effort to not say MI when speaking with patients. And Cabbage (CABG)- patients do not want to hear about vegetables.

Acute Coronary Syndrome (ACS)

Definition: ACS includes unstable angina and evolving myocardial infarction, both ST-elevation MI (STEMI) and non ST-elevation MI (NSTEMI). These come under the umbrella term of Ischaemic Heart Disease (IHD), resulting from decreased blood supply to the heart muscle, alongside stable angina. MI refers to cardiac muscle necrosis resulting from ischaemia.

Aetiology/ risk factors:

-Unstable angina and MI share a common pathology- atheromatous plaque rupture, thrombosis and inflammation- with variable degree of irreversible myocyte death in MI.

-ACS may rarely be due to emboli or coronary spasm in normal coronary arteries, or vasculitis

Risk factors:

Non-modifiable- age, male gender, family Hx of IHD (MI in 1st degree relative < 55 years)

Modifiable- smoking, hypertension, diabetes, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use

Controversial risk factors– stress, type A personality, left ventricular hypertrophy, increased fibrinogen, hyperinsulinaemia, raised homocysteine levels, ACE genotype.

Epidemiology: STEMI- 5/1000/year (UK)

Declining in UK and US


-Acute central chest pain, lasting > 20 minutes (‘crushing/ gripping/ tight’)

-Chest pain radiates to arms (usually left), neck, jaw or epigastrium

-Associated nausea, sweatiness, breathlessness, palpitations

-May present without chest pain (silent infarct), especially in diabetics and elderly

Silent MI presentation may include: syncope (blackout), pulmonary oedema, epigastric pain and vomiting, post-operative hypotension or oliguria, acute confusional state, stroke and diabetic hyperglycaemic states.


-Distress, anxiety

-Pallor, sweatiness

-Pulse and BP may be increased or decreased (check both radial pulses for aortic dissection)

4th heart sound

-May be signs of heart failure (as a complication): raised JVP, 3rd heart sound, basal crepitations

-Cardiogenic shock (complication): hypotension, cold peripheries, oliguria

-May have a pansystolic murmur (papillary muscle dysfunction/rupture, VSD)

-Low-grade fever may be present

-Pericardial friction rum or peripheral oedema- may develop later




ST Elevation = elevation >  1mm in 2 or more limb leads or > 2 mm in 2 or more chest leads.

New left bundle branch block (LBBB) in the context of this acute presentation is also considered as the equivalent of an acute STEMI and is treated as such.

Classical changes

1Image result for ecg evolution in stemiTented T waves in affected leads within minutes of occlusion (localised hyperkalaemia following myocyte ischaemia)

2- ST elevation in affected leads, with ST depression in the reciprocal leads within hours, lasting 24-48h.

3-T wave inversion, developing in 1-2 days and persisting for weeks or months unless the MI is treated

4- Pathological Q waves developing within days and remaining permanently.

Leads affected reflect the site of infarct:

Inferior infarct (Right Coronary Artery): II, III, aVF

Anteroseptal infarct (LAD artery): V1-V4

Lateral infarct (Circumflex/LAD arteries): V5-V6, I, aVL

Posterior infarct (Circumflex artery): deep ST depression in V1-3 with tall R waves

(Posterior infarct can be difficult to distinguish from LAD territory ischaemia- ST depression- so look for a dominant R wave in V1 and inferior lead ST elevation in infarction. A true posterior MI counts as a STEMI).

NSTEMI or Unstable angina– can present with ST depression, T wave inversion, non-specific changes or normal ECG.

⇒In 20% of MI, the ECG may be normal initially.

-Cardiac enzymes:

Cardiac troponin levels are the most sensitive and specific markers of myocardial necrosis (cell death) and is most used clinically. Serum levels are elevated within 3-12 hours from the onset of chest pain, peak at 24-48h, and return to baseline over 5-14 days. Will be raised in STEMI and NSTEMI but normal in unstable angina (= not enough ischaemia to cause sufficient necrosis to raise troponin).

Creatine kinase (CK-MB) levels rise within 3-12 hours of onset of chest pain, reach peak values within 24h and return to baseline after 48-72h. Levels peak earlier if reperfusion occurs. Can be useful in identifying a re-infarction because troponin may still not have returned to baseline. (Sensitivity ~95%, high specificity).

Myoglobin levels rise within 1-4h from pain onset. Highly sensitive but not specific.

Bloods- FBC, U&Es, glucose, lipids

CXR: look for cardiomegaly, pulmonary oedema (heart failure) or widened mediastinum (aortic rupture). Don’t delay treatment for a CXR.


Pre-hospital– arrange ambulance.

                     Aspirin 300mg

                     GTN sublingual

                     Analgesia e.g. morphine 5-10mg IV+ metoclopramide (anti-emetic) 10mg IV

In hospital- O2 ( if sats < 95%, patient breathless or in acute left ventricular failure)

                       IV fluids


                       Aspirin + clopidogrel

This can be summarised by the mnemonic: MONA

Morphine + metoclopramide



Antiplatelets: aspirin + clopidogrel

-At some point from ambulance to hospital, an ECG will  be performed.



Primary Percutaneous Coronary Intervention (PCI) if available, or fibrinolysis, if no contraindication = definitive treatment

PCI is performed if it can be made available within 120 minutes of first medical contact. Otherwise, the patient is given fibrinolysis because time is of the essence. They can then be transferred to a primary PCI centre after the infusion for rescue PCI (if fibrinolysis unsuccessful) or angiography if successful. 

Injectable anticoagulant must be used in PCI-Bivalirudin (Direct Thrombin Inhibitor), and if not available- enoxaparin (LMWH) +/- GPIIB/IIIa antagonist (e.g. Tirofiban).

Fibrinolysis target time is < 30 min from admission and it is contraindicated > 24h from symptom onset.  Alteplase is given, followed by an unfractionated heparin infusion.

Fondaparinux (enoxaparin/unfractionated heparin if not available)- for STEMI patients that do not receive reperfusion.

Beta-blocker e.g. atenolol 5mg IV (if tachycardic or hypertensive and no signs of heart failure. CI in asthma.)

ACE inhibitor e.g. Lisinopril 2.5mg. Consider in all normotensive patients within 24h of acute MI.  -if not already given

Aspirin (300 mg)+ Clopidogrel (300m) -if not already given

If NSTEMI or Unstable Angina:

Patients are managed medically until symptoms settle, unless high risk. They are then investigated by angiography with a view to possible PCI or surgery (Coronary Artery Bypass Graft- CABG)

Aspirin (300 mg)+ Clopidogrel (300mg) -if not already given

Beta-blocker e.g. atenolol 5mg IV

-Nitrates IV or PO for recurrent chest pain.

Antithrombotic fondaparinux- if low bleeding risk and no angiography planned for 24h, otherwise consider LMWH (e.g. enoxaparin 1mg/kg/12h sc for 2-8d)- until discharge.

NSTEMI patients are candidates for immediate PCI if they are haemodynamically unstable, have severe left ventricular dysfunction, ongoing chest pain despite maximal medical management, new mitral regurgitation or ventricular septal defect or sustained ventricular arrhythmias. NSTEMI patients should not be given fibrinolysis.

-For more stable patients, assess risk  e.g. GRACE SCORE

High risk: persistent or recurrent ischaemia, ST depression, diabetes, raised troponin (elevated troponin = NSTEMI)

GPIIB/IIIa antagonist (e.g. Tirofiban– antiplatelet) or bivalirudin (Direct Thrombin Inhibitor) + coronary angiography  within 96h (image coronary vessels) + clopidogrel for up to 12 months (in addition to aspirin).

Low risk: no further pain, flat or inverted T waves, or normal ECG, and negative troponin (-ve troponin = unstable angina)

Clopidogrel if risk 1.5-3%/yr. Discharge if a repeat troponin is negative. Treat medically and arrange further investigation if recurrent ischaemia.

Coronary Artery Bypass Graft (CABG)

Performed in left main stem disease, multi-vessel disease, multiple severe stenoses, patients unsuitable for angioplasty (PCI), failed angioplasty, refractory angina.

Subsequent management:

-Bedrest for 28h with continuous ECG monitoring

-Daily examination for complications, 12 lead ECG, U&Es

-Thromboembolism prophylaxis (LMWH) until fully mobile- consider 3 month warfarin if large anterior MI to prevent LV mural thromboembolism

Aspirin– low dose aspirin for life (e.g. 75 mg/d) to decrease vascular events (MI, stroke) + Clopidogrel for 12 months (75 mg/d)

-Long term beta-blocker (e.g. bisoprolol 2.5-5 mg/d). Consider calcium channel blocker- verapamil or diltiazem– if contraindicated.

-Continue ACE inhibitor.

-Start a statin, e.g. simvastatin 40mg.

-Address modifiable factors- smoking cessation, exercise, treat diabetes, hypertension and hyperlipidaemia.

-Assess left ventricular function in all patients post-MI (echo).

If uncomplicated, discharge after 5-7 days. Refer for structured rehabilitation programme. Review e.g. at 5 weeks and 3 months.

-Encourage diet high in oily fish, fruit, vegetable and fibre and low in saturated fats, and regular exercise. Avoid sex for 1 month and air travel and return to work for 2 months

This can be summarised further by the mnemonic: MONABASH

Morphine + metoclopramide



Antiplatelets: aspirin + clopidogrel


ACE inhibitor


Heparin (LMWH) or similar mechanism drug such as Fondaparinux.


MI complications

-Recurrent ischaemia or failure to reperfuse  (detected as persisting pain and ST segment elevation immediately after thrombolysis)- not uncommon so all STEMI patients should be transferred to PCI centre for ongoing management


Cardiac arrest

-Cardiogenic shock

-Unstable angina

-Left ventricular hypertrophy

-Bradycardias, heart block

-Tachyarrhythmias- AF, Atrial Flutter, SVT, non-sustained VT, sustained VT, VF. Ventricular arrhythmias can also occur 1-3 weeks post-MI.

-Right ventricular failure-presents with low cardiac output and raised JVP

-Pericarditis-presents 2-4 days after MI (simple post-MI pericarditis)

-Dressler’s syndrome = autoimmune pericarditis 2-10 weeks after MI

-DVT & PE-so, LMWH (enoxaparin) until fully mobilised

-Systemic embolism- may arise from left ventricular mural thrombus

-Cardiac tamponade

-Mitral regurgitation

-Ventricular septal defects

-Left ventricular aneurysm- this occurs late (4-6 weeks post-MI)

WOW! Lesson- don’t have a heart attack.

Can be summarised by DARTH VADER, whom I recently was shocked and saddened to learn is the little boy at the start of the movie who enters the space race, turned evil (that’s the only scene I’ve ever watched of Star Wars, and I’ve seen it a couple of times).



Rupture (of septum or outer wall)


Heart failure

Valve disease


Dressler’s syndrome and other pericarditis



Prognosis: 50% of deaths occur within 2h or onset of symptoms. Up to 7% due before discharge.

Worse prognosis if elderly, LV failure, and ST changes.

References: Cheese & Onion, Oxford Cases in Medicine and Surgery, Rapid Medicine



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