Myocardial Infarction and ACS

Question 1

What is the basic pathophysiology behind ACS?

Answer 1

Rupture of atheromatous plaque in coronary artery → thrombus formation → vessel occlusion locally or elsewhere in the heart.

Question 2

What are the three types of ACS?

Answer 2

ST elevation myocardial infarction (STEMI): ↑troponin and ST elevation on ECG. In practice, the ST elevation alone is sufficient to treat as the troponins take time to rise.
Non-ST elevation MI (NSTEMI): ↑troponin and ischaemic 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

What are the 5 types of MI, classified according to cause?

Answer 3

Type 1: atherosclerotic plaque rupture. Commonest.
Type 2: imbalance in myocardial O2 supply and demand e.g. because of anaemia, ↑heart rate, ↓BP, arterial spasm, embolism, or arrhythmia. May happen during surgery or illness.
Type 3: sudden cardiac death with ischaemic features (on ECG, angiography, or autopsy) but before troponin could be checked.
Type 4: MI during PCI.
Type 5: MI during CABG.

Question 4

What are the important clinical signs and symptoms in ACS?

Answer 4

Evaluate chest pain 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 factors: Exertion, Emotion, Eating. Relieving factors: ACS less likely if relieved by GTN <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.
Sometimes no symptoms at all: 'silent MI'.

Signs:

HR and BP may be ↑ or ↓.
Pallor
S3 or S4 heart sounds (especially in STEMI).

Question 5

How would you approach investigation of ACS?

Answer 5

ECG:

Do immediately, and if negative repeat after 20 minutes if pain continues or suspicion is high.
See ECG findings in acute coronary syndrome.

Troponin T or I:

Test on admission and at 3-6 hours. Troponin peaks at 12-24 hours, then declines over 10 days.
Values >99th centile are diagnostic of acute MI. STEMI diagnosis is initially from the ECG alone so as not to delay treatment.
Causes of ↑troponin, HEART DIES: HF, Embolus (pulmonary), AF, Renal failure (due to ↓clearance), Thrombus (acute MI), Dissection of the aorta, Inflammation (myo/pericarditis), Excercise (very strenuous), Sepsis.

Other investigations:

FBC: ↓Hb may exacerbate heart strain, and baseline Hb and PLT needed before anticoagulation.
U+E: baseline before anticoagulants and ACEi, and screens for co-morbid renal disease from HTN.
Glucose: tight control improves outcomes.
Lipids: check on admission, as cholesterol can dip 24 hours post-MI.
CXR: rule out other causes and check for HF.
Exercise tolerance test: consider in ↓risk patients.

Question 6

What is the medical management of ACS?

Answer 6

Medical therapy

Initial medical treatment:

Dual antiplatelet therapy: aspirin and P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel). Loading dose for both.
Analgesia PRN: morphine IV and/or nitrates (oral spray, sublingual tablet, or IV infusion in refractory chest pain).
Other therapies: oxygen if hypoxemic, β-blockers IV if tachycardic/hypertensive (but not if unstable).

Anticoagulation:

Unfractionated heparin or bivalirudin IV in those going for immediate or early angiography. Glycoprotein IIb/IIIa inhibitor IV (eptifibatide, tirofiban, or abciximab) is sometimes added as an adjunctive antiplatelet, but not routinely.
Enoxaparin or fondaparinux SC for those without angiography planned.

Question 7

How is reperfusion therapy approached in ACS?

Answer 7

Reperfusion

STEMI presenting within 12 hours of onset:

Immediate (within 90-120 mins) primary PCI (percutaneous coronary intervention) i.e. dilation of artery with balloon catheter ± stent placement.
If PCI not available within 120 mins, consider thrombolysis (alteplase, reteplase, or tenecteplase) and transfer to PCI centre.
Patients presenting beyond 12 hours are essentially managed like NSTEMI.

NSTEACS:

Angiography ± revascularisation within 48 hours (‘early invasive strategy’) if high risk as per TIMI or GRACE score. Revascularisation is usually PCI, but sometimes CABG if left main or triple vessel disease.
Immediate PCI if unstable, refractory chest pain, or acute severe heart failure.
Conservative management otherwise.

Question 8

What further management should be done in ACS?

Answer 8

• Start BAGS within 24 hours:
  
  • β-blocker PO e.g. metoprolol, atenolol. Started in the acute phase as it prevents recurrent ischaemia and arrhythmias. May initially be given IV (see ‘Initial medical treatment’ above).
  • ACEi, especially if ↓LVEF, but even others benefit.
  • Maintain Glucose <11 mmol/L. May require insulin infusion.
  • Statin. Evidence of short-term benefit is unclear, but it will be needed for secondary prevention anyway.
• Other issues:
  
  • Anticoagulation is usually stopped post-PCI, or continued until discharge in those managed without reperfusion. However, it is continued for 3 months in anterior MI.
  • Discharge on CVD secondary prevention medication and offer cardiac rehab.
  • Avoid NSAIDs, especially diclofenac.

Question 9

What are the short term complications of ACS?

Answer 9

• Short term complications
⅓ of MIs are fatal: 20% pre-hospital, and a further 10% within 30 days.
Electrical:
  
  • Heart block or sinus bradycardia following inferior MI (right coronary artery) as supply to the AV and SA node is disrupted.
  • Bundle branch block following anterior MI (left anterior descending artery).
  • Ventricular fibrillation.
• Structural:
  
  • Acute mitral regurgitation.
  • Papillary muscle rupture.
  • Ventricular free wall rupture leading to haemopericardium.
  • Ventricular septal rupture. Causes pan-systolic murmur. May lead to cardiogenic shock days later.
  • Ventricular aneurysm: blood pools under dyskinetic, thin area of LV wall. Causes persistent (>6 weeks) ST elevation.
• Inflammatory:
  
  • Peri-infarction pericarditis.
  • Dressler’s syndrome: pericarditis weeks later.

Question 10

What are the long term complications of ACS?

Answer 10

Long term complications
Myocyte death + ↓stroke volume → ↓HR + ↓BP → sympathetic neurohumoral response + LV changes → HF.

Question 11

How is risk calculated in ACS?

Answer 11

• Risk calculation
  
  • The 10 year risk of MI or stroke can be quantified using CVD risk calculators such as QRISK2 (if age <85) or the Framingham risk equation.
  • This is appropriate for people with intermediate risk and without previous CVD events, but less useful for people with major risk factors (e.g. severe dyslipidaemia).
  • Those with previous CVD (MI, stroke, PVD) automatically have a 10 year risk >30%.

Question 12

What lifestyle strategies should be employed to reduce cardiovacular risk?

Answer 12

• Lifestyle
  
  • Weight loss and dietary change. The Mediterranean diet (fruit, veg, vegetable oil, fish) has the most evidence for CVD prevention. Also recommend reducing sugar intake and replacing starch with wholegrains.
  • Physical activity: 150 minutes/week moderate activity.
  • Smoking cessation.
  • Reduce alcohol intake: ≤14 units/week

Question 13

What medical therapies are employed to modify risk factors?

Answer 13


Involves modifying risk factors, namely hypertension, dyslipidaemia, and diabetes.


Secondary prevention post-ACS
 Block An ACS:

* β-blocker.
* ACE inhibitor, aiming for BP of 140/90.
* Aspirin for life.
* Clopidogrel or ticagrelor for 1 year after an ACS.
* Statin: high dose e.g. atorvastatin 80 mg.

Question 14

Which ECG changes might you expect to see in a STEMI over time?

Answer 14

• STEMI

  Changes over time:
  
  • Acute: peaked T waves (<5 mins) then ST elevation (<20 minutes). Resolve in hours to days. ST elevation (STE) at the J point (end of QRS) must be in ≥2 consecutive leads, ≥1 mm in all leads except V2-3, where it must be ≥1.5 mm in women, ≥2 mm in men ≥40 years, and ≥2.5 mm in men <40 years.
  • Within days: Q waves then T wave inversion. Occasionally, transient Q waves appear much earlier.
  • Long-term: Q waves, ST changes.

Question 15

What are other causes of ST elevation?

Answer 15

• Other causes of ST elevation:
  
  • Benign early repolarisation (BER, aka high take off): concave up (saddle) ST elevation <2mm high (at J point).
  • Pericarditis: diffuse, concave up ST elevation. Myocarditis: similar to pericarditis, though sometimes ST elevation may be localised and mimic STEMI.
  • LVH: LV strain pattern causing ST elevation in V1-3.
  • Aortic dissection: can cause MI if it extends proximally to the coronary ostia, the holes in the aortic valve which supply the coronary arteries. Do not thrombolyse, as there is a risk of cardiac tamponade.
  • LBBB and RBBB.
  • PE
  • Brugada syndrome: coved (type 1) or saddle (type 2) ST elevation in V1-3, with T wave inversion.
  • Hyperkalaemia

Question 16

What ECG changes might you expect to see in a NSTEACS?

Answer 16

• NSTEACS
  
  • ST depression and/or T-wave inversion.
  • Note that T-wave inversion is normal in aVR, where it is concordant with the QRS complex (dominant S waves). In children they are also seen in V1 and V2, and their persistence in adulthood is the non-pathological ‘persistent juvenile T-wave pattern’.
  • Unlike in STEMI, difficult to localise lesion based on ECG.