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Unstable angina
Unstable angina

Unstable angina

Unstable angina or sometimes now as crescendo angina is the presence of myocardial ischaemia at rest or upon minimal exertion, in the absence cardiomyocyte injury or necrosis. This is the defining difference between unstable angina and NSTEMI. NSTEMI has elevated cardiac markers → implying cardiac damage. However, in unstable angina, they are normal, meaning no injury has occurred.

Pathophysiology

What occurs in unstable angina is very similar to NSTEMI, in which there is a partial occlusion due to a thrombus formation (after atherosclerotic plaque rupture). This leads to stenosis of the coronary artery → deoxygenation of the myocardium. However, in unstable angina, there is no death as it is a more transient attack.

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⚠️ Risk factors

  • Ischaemic heart disease
  • Diabetes mellitus
  • Hypertension - worsens angina symptoms as it increases afterload and thus coronary oxygen demand.
  • Metabolic syndrome - diabetes mellitus, obesity and hypertension altogether.
  • Hyperlipidaemia
  • Renal impairment - increases risk of cardiovascular events.
  • Peripheral arterial disease
  • Older age - men >45 and women >55.
  • Smoking
  • Cocaine use
  • Sedenterism
  • Family history

😷 Presentation

Any ACS should be suspected in a patient who presents with chest pain radiating to other areas (such as arms, back, or jaw) and has associated breathlessness, diaphoresis, nausea and vomiting.

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  • ⭐️ Chest pain - this is the classical, most notable symptom. It is typically on the left side of the chest and may radiate to the left arm, jaw, or back. It is described as a crushing chest pain as if there was a heavy pressure sitting on the chest. However, this presentation differs sometimes. Pain is also reported in the neck and shoulder blades or even the epigastric area. It may occur at rest or with activity. It may be constant or it may be intermittent.
  • Palpitations
  • Dizziness
  • Dyspnoea
  • Nausea and vomiting
  • Sweating (diaphoresis)

🔍 Investigations

  • FBC - look for thrombocytopenia or anaemia as NSTEMI management increases bleeding risk.
  • U&E’s & creatinine - to calculate GRACE score.
  • LFTs and coagulation profile
  • Blood glucose
  • CRP
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ECG

🥇 ECG is the first-line investigation. It is needed to distinguish between a STEMI, and NSTEMI/UA:

In unstable angina there should be no new ECG changes present.

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High-sensitivity cardiac troponin (HS-cTn):

Needs to be done within 60 minutes of any query ACS. It looks at TnT and TnI.

An acute MI is definitively confirmed by a rise and/or fall in cardiac troponin (with at least one value >99th percentile of the upper limit) with a patient that signs or symptoms of ischaemia. A rise and fall >20% with a convincing history suggests ACS diagnosis.

This upper limit varies between men and women and varies for each specific assay. They are not standardised and cannot be compared.

The troponin should be interpreted in the context of ECGs (present and prior), signs and symptoms, alternative causes, and historical levels.

At NCIC, the following guidelines are present:

  • Low HEART score and presented with pain <6 hours ago and there is high likelihood of ACS → repeat troponin after 3 hours.
  • High HEART score → repeat troponin after 6 hours.

Once we have ruled out a STEMI, we may consider NSTEMI/UA with the following investigations:

  • FBC - look for thrombocytopenia or anaemia as NSTEMI management increases bleeding risk.
  • U&E’s & creatinine - to calculate GRACE score.
  • LFTs and coagulation profile
  • Blood glucose
  • CRP

🧰 Management

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NSTEMI/unstable angina management:

Once diagnosis of NSTEMI or UA is made:

  1. Aspirin - 300mg loading dose and continue on 75mg OD lifelong.
  2. Antithrombin therapy
    1. Fondaparinux - unless patient has high risk of bleeding or is going for immediate coronary angiography.
    2. Enoxaparin - if the patient has renal impairment (creatinine >265umol/L).
  3. GRACE risk assessment - to formally assess risk of future CVS event.

GRACE risk assessment:

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It predicts 6-month mortality using:

  1. Age
  2. Heart rate and BP
  3. Cardiac function (Killip classification) and renal function (serum creatinine)
  4. Cardiac arrest on presentation
  5. ECG findings
  6. Troponin levels

It can be calculated online with a predicted risk outcome:

Predicted 6-month mortality
Risk of future CVS events
<1.5%
Lowest
1.5% - 3%
Low
3% - 6%
Intermediate
6% - 9%
High
9%
Highest

Low risk patients:

  • Conservative management without coronary angiography - this involves dual antiplatelet therapy:
    1. Aspirin
    2. Prasugrel (P2Y12 inhibitor) if they are taking an oral anticoagulant or clopidogrel if they are already taking an oral anticoagulant.

Intermediate - highest risk patients:

  • If clinically unstable:
    • Coronary angiography ± revascularisation within 72 hours
    • Dual antiplatelet therapy
    • Anticoagulant (heparin)
    • ACEI or ARB
  • If clinically stable:
    • Immediate coronary angiogrpahy + revascularisation with PCI or CABG
    • Dual antiplatelet therapy
    • Anticoagulant (heparin)
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Secondary prevention:

All 3 types of ACS need lifelong drug treatment to reduce the risk of another CVS event. This includes:

  1. Dual antiplatelet therapy - continue 75mg aspirin lifelong and stop the P2Y12 inhibitor after 1 year.
  2. Start/continue B-blocker (bisoprolol) or a non-dihydropyridine CCB (verapamil or diltiazem)
  3. Start/continue ACEI (enalapril) or ARB if the ACEI is not tolerated.
  4. Start statin (atorvostatin)
  5. Cardiac rehab - with exercise, health education, stress management and psychological + social support.