- Chest Pain Characteristics
- The 12-Lead ECG
- Plasma Troponin
- Risk Assessment in NSTE-ACS
- Treatment of Confirmed or Suspected NSTE-ACS
- Assessment of Bleeding Risk
- Anticoagulation
- Invasive Coronary Angiography
- Non-Invasive Assessment
- NSTE-ACS with Normal Coronary Arteries
The initial assessment of acute chest pain is dominated by the ECG. If this does not show ST-segment elevation or new left bundle branch block, pain characteristics, coronary risk scoring and troponin concentration are used to make the diagnosis of non-ST-segment elevation ACS and to guide further management. Investigations required urgently are given in Table 46.1.
Typical cardiac chest pain is retrosternal pressure or heaviness/tightness radiating to the left arm (occasionally right or both arms) or to the neck or jaw and sometimes associated with sweating and nausea.
Atypical symptoms occur more commonly in the elderly, female patients, those with diabetes and renal failure and can include:
- Epigastric pain
- Dyspeptic symptoms
- Breathlessness
- Delirium
The likelihood of cardiac ischaemia causing the pain is increased if there has been previous similar exertional pain or there is known coronary artery disease. Response to nitrate administration is not specific to cardiac ischaemia. The differential diagnosis of acute chest pain is discussed in Chapter 7.
This may be entirely normal, particularly if pain has resolved. If there is a high clinical suspicion or chest pain persists, repeat every 15 minutes and include modified leads (lateral and right-sided leads) as left circumflex coronary territory or right ventricular ischaemia may not appear with standard lead positions.
Typical ECG findings are:
- ST depression >0.05mV in two or more contiguous leads
- T wave changes:
- Inversion
- Flattened T waves
- Pseudo-normalization of inverted T waves
- The measurement of plasma troponin (released during myocardial ischaemia) complements but does not supplant the history, examination and ECG findings.
- Measurement of plasma troponin using a high-sensitivity assay is recommended, as increases in plasma troponin can be detected within 1–2hours of symptom onset. Point-of-care assays are less sensitive and may take several more hours to become abnormal.
- The universal definition of myocardial infarction is given in Table 46.2. For spontaneous non-ST-segment-elevation myocardial infarction, or infarction as a result of low coronary perfusion (e.g. prolonged syncope or hypotension), one troponin level above the 99th centile for a normal person is abnormal. If the baseline level is raised, a >20% rise in 3hours is required.
- A similar definition applies to Types 4b and 4c. Type 4a requires one level >5 times the 99th centile or a new rise by >20%. Type 5 requires a level >10 times the 99th centile
- Many conditions are associated with a raised plasma troponin, and should be considered in the differential diagnosis (Table 46.3).
- Avoid unnecessary measurement of troponin or other biomarkers to ‘rule-out’ ACS without consideration of the history and serial ECGs.
- The recognition of a NSTE-ACS requires the additional presence of chest pain or other significant symptom or an acute change in the 12-lead ECG.
If the diagnosis of NSTE-ACS is confirmed by the history, ECG findings and plasma troponin results, the risk of mortality in hospital and at six months can be calculated and used to guide further management. A number of risk models are available; the GRACE 2.0 risk calculator is widely preferred and is based on the following clinical factors:
- Age
- Systolic blood pressure
- Heart rate
- Serum creatinine
- Killip class:
- I – no evidence of pulmonary oedema
- II – audible crepitation, raised venous pressure, third heart sound
- III – acute pulmonary oedema
- IV – cardiogenic shock
- Cardiac arrest at admission to hospital
- Elevated cardiac biomarkers
- ST segment deviation
The GRACE calculator is available online at: http://gracescore.org/WebSite/WebVersion.aspx.
Treatment of Confirmed or Suspected NSTE-ACS
- Insert an IV cannula and relief pain with IV morphine
- Give oxygen therapy if saturations <92% or obvious respiratory distress
- Intravenous nitrates therapy with close blood pressure monitoring:
- More effective than sublingual nitrates
- Contraindicated if recent intake of phosphodiesterase type-5 inhibitors (e.g. sildenafil)
- Start a beta blocker, oral or IV unless:
- Risk of cardiogenic shock – heart rate >110/min and systolic <120 mmHg
- Bronchospasm
- Ischaemia due to vasospasm or cocaine intake (unopposed alpha-mediated vasoconstriction)
- Give antiplatelet agents and continue for one year, unless there is excessive risk of bleeding:
- Aspirin 300 mg orally unless already administered (lifelong at a dose of 75 mg daily)
- Clopidogrel 300 mg or alternative P2Y12 inhibitor, for example prasugrel 60 mg or ticagrelor 180 mg
Clinical factors that may influence bleeding risk include:
- Increasing age
- Female gender
- Low body weight, for example <65kg
- Diabetes
- Peripheral vascular disease
- Renal function
- Prior bleeding
Combining dual anti-platelet therapy with anticoagulation to reduce thrombin generation or activation is more effective than antiplatelet or anticoagulant therapy alone. Protocols vary by institution but typically recommend the addition of one of the following:
- Intravenous unfractionated heparin, for example 60IU/kg bolus and 12–15IU/kg infusion
- Subcutaneous low molecular weight heparin, for example enoxaparin 1 mg/kg twice daily
- Subcutaneous factor Xa inhibitor, for example fondaparinux 2.5 mg/day
- Intravenous thrombin inhibitor, for example bivalirudin 0.75 mg/kg bolus and 1.75 mg/kg/h infusion
Anticoagulation should not be continued indefinitely alongside dual antiplatelet therapy as there is a marked increase in bleeding risk. Triple therapy should be avoided in all but highly selected cases with a clear indication for both anticoagulation and dual antiplatelet therapy at high risk of thrombotic complications if discontinued. This should be discussed with cardiology and a management plan agreed before coronary intervention.
Risk factors mandating invasive management are summarized in Table 46.4.
Patients with no high risk features, and without diabetes, renal impairment, LV systolic dysfunction or prior revascularization who settle on medical therapy with no on-going symptoms can be managed with non-invasive assessment of ischaemia. If this shows a significant volume of ischaemia (>10% of viable myocardium) then invasive angiography is indicated. If ischaemia is absent or confined to a small volume then medical therapy is appropriate.
NSTE-ACS with Normal Coronary Arteries
Up to 10% of patients presenting with NSTE-ACS will not have a culprit lesion identified at angiography. Cardiac causes are given in Chapter 45. Always revisit the initial diagnosis and ensure an alternative major pathology has not been missed and consider computed tomography to exclude aortic dissection or pulmonary embolism.