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Chapter 2: Ischaemic heart disease 37

Investigations Low-risk patients should be discharged with an elec-
Serial ECGs are essential to exclude the development tive exercise/stress test pre- or post-discharge.

of an acute myocardial infarction (ST segment ele- Intermediate-risk patients should have an inpatient
vation or new left bundle branch block). In non-ST stressorexercisetest.Ifthisshowsreversibleischaemia
elevation ACS, the ECG may be normal or show ST angiography and revascularisation should be consid-
depression and/or T wave changes corresponding to ered.
the area of the lesion. There may also be signs of High-risk patients may benefit from a glycoprotein
hypertrophy or previous infarction (Q waves). The IIb/IIIa inhibitor (which prevents platelet aggrega-
evolution of ECG changes is also useful for prognostic tion) together with unfractionated intravenous hep-
informationandplanningofmanagement.Additional arin in place of low-molecular-weight heparin. They
ECGs should also be performed during subsequent should undergo inpatient angiography and revascu-
episodes of chest pain. larisation as appropriate.
Twelve hours after the onset of chest pain, a troponin Very high risk patients should be given a glycoprotein

TorI level should be checked. If this is raised, this is IIb/IIIa inhibitor together with unfractionated intra-
diagnostic of a NSTEMI. If the level is normal patients venousheparininplaceoflow-molecular-weighthep-
are defined as having unstable angina. arin and where possible undergo emergency angiog-
raphy with revascularisation unless contraindicated.

Management
Once diagnosed with non-ST elevation ACS, all patients Prognosis
should be commenced on aspirin and subcutaneous Unless aggressively treated, approximately 10% of pa-
low-molecular-weight heparin. Coexisting arrhythmias tients (excluding those with a normal ECG) will proceed
should be treated and oxygen given as appropriate. Con- to myocardial infarction or death within 1 month.
tinuing chest pain is treated with intravenous glyceryl
trinitrate infusion. Patients should be commenced on
a β-blocker (unless contraindicated) and an oral ni- Acute myocardial infarction (STEMI)
trate once the intravenous infusion is not required. In
Definition
patients with contraindications to β-blockers, a non-
Myocardial infarction (MI) is death of myocardial tissue
dihydropyridine calcium channel antagonist, e.g. dilti-
as an end stage to ischaemia. An acute, evolving or recent
azem should be used.
myocardial is diagnosed by a rise and fall of biochemical
Patients can be stratified as to acute ischaemic
markers of myocardial damage (e.g. troponin or CK-
risk depending on symptoms and investigations (see
MB) with at least one of the following:
Table 2.5).
Ischaemic symptoms.

Development of pathologic Q waves on the ECG.

Table 2.5 Risk stratification of unstable angina ECG changes indicative of ischaemia (ST segment el-
and NSTEMI evation or depression).
Following coronary artery intervention (e.g. angio-
Low risk Clinically stable, normal ECG, negative
12-hour troponin plasty).
Intermediate Recurrent symptoms without new ECG
risk changes or persistence of previous
abnormal ECG Incidence
High risk Raised 12-hour troponin level without ST 240,000 cases per year in England and Wales.
elevation or new Q waves
Highest risk Refractory or recurrent symptoms with
ischaemic ECG changes Aetiology
Ischaemia with haemodynamic Myocardial infarction almost always occurs in patients
compromise or arrhythmia. Elevated with atherosclerosis of the coronary arteries (see page
troponin with recurrent ECG changes
33).