THE ECG IN ACUTE CORONARY SYNDROMES

‘Acute coronary syndrome’ is a term that covers a spectrum of clinical conditions caused by the rupture of atheromatous plaque within a coronary artery. On the exposed core of the plaque, a thrombus forms, and this can cause total or partial occlusion of the artery. The clinical syndrome ranges from angina at rest (unstable angina) to transmural myocardial infarction, and some definitions of acute coronary syndrome also include sudden death due to coronary occlusion. The diagnosis of acute coronary syndrome is based on the clinical presentation (including a previous history of coronary disease), ECG changes, and biochemical markers, principally troponin.

If a patient has chest pain and there is ECG evidence of myocardial ischaemia but a normal plasma troponin level, then the diagnosis is acute coronary syndrome due to unstable angina. Myocardial necrosis causes a rise in the level of plasma troponin (either troponin T or troponin I), and a high-sensitivity assay can detect a very small rise. By some definitions, any such rise in a clinical situation suggesting myocardial ischaemia justifies a diagnosis of myocardial infarction. However, the plasma troponin level may also rise in other conditions, which may also be associated with chest pain ( Box 6.2). It is essential to remember that the plasma troponin level may not rise for up to 12 h after the onset of chest pain due to a myocardial infarction.

Thus the ECG is an essential tool in the diagnosis of an acute coronary syndrome. Importantly, it also distinguishes between two categories of myocardial infarction whose management is different. The first is infarction associated with ST segment elevation, known as ‘ST segment elevation myocardial infarction’ or ‘STEMI’, and the second is ‘non-ST segment elevation myocardial infarction’ or ‘NSTEMI’. Differentiation is important because a STEMI requires immediate treatment by thrombolysis or percutaneous intervention (PCI – i.e. angioplasty and probably stenting), although after 6 h the benefit of this treatment is largely lost. An NSTEMI may also require PCI but with considerably less urgency, and the patient is initially treated with some form of heparin, anti-platelet agents and a beta-blocker.

During the first few hours after the onset of chest pain due to myocardial infarction the ECG can remain apparently normal, and for this reason ECGs should be recorded repeatedly in a patient with chest pain that could be due to cardiac ischaemia, but whose ECG is nondiagnostic.

UNSTABLE ANGINA

In unstable angina there is ST segment depression while the patient has pain ( Fig. 6.1). Once the pain has resolved the ECG returns to normal, or to its previous state if the patient has had a myocardial infarction in the past.

STEMI

In STEMI the ST segments rise in the ECG leads corresponding to the part of the heart that is damaged: the V leads with anterior infarction, lead VL and the lateral chest leads with lateral infarction, and leads III and VF with inferior infarction. STEMI is diagnosed when there is more than 1 mm of ST segment elevation in at least two contiguous limb leads (e.g. I and VL; III and VF), or more than 2 mm of ST segment elevation in at least two contiguous precordial leads. The diagnosis of STEMI can also be accepted if there is left bundle branch block which is known to be new.

Prompt treatment by PCI or thrombolysis may prevent myocardial damage, so that Q waves do not develop. Otherwise, after a variable time, usually within a day or so, the ST segments return to the baseline, the T waves in the affected leads become inverted, and Q waves develop (see p. 91). Once Q waves and inverted T waves have developed following infarction, these ECG changes are usually permanent. If anterior ST segment elevation persists, a left ventricular aneurysm should be suspected.

Figures 6.2–6.5 show ECGs from different patients with anterior infarctions, at increasing times from the onset of symptoms.

An old anterior infarction can also be diagnosed from an ECG that shows a loss of R wave development in the anterior leads without the presence of Q waves ( Fig. 6.6). These changes must be differentiated from those due to chronic lung disease, in which the characteristic change is a persistent S wave in lead V₆. This is sometimes called ‘clockwise rotation’ because the heart has rotated so that the right ventricle occupies more of the precordium, and seen from below the rotation is clockwise ( Fig. 6.7).