Section 6 Ischaemic heart disease

Myocardial ischaemia – ST depression

Myocardial ischaemia – T wave inversion

Myocardial ischaemia – non-specific changes

Acute extensive anterior myocardial infarction

Acute anterolateral myocardial infarction

Acute anteroseptal myocardial infarction

Acute ‘high’ lateral myocardial infarction

Acute inferior myocardial infarction

Very early acute inferior myocardial infarction

Acute right ventricular infarction

Acute posterior myocardial infarction

Acute anterior myocardial infarction in the presence of left bundle branch block

Case 57 A 47-year-old man during an exercise tolerance test

Myocardial ischaemia – ST depression

Horizontal ST depression is strongly suggestive of ischaemia in an appropriate clinical setting. Sloping ST depression is a less reliable indicator of ischaemia.

Features of this ECG

• Sinus tachycardia, 110 b.p.m., normal QRS axis

• Horizontal ST epression in the inferior and lateral leads (Fig. 57.1)

Fig. 57.1 Horizontal ST depression.

Clinical Note

This ECG was taken at 3 minutes 20 seconds. The patient developed chest pain and the above ECG changes.

Common causes of ST depression

→ Horizontal:

– ischaemia

– subendocardial infarction

– reciprocal to ST elevation (acute injury)

→ Sloping:

– ventricular hypertrophy

– digoxin

– ischaemia

– hyperkalaemia

– bundle branch block

Case 58 A 42-year-old man with chest pain

Myocardial ischaemia – T wave inversion

There are no definitive criteria for the normal T wave and numerous conditions other than ischaemia can cause T wave changes (see CASE 58). Inversion of the T wave is considered abnormal in V3-6, I, II and aVF in most adults. T wave inversion is relatively non-specific for ischaemia unless it is deep and symmetrical (‘arrowhead’) inversion.

Features of this ECG

• Sinus rhythm, 75 b.p.m., normal QRS axis

• Deep and symmetrical T wave inversion in the anterior leads, V1-5, I and aVL (Fig. 58.1)

• Long QT interval (QT = 480 ms, QTc = 540 ms)

Fig. 58.1 Lead V2. ‘Arrowhead’ T wave inversion.

Clinical Note

This patient had post-infarct angina. His ECG the previous day had been normal. Subsequent angiography showed a 50% stenosis in the left anterior descending coronary artery with thrombus visible in the lumen. The ECG returned to normal with 4 days of i.v. heparin.

Causes of deep symmetrical T wave inversion

→ Subendocardial ischaemia

→ Subendocardial infarction (non Q-wave infarction)

→ Hypertrophic obstructive cardiomyopathy

→ Juvenile pattern

→ Intracranial haemorrhage

Case 59 A 61-year-old lady – routine preoperative ECG

Myocardial ischaemia – non-specific changes

Usually the ECG changes of ischaemia are more subtle than those shown in the previous two examples and are referred to as non-specific ST and T wave changes. These changes include minimal or sloping ST depression, T wave flattening, abnormally tall T waves, and minimal T wave inversion.

Features of this ECG

• Sinus rhythm, 72 b.p.m., normal QRS axis

• T wave flattening in the lateral leads V4-6 (Fig. 59.1)

• Flattened T wave in II, minimal T wave inversion in leads aVF and III (Fig. 59.2)

Fig. 59.1 T wave flattening.

Fig. 59.2 T wave inversion.

Clinical Note

This patient had a history of stable angina. This ECG was done routinely prior to hip joint replacement surgery.

Common causes of T wave changes

→ Myocardial ischaemia

→ Physiological (race, hyperventilation, anxiety, iced water)

→ Left ventricular hypertrophy

→ Drugs (e.g. digoxin)

→ Myocarditis/pericarditis

→ Pulmonary embolus

→ Intraventricular conduction delay

→ Electrolyte abnormalities

Case 60 A 36-year-old man with 40 minutes of ‘crushing’ chest pain

Acute extensive anterior myocardial infarction

• Changes of acute injury (ST elevation) in most or all anterior leads V1-6, I and aVL.

• With or without reciprocal changes (ST depression) in the inferior leads.

(NB: Infarction can be divided into regions depending on which leads show changes; however, these should not be treated rigidly as lead positions may vary. What is important is that the pattern of acute injury is recognised and distinguished from other causes of ST elevation.)

Features of this ECG

• Sinus rhythm, 66 b.p.m., normal QRS axis

• ‘Hyperacute’ changes, indicating first few hours of infarction, in anterior leads (Fig. 60.1):

– increased ventricular activation time (normal < 1 small square)

– increased height of R wave

– upsloping ST elevation

– broad T wave with increased height

Fig. 60.1 Acute injury.

(note V5 and V6 do not seem to fit the pattern, chest leads can be easily misplaced when in a hurry)

• Reciprocal ST depression in leads II, III and aVL (Fig. 60.2):

– the mirror image of the acute injury

• Two consecutive ventricular premature beats from different ectopic foci (Fig. 60.3)

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