The Relevance of Silent Ischaemia for the Clinician

Summary

Studies involving haemodynamic monitoring and scintigraphy have shown that asymptomatic ST depression truly represents myocardial ischaemia. It is also clear that the mechanisms causing silent ischaemia are similar to those responsible for the generation of angina pectoris, that is, increase in myocardial oxygen demand, reduction in coronary blood flow or a combination of both. Treatment with agents that are effective in the treatment of angina pectoris are also effective in the treatment of silent ischaemia. However, the role in clinical practice of drug treatment for silent ischaemia is uncertain.

In patients with angina pectoris 24-h ambulatory monitoring has shown that STsegment changes occur not only as expected during episodes of angina pectoris, but also in the absence of chest pain [1, 2]. Since ST-segment changes can occasionally occur in normal individuals, it was argued that such changes did not necessarily reflect myocardial ischaemia. Studies using a nuclear stethoscope, however, have shown that both painful and silent episodes of ST-segment depression are associated with increases in left ventricular volume, and these increases precede the development of chest pain where it occurs. Using positron tomography it has been possible, on occasions, to record positron scans during painless ST-segment changes. Positron scans using the isotope rubidium 82 provide a quantitative means of measuring the uptake of potassium in regions of the myocardium. Due to the high energy nature of the isotope, tomographic scans may be recorded, and also, since the isotope is short lived, the changes in the uptake of the isotope with time may be followed. Thus, in patients with angina pectoris, it is possible to observe them while they are lying within the positron camera. The ECG can be continuously recorded, and ST-segment changes, both accompanied and unaccompanied by chest pain, can be detected. During such episodes, it is possible to inject the isotope, and it has been found that similar defects in the regional myocardial uptake of rubidium 82 occur in painful and painless episodes of ST-segment depression.

Invasive investigations following cardiac catheterisation in which catheters have been left in the left ventricle have shown that during painless ST-segment depression, there is an increase in left ventricular filling pressure although this increase is not as great as during episodes of painful ST-segment depression. The recent development of ambulatory pulmonary artery monitoring has provided a continuous means of measuring left ventricular end diastolic pressure [3]. In the absence of obstructive lesions of the mitral valve and in the absence of pulmonary hypertension, the pulmonary artery diastolic pressure equates with left ventricular filling pressure. This permits an indirect assessment of left ventricular function to be made whilst the patient is going about his everyday activities. Such recordings have shown that during painless ST-segment depression, there is an increase in pulmonary artery diastolic pressure. Such increases in pulmonary artery diastolic pressure were not seen in normal controls and indeed were equal in magnitude to the increases that occurred during painful ST-segment depression [4].

These studies have shown conclusively that painless ST-segment changes in patients with coronary artery disease truly reflect silent ischaemia.