Stress Echo
Stress echo is based upon the principle that an abnormality in myocardial perfusion leads to a change in myocardial function. Stress echo therefore plays a valuable role in the assessment of myocardial perfusion (and, therefore, of underlying coronary artery disease). It also can make an important contribution to the assessment of certain patients with aortic and mitral stenosis. This chapter will consider each of these indications.
PRINCIPLES OF STRESS ECHO
The principal role of stress echo is in the detection of regional wall motion abnormalities – areas of left ventricular (LV) myocardium that show abnormal function at rest and/or during stress. Each region of the myocardium is supplied with blood (and therefore oxygen) by one of the coronary arteries (see Chapter 16), and an imbalance between supply and demand will cause myocardial ischaemia.
Even a relatively severe stenosis in one of the major epicardial coronary arteries does not cause myocardial ischaemia at rest, as the myocardial vasculature compensates to maintain resting blood flow by dilating the arterioles downstream of the stenosis. However, this is inadequate to prevent ischaemia with stress, as the increase in myocardial oxygen demand exceeds the ability of the arterioles to dilate further. Thus a patient with a significant coronary stenosis will usually have normal myocardial perfusion (and therefore contractility) at rest, but will develop myocardial ischaemia (and abnormal wall motion) with stress.
The myocardium can be ‘stressed’ by increasing myocardial oxygen demand, either with physical exercise or pharmacologically using an intravenous (IV) infusion of dobutamine. Alternatively, an IV infusion of a vasodilator (e.g. dipyridamole, adenosine) can be used as the stressor. Vasodilators work by redistributing coronary blood flow, causing dilatation of normal coronary arteries but not of abnormal ones. This increases blood flow down the normal arteries but leads to a reduction in blood flow to areas supplied by stenosed coronaries, via a ‘steal’ mechanism, leading to ischaemia.
For the purposes of a stress echo study, the LV is subdivided into 16 or 17 myocardial segments, and the function of each segment is assessed at rest and with stress. A number of distinct patterns of response can be identified:
A normal response is indicated by normal contractility (normokinetic) at rest, with normal or increased contractility (hyperkinetic) with stress.
An ischaemic response is indicated by normokinetic myocardium at rest, but worsening function on stress, shown by reduced (hypokinetic), absent (akinetic) or paradoxical (dyskinetic) contractility. This is usually due to a stenosis in the supplying coronary artery.
A necrotic response is indicated by abnormal contractility (akinetic, hypokinetic) at rest which remains unchanged with stress. This is usually due to an area of myocardial infarction (scar tissue) resulting from an occlusion in the supplying coronary artery.
A viability response is indicated by abnormal contractility (akinetic, hypokinetic) at rest which improves with stress:
If the improvement is sustained throughout stress, the myocardium is said to be stunned. Stunned myocardium can result from a brief period of coronary occlusion and gradually improves with time.
If the improvement only occurs at low-level stress, and the myocardium worsens again at higher levels of stress (‘biphasic response’), it is said to be hibernating. Hibernating myocardium will not recover spontaneously but may improve following coronary revascularization.
All stress studies (exercise, dobutamine, dipyridamole and adenosine) permit the identification of normal, ischaemic and necrotic myocardium. To assess viability, a dobutamine stress study (using low-dose as well as higher doses of dobutamine) is necessary, in order to assess wall motion at different levels of stress.
INDICATIONS FOR STRESS ECHO
Because it can provide valuable information about the presence and extent of coronary artery disease, the indications for a stress echo study include:
diagnosis of suspected coronary artery disease
risk assessment of patients with known coronary artery disease
identification of viable myocardium prior to revascularization
localization of myocardial ischaemia (‘culprit coronary lesion’ identification prior to revascularization)
assessment of myocardial perfusion following revascularization.
Stress echo is reported as having a sensitivity of 88 per cent and a specificity of 83 per cent in the detection of coronary artery disease (coronary stenosis >50 per cent). This is similarly sensitive to, but more specific than, nuclear myocardial perfusion imaging (p. 109). Stress echo does not, however, involve exposure to ionizing radiation.
In addition to its role in the assessment of myocardial ischaemia, stress echo can be useful in assessing:
low-gradient aortic stenosis with LV dysfunction
mitral stenosis where there is disparity between severity and symptoms.
CONTRAINDICATIONS TO A STRESS ECHO STUDY
For all forms of stress:
acute coronary syndrome in first 24-72 h (high-dose dobutamine should not be used for 7 days after myocardial infarction)
known left main stem coronary artery stenosis
LV failure with symptoms at rest
recent life-threatening arrhythmias
severe dynamic or fixed left ventricular outflow tract obstruction
severe systemic hypertension (systolic blood pressure >220 mmHg and/or diastolic blood pressure >120 mmHg)
recent pulmonary embolism or infarction
thrombophlebitis or active deep vein thrombosis
hypokalaemia
active endocarditis, myocarditis or pericarditis.
For atropine:
closed-angle glaucoma
severe prostatic disease.
For vasodilator (dipyridamole, adenosine) stress:
suspected or known severe bronchospasm
sick sinus syndrome, second or third degree atrioventricular block (unless a functioning pacemaker is present)
hypotension (systolic blood pressure <90 mmHg)
xanthine (e.g. caffeine, aminophylline) use in the last 12 h or dipyridamole use in the last 24 h.
Vasodilator stress is relatively contraindicated by bradycardia of <40 beats/min, equivocal left main stem coronary artery stenosis, recent cerebral ischaemia or infarction.
PATIENT PREPARATION
Patients should receive a clear explanation of what a stress echo study entails and be offered an information leaflet. Ensure that patients taking beta-blockers are informed, where necessary, to omit the beta-blocker for 48 h prior to the stress echo. Advise patients to bring a companion to drive them home.
A minimum of two personnel should be present throughout the stress echo study, one of whom should be trained in advanced life support and the other in basic life support. The sonographer should be experienced in stress echo, and a physician should be immediately available if not present during the study. Appropriate cardiopulmonary resuscitation equipment must be available.
Prior to undertaking the stress echo study, ensure that the patient understands what is planned and has given informed consent. Review the patient’s history and prior investigation findings and check for contraindications or anything that may increase the risk of complications.
A 12-lead ECG must be recorded (and reviewed) at baseline and every minute during the stress study. Attach the ECG
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