A diagnosis of ischaemic heart disease (IHD), including exertional or unstable angina, ST segment elevation myocardial infarction (STEMI) or non-ST segment elevation myocardial infarction (NSTEMI), involves a broad range of risk; therefore, exercise prescription s should be developed on an individual patient basis. The appropriate mode and intensity of exercise is based on clinical risk and effort/exercise tolerance.

When assessing risk, the following should be considered:

Volume of infarcted myocardium (troponin rise)

• Degree of ventricular impairment – on echocardiogram, refer to left and right ventricular function, and whether regional wall motion is hypokinetic or akinetic. On angiogram, refer to left ventriculogram
• Region of infarcted myocardium – anterior vs inferior, apical vs basal
• Potential for current or future ischaemia – other untreated stenosis or risk of restenosis
• Type of intervention (angioplasty only vs drug eluting stent vs bare metal stent) – this can determine risk of future restenosis of the treated segment
• Location of stenosis and the volume of myocardium effected
• Inability to treat an occlusion, or a failed revascularisation

TIP: Individuals with good exercise tolerance or who demonstrate no symptoms on exertion can still be at significant risk. Exercise prescription should consider clinical risk, not just exercise tolerance.

Moderate-to-large myocardial infarctions require lower-intensity exercise in the first 4 weeks to allow for remodelling of the infarcted area, recovery of hibernating myocardium and reduction in risk of ventricular wall rupture. This applies to those with significant troponin rise, moderate-to-severe impairment of ventricular function or resting wall motion abnormalities at the time of the infarction.

While angiograms are extremely valuable in stratifying risk, the severity of a stenosis does not predict the risk of myocardial infarction (MI). Approximately 65% of MI's occur in arteries that are <50% occluded; 20% in arteries 50-70% occluded and 15% in arteries that are >70% occluded.[#falk-e-shah-pk-fuster-v.-1995]

Patients with ischaemia or coronary artery occlusion for ‘medical management’ may vary in risk. Medical management refers to the use of medications to affect the stenosis progression and minimise the likelihood of ischaemia or symptoms.

The decision to avoid procedural intervention may indicate:

• Occlusion is not significant enough to require revascularisation
• Small calibre vessel is not suitable for PCI
• Small calibre vessel affects an insignificant volume of myocardium
• Failed or aborted attempt to revascularise
• Collateral circulation supplies the myocardium distal to the stenosis
• Chronic total occlusion (i.e., there may be distal ischaemia)
• Majority of myocardium distal to the stenosis is necrotic

TIP: The intention to ‘treat medically’ without intervention does not necessarily imply the absence of myocardial ischaemia or that the individual is at low risk.

All available clinical information (angiogram, myocardial perfusion scan, stress echo) should be reviewed to determine the following:

• Location of the stenosis
• Volume of myocardium distal to the stenosis
• Likelihood of collateral circulation (where the area distal to the stenosis is supplied by other vessels)
• Likelihood of ischaemia (perfusion defect or regional wall motion)
• Maintenance or decline in left ventricular function on exertion

On an ongoing basis, it is important to determine whether:

• Prescribed medication is providing symptomatic relief
• Medications are well tolerated (i.e., side-effects)
• ‘Medical management’ requires review to ensure it is achieving the desired outcome

Monitoring the patient’s response to exercise is essential.

TIP: Always reinforce the appropriate use of anti-anginal medications (glyceryl trinitrate; GTN) in patients who may experience angina. See section on exertional angina.

Myocardial infarction (MI) is associated with a broad array of clinical risk, with management depending on presenting features. Some form of revascularisation intervention is usual. The level of troponin released upon myocardial damage reflects the size of the infarct. This is often in keeping with the degree of ventricular dysfunction or wall motion abnormalities at the time of admission. This may improve over the first 4 weeks as ‘stunned’ myocardium restores its function, although detrimental remodelling may occur, leading to no improvement or even worsening HF.

Thorough screening and risk stratification are crucial; see previous section on ischaemic heart disease.

TIP: During hospital admission, sometimes only the culprit lesion will be revascularised, postponing treatment or reassessment of other stenosis for a later time, typically, 4-6 weeks.

Exercise prescriptions should commence at a low, well-tolerated level and progress gradually. The duration of exercise should progress before the intensity to avoid excessive load on the myocardium via increased HR and BP.

Larger infarcts with some degree of ventricular dysfunction or wall motion abnormality require greater precaution and slower graduation of exercise. Small infarcts with preserved myocardial function and no other stenosis allow exercise progression with less restriction.

Microvascular, or small vessel, coronary artery disease (CAD) involves the arterioles and capillaries that perfuse the heart muscle. Large vessels and branches may still be patent on coronary angiography.

Microvascular disease is treated medically, so exercise considerations are identical to ischaemic heart disease for medical management.

Medical management with pharmacological agents aims to:

• Increase myocardial blood supply using vasodilators (nitrates and some calcium channel blockers)
• Reduce cardiac oxygen demand by lowering HR and BP (beta-blockers and antihypertensives)
• Prevent angina by promoting vasodilation or altering the myocardial oxidative metabolism.

It is important to clarify which medications have been prescribed to the patient to reduce myocardial ischaemia, and the time they are taken in relation to exercise. Some medications, particularly nitrates, have an 8-10 hour duration of effect, but typically take 1-1.5 hours to generate a therapeutic effect. The timing can affect safety and symptomatic benefit of these medications during exertion.

TIP: Educate patients about the timing and duration of their anti-anginal medications to ensure patient confidence and safety so that they can exercise safely.

Typical characteristics of angina symptoms should be assessed, including:

• How the patient senses their angina (chest, back, arm, shoulder, jaw)
• Type of activities/intensity of exercise that typically produces angina
• How the patient resolves the symptoms (rest, GTN)
• Severity of discomfort (scoring system out of 10)

TIP: When reviewing exercise tests, establish whether ischaemic ECG changes are accompanied by symptoms. A patient is at greater risk if ECG changes occur in the absence of overt symptoms.

The volume and territory of the possible ischaemia should be determined. A larger volume of affected myocardium implies a greater risk, as does anterior ischaemia compared with inferior wall ischaemia.

The following strategies can be considered to reduce physiological demand:

• Prescribe exercise using less volume of muscle mass – rowing ergometer > cycling > unilateral leg extension
• Prescribe small bouts of exercise with periods of rest – weight resistance or brief aerobic exercise
• Reduce the intensity of exercise
• Use prophylactic GTN

An important component of each exercise session is a warm-up and cool-down. Patients with exertional angina benefit from a very prolonged and gradual warm-up.

Prophylactic use of GTN

In consultation with the treating doctor, GTN can be used before or during exercise to prevent myocardial ischaemia.

Prophylactic GTN dilates the vasculature, increasing blood flow to the myocardium prior to the onset of symptoms. However, this systemic vasodilation may also reduce BP to the point of hypotensive symptoms. Therefore, BP should be recorded before and after GTN administration, both in a seated and standing position. Maximum dilation from GTN will occur within 5 minutes.