Ischaemic burden myocardial ischaemia

The presence of ischaemia during exercise can be explained in terms of physiological response. As an individual steps up his or her level of activity, myocardial oxygen consumption rises (Rate Pressure Product (RPP) = HR x SBP). Simultaneously, there is a shortening of diastole and subsequently a decrease in coronary perfusion time. Consequently, there is a transient oxygen deficiency to the myocardium. Myocardium deprived of oxygen is unable to meet the demand of the increased activity, and the individual complains of angina, or ST depression is identified on the ECG.

From the clinician's perspective the outcome may be that the patient develops life-threatening electrical disturbances. As the exercise level increases, the resulting increased sympathetic activity leads to an alteration in the depo-larization/repolarisation mechanism, with resulting distortion in the conduction velocity. This may give rise to increased ventricular ectopic activity and potentially ventricular tachycardia and/or fibrillation. The degree of ischaemia present and the workload at which this occurs is of enormous importance to the exercise leader. This information will guide the exercise prescription of the individual or ultimately determine entry to the exercise component of CR.

To establish the ischaemic burden or degree of myocardial ischaemia in an individual patient, the CR professional can refer to both technological and clinical examination of the patient. A clinical history of angina, relieved by rest and/or GTN spray, can help the exercise professional classify the individual. A dialogue about the precipitation of chest pain in relation to everyday activities can direct the exercise professional to the level of prescription required to work beneath the ischaemic threshold.

Stress testing can elicit ischaemic changes, revealing ST segment changes and/or myocardial perfusion rates. In general terms, ST displacement of 12 mm would be considered as confirmation of moderate myocardial ischaemia, with anything greater that 2 mm regarded as significant. Patients with ischaemia on ECG, or angina at a low workload have a poorer prognosis. This is in line with previous trials (Jesperson, et al., 1993) where a positive test doubles the risk of reinfarction and death in the short to medium term and early ST-segment depression of >2 mm increases the risk of an unfavourable conclusion. They conclude that symptomatic exercise-induced angina at a low workload were independent predictors of mortality with a relative risk of 2.07 and 1.78 respectively. Studies of perfusion abnormalities similarly would consider that the magnitude of the abnormality is the single most effective prognostic indicator of risk, with those patients with mildly abnormal single photon emission computed tomography (SPECT) scan after ETT being in a low-risk category of cardiac death but intermediate risk of non-fatal MI. Conversely, those with extensive scan abnormalities have significant risk of cardiac death (Hachamovitch, et al., 1998).

Occasionally these ischaemic changes may be established from ambulatory, 24hr Holter monitoring. These data are particularly useful in those individuals with 'silent ischaemia', i.e. absence of pain. Silent ischaemia has been found to occur in 2.5% of the male population (McMurray and Stewart, 2000) and represents impaired myocardial perfusion. A number of patients, diabetics especially, may have silent ischaemia. This can present the exercise professional with an additional challenge when risk stratifying and prescribing exercise, unless information on ischaemic threshold is available. In general, the greater degree of ST depression, the greater the likelihood of the patient experiencing chest pain.

Arrhythmic potential

The increase in myocardial oxygen consumption associated with vigorous activity, and the corresponding decrease in coronary perfusion time, can result in a temporary deficit of oxygen to the myocardium. At the same time the effect of the increased workload results in an increase in circulating catecholamines, with an alteration in the sodium-potassium balance that results in an increased myocardial irritability and produces amplified ventricular activity (ACSM, 2001). It is important to establish the level of arrhythmia production, in particular ventricular tachycardia (subsequently associated with ventricular fibrillation), prior to entry into CR. This can be gained from either an ETT or through 24-hour ambulatory monitoring. However, careful interpretation is required, as a single occurrence of ventricular tachycardia during a stress test is not necessarily an indication of the onset of fatal ventricular fibrillation. Nevertheless, it should be highlighted that an individual who has experienced an episode of ventricular fibrillation (VF) that did not occur in the presence of an acute event or cardiac procedure would be considered moderate to high risk (AHA, 2001). Similarly ventricular arrhythmias (VA) which are uncontrolled at low to moderate workloads with medication would be considered at greater risk for cardiac-related complications during exercise.

Those at greatest risk of exercise-induced ventricular fibrillation are individuals with significantly impaired left ventricular function: namely those who have serious/major myocardial damage, due either to a large infarct, multiple infarctions or other conditions affecting ventricular function, e.g. valve disease, myocarditis, hypertension and cardiomyopathy. There is a lack of recent evidence on the incidence of arrhythmic events during CR. In a study cited by Belardinelli (2003) a programme of exercise training for heart failure patients had only one episode of cardiac arrest in 16 years, i.e. 1 per 130000 patient hours. However, as Belardinelli (2003) suggests, the low incidence of arrhythmia, as with other complications, during CR is because exercise is safe if the exercise prescription is 'tailored to the patient's clinical picture and needs'.

Left ventricular function

It is generally accepted that impairment of left ventricular (LV) function is a strong predictor of prognosis, with a number of authors rating it as the most powerful predictor (Specchia, et al., 1996). The most widely practised method of assessing LV function is echocardiography. LV function can be expressed as a verbal description, as an ejection fraction (%) or wall motion index. Although less common, LV function can also be assessed during angiography or perfusion scanning. Although ejection fraction as a percentage is less commonly available to exercise practitioners, it is accepted that normal ejection fraction approximates to 60-70%. Variations exist within the literature as to clearly defined links between ejection fraction percentages, verbal descriptors

Figure 2.1. Possible adverse physiological consequences of exercise in presence of heart failure (Adapted from Belardinelli, 2003).

and level of risk. Some of the risk table summary data report that only at the level of poor LV function is this considered a high risk variable (PaulLabrador, et al., 1999). However, the Canadian guidelines (Stone, et al., 2001) classify high risk as <40%, moderate as >40%, and low risk as >50%.

In relation to risk stratification for exercise, LV dysfunction is an indicator of increased risk of complication during exercise. Figure 2.1 illustrates a proposed physiological response to exercise in the presence of heart failure. This explains the link between exercise and adverse event in individuals with impaired LV function.

This figure shows that the sequence of events links LV dysfunction directly to other components of risk stratification already discussed, namely, arrhythmic potential and exercise capacity, due to compromised cardiac output and ischaemic burden.

The information the exercise professional can gather regarding LV function will be relevant for only a specific time. Predicted spontaneous recovery and pharmaceutical interventions (especially ACE inhibition) may have an effect on LV function between time of event and commencement of phase III exercise. Contrary to historical evidence, which suggested LV-impaired patients could not increase cardiac output sufficiently to benefit from rehabilitation, recent research shows that exercise training itself improves survival in the presence of LV dysfunction (Specchia, et al., 1996). Goebbels, et al. (1998) conducted a randomised controlled trial that showed a more favourable benefit from exercise rehabilitation for those with reduced ejection fractions (<40%).

32 Exercise Leadership in Cardiac Rehabilitation

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