This thesis investigates the use of exercise training as a
therapy in the management of angina pectoris. The hypothesis
underlying this work is that in the presence of ischaemia the
myocardium will, if possible, respond in such a way as to minimise
the effects of ischaemia. Improved collateral function was felt
to be the most likely mechanism.A series of non-invasive investigations was developed in such
a way as to make them useful for the detection of any possible
improvement in myocardial ischaemia. These investigations
included treadmill exercise tolerance testing, Thallium
scintigraphy, Technetium ventriculography, exercise
echocardiography and 24 hour ambulatory ECG monitoring. These
techniques were refined for use in this study by the development
of computerised analysis where appropriate.Forty male patients under 60 years of age with angina
pectoris and no prior myocardial damage were recruited and
randomised into exercise and control groups. Both groups were
followed up over a one year period, the exercise group carrying
out a brief daily home-based exercise programme, using the
Canadian Airforce PBX Program for Physical Fitness.The techniques developed proved to be effective follow up
tools in this group. Using them significant improvements in
treadmill performance were demonstrated in the exercise group.
These improvements were found to be partly due to changes in the
peripheral control of exercise induced heart rate increases but
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also due to myocardial improvements. The peripheral effects were
compared to and contrasted with betablockade. Within the
myocardium significant reductions in ischaemic area were
demonstrated, particularly in the territory of the left anterior
descending coronary artery. These improvements in perfusion were
accompanied by improvements in left ventricular function and
regional wall motion. The improvements demonstrated in the
laboratory were also evident during ambulatory ECG monitoring.The results demonstrated support the hypothesis outlined that
controlled myocardial ischaemia can induce improvements in
myocardial perfusion, perhaps due to collateral enhancement, and
furthermore support the use of these techniques in such follow up
studies.Further studies would be justified and indeed necessary to
convincingly prove the hypothesis. Such studies may need to be
multicentre in order to recruit sufficient numbers and ideally
should involve coronary angiography and coronary perfusion
assessment
