Marchant, Bradley G; (1994) Mechanisms affecting the symptomatic expression of myocardial ischaemia. Doctoral thesis (M.D), UCL (University College London).

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Abstract

The symptomatic expression of myocardial ischaemia varies between and within patients and mechanisms are poorly understood. The aim of this thesis has been to determine factors which account for this variation in patients with stable angina and acute myocardial infarction. In stable angina, myocardial ischaemia will only provoke symptoms if the magnitude of the ischaemic stimulus exceeds the sensory threshold for experiencing angina and this explains much of the within patient variation. Ischaemic mass may also account for the between patient variability, although in diabetic patients, perceptual dysfunction caused by subclinical neuropathy plays an additional role. Endogenous opiates do not appear to influence the perception of myocardial ischaemia. Other factors affecting the symptomatic expression of myocardial ischaemia include environmental temperature and cold-intolerant patients appear to have impaired baroreceptor function which may result in a greater increase in heart rate in the cold. In acute myocardial infarction, cold also appears to play a role, with more infarcts occurring on colder days in both summer and winter. Following acute myocardial infarction, myocardial ischaemia is common and frequently silent. Damage to the innervation of the myocardium may account for the low level of symptoms in the early post-infarction period, but does not account for the variation between and within patients. As in stable angina, the magnitude of the ischaemic stimulus is an important determinant of symptoms in these patients. Comparison of patients with stable angina and acute myocardial infarction demonstrates an association between circadian variation in sympatho-vagal balance and episodes of ambulatory myocardial ischaemia. Thus patients with stable angina have a peak in sympatho-vagal balance in the waking hours which corresponds with a peak in ambulatory ischaemia. This is in distinction to patients with acute myocardial infarction, in whom the circadian variation in sympatho-vagal balance and ambulatory ischaemia is reduced. In most patients with stable angina, the absence of symptoms during an episode of myocardial ischaemia probably reflects an inadequate intensity of ischaemia. A logical consequence may be that it is relatively unimportant to detect and treat asymptomatic myocardial ischaemia. However, in some patients, particularly those with diabetes, a subclinical neuropathy may impair the perception of myocardial ischaemia despite what would be considered an adequate stimulus in another patient. It may be worthwhile screening such patients for myocardial ischaemia even if symptoms are not prominent.

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