Why the study?
How does previous transmural anterior myocardial infarction and the presence of multivessel disease modify the left ventricular response to exercise?
How does previous transmural anterior myocardial infarction and the presence of multivessel disease modify the left ventricular response to exercise?
In patients with prior anterior myocardial infarction, the presence of additional multivessel disease leads to a decrease in ejection fraction during exercise due to a disproportionate increase in end-systolic volume.
Left ventricular response to exercise after transmural anterior myocardial infarction. A. T. H. Tan, N. Sadick, P. J. Harris, J. Morris and D. T. Kelly. Aust. N.Z. J. Med., 1982,12, pp. 489–494. The purpose of this study was to determine the effect of a previous myocardial infarction on the left ventricular response to exercise and to see how this response is modified by the presence of multivessel versus single vessel coronary artery disease. Twenty-seven patients with a past history of transmural anterior myocardial infarction underwent rest and exercise gated equilibrium blood pool imaging. All 27 patients had a total occlusion of the left anterior descending coronary artery and akinesis of the anterior wall of the left ventricle. Sixteen patients had isolated, left anterior descending artery occlusion (Group A). Eleven patients had multivessel disease with 70% or greater stenosis of one or more major coronary arteries in addition to the total left anterior descending artery occlusion (Group B). Seventeen subjects with atypical chest pain and normal exercise test were selected as controls. Seven Group B patients but no Group A patients developed angina and/or ischaemic ST changes with exercise. Control subjects achieved an average 94±2% (mean) of their predicted work capacity whereas the post-infarct patients had a diminished work capacity (Group A 73±6%, P <0.001; Group B 65±5%, p< 0.001). Control subjects showed an increase in ejection fraction (EF) from rest (0.53 ±0.02) to peak exercise (0.63±0.02). This increase was primarily due to a 33±6% decrease in end systolic volume since the end diastolic volume did not change significantly from rest to peak exercise (-1.4±4%). In Group A patients, EF did not change from rest (0.32±0.03) to peak exercise (0.30±0.03) because there was a similar increase in end-diastolic volume (76±4%) and end-systolic volume (19±4%). However, in Group B patients EF decreased from 0.32±0.03 to 0.23±0.02 (p<0.01) because of a disproportionate increase in endsystolic volume (45 ± 13%) compared to enddiastolic volume (27± 7%). When patients with abnormal resting left ventricular function due to previous myocardial infarction exercise there is little change in the ejection fraction and the increase in cardiac output is heart rate dependent. If additional myocardial ischaemia develops the ejection fraction and stroke volume decrease due to a disproportionate increase in endsystolic volume.
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Tan et al. (1982) studied this question.
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