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Exercise training after anterior Q wave myocardial infarction: Importance of regional left ventricular function and topography,☆☆

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Abstract

To determine whether the extent of left ventricular dysfunction and the degree of shape distortion can predict outcome in survivors of moderate-sized anterior Q wave myocardial infarction who are undergoing exercise training, these variables were measured by two-dimensional echocardiography before and after 12 weeks of a low level exercise training program starting 15 weeks after infarction in 13 patients (7 in group 1 and 6 in group 2) and 12 weeks apart in 24 matched control patients without training. By the end of training, the functional class score had increased in group 2 (from 2.25 to 2.67, p < 0.005) but had not changed in group 1. Further discrimination of groups 1 and 2 was provided by an initial asynergy (akinesia or dyskinesia, or both) < 18% or ≥ 18%. Compared with group 1, group 2 had greater initial asynergy (32 versus 6%, p < 0.001), expansion index (asynergic/normal endocardial segment length: 1.8 versus 1.6, p < 0.025) and peak shape distortion index (12.2 versus 1.0 mm, p < 0.005) but lower ejection fraction (43 versus 59%, p < 0.05) and thinning ratio (asynergic/normal wall thickness: 0.61 versus 0.74, p < 0.05).

These variables did not change with training in group 1. However, in group 2, training caused significant increase in asynergy (from 32 to 40%, p < 0.05), expansion index (from 1.8 to 2.0, p < 0.01) and peak shape distortion (from 12.2 to 20.9 mm, p < 0.05) associated with a decrease in thinning ratio (from 0.61 to 0.51, p < 0.001) and ejection fraction (from 43 to 30%, p < 0.005). Initial values for these variables were similar for corresponding control groups but did not change over the 12 weeks. Thus, patients with ≥ 18% left ventricular asynergy on the initial echocardiogram showed more shape distortion, expansion and thinning before exercise training and developed further functional and topographic deterioration with training.

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This study was supported in part by a grant from the Canadian Heart Foundation, Ottawa, Ontario, Canada.

☆☆

This paper was presented in part at the Annual National Meeting of the American Federation for Clinical Research, San Diego, California, May 2, 1987.

1

Dr. Michorowski was a Clinical Research Fellow (1985 to 1987) supported by the Alberta Heritage Foundation for Medical Research, Edmonton.