Influence of exercise rehabilitation on myocardial perfusion and sympathetic heart innervation in ischaemic heart disease.

Exercise rehabilitation improves the clinical status in ischaemic heart disease. The purpose of this study was to assess the influence of exercise rehabilitation on myocardial perfusion and sympathetic heart innervation. Sixteen patients with ischaemic heart disease and previous myocardial infarction were investigated by means of exercise/rest tetrofosmin and metaiodobenzylguanidine (MIBG) exercise/rest single-photon emission tomography (SPET) studies, before and 6 months after starting an exercise rehabilitation programme. Tomograms were divided into 15 segments, and these were grouped into five myocardial anatomical regions. Regional uptake of both tracers was quantified and expressed as a percentage of maximum peak activity. The percentage < or =55% was chosen to evaluate defect size, and the results were expressed as a percentage of left ventricular mass. Areas with perfused and denervated myocardium and areas with ischaemic myocardium were calculated. In addition, regions with <75% of peak activity in the exercise perfusion study at baseline were divided into two groups according to whether there was an increase in peak activity of >10% (representing reversible regional defects) or an increase of <10% (representing fixed regional defects) in the rest study. These percentages were compared with the percentages obtained in the innervation study, and with the percentages obtained in exercise/rest perfusion and innervation studies performed 6 months after starting rehabilitation. Myocardial perfusion defects were significantly smaller than myocardial innervation defects before and 6 months after starting exercise rehabilitation. The area of ischaemia 6 months after starting exercise rehabilitation was significantly smaller than that before rehabilitation (0.31%+/-1.4% vs 1.4%+/-1.6%, P<0.01). The size of innervation defects and the area of perfused and denervated myocardium did not show significant differences between the two studies performed before and 6 months after starting exercise rehabilitation. In reversible regional defects the percentage of peak activity was significantly increased 6 months after starting exercise rehabilitation in exercise and rest studies (P<0.001), while in fixed regional defects it was significantly increased only in exercise studies (P<0.001). There was no significant change in the regional MIBG percentages. We conclude that in ischaemic heart disease, exercise rehabilitation over a period of 6 months improves myocardial perfusion, but does not cause changes in sympathetic myocardial innervation.