Evaluation of the left ventricular hemodynamic function and myocardial perfusion by gated single photon emission tomography, in patients with type 1 diabetes mellitus; prodromal signs of cardiovascular disease after four years

The aim of this study was to assess the changes in hemodynamic function and myocardial perfusion of the left ventricle occurring in patients with type 1 diabetes mellitus (DM1) 47-49 months after the first assessment. We have studied 20 asymptomatic patients, five females and 15 males, aged 22-46 y. The patients were under intensive insulin treatment and had normal electrocardiogram (ECG) at rest. In all patients gated single photon emission tomography (GSPET) was performed at rest and after exercise (examination I). After 47-49 months this test was repeated (examination II). GSPET was performed 60 min after the intravenous injection of 740 MBq of technetium-99m 2-methoxy-isobutyl-isonitrile ((99m)Tc-MIBI), using a dual-headed gamma-camera. Left ventricular ejection fraction (LVEF), end diastolic volume (EDV) and end systolic volume (ESV) were calculated using quantitative GSPET (QGS). The intensity of perfusion defects was also evaluated based on a four degree QGS scale. Our results were as follows: a) In examination I, performed at rest: LVEF was 56.1%+/-7.5%, EDV 96.9+/-25.8 ml and ESV 42.6+/-16.3 ml. b) In examination I at stress: LVEF was 57.2%+/-7.5%, EDV 94.1+/-24.0 ml and ESV 40.5+/-15.5. c) In examination II performed at rest: LVEF was 58.1%+/-6.5%, EDV 112.1+/-26.1 ml and ESV 46.6+/-14.9 ml and d) In examination II at stress: LVEF 57.8%+/-5.6%, EDV 107.9+/-27.4 ml and ESV 44.9+/-14.4 ml. Significant differences were found between examinations I and II, regarding: a) EDV at rest (P<0.001) and at stress (P<0.001) and b) ESV at rest (P<0.05) and at stress (P<0.005). Correlation analysis revealed significant correlation between LVEF at rest and at stress both in examination I (r=0.83; P<0.001) and also in examination II (r=-0.897; P<0.001). Intensity of myocardial perfusion defects in examination I at rest and at stress was: 1.68+/-0.5 and 2.2+/-0.6 degrees respectively. Intensity of myocardial perfusion defects in examination II at rest and at stress was: 1.75+/-0.4 and 2.2+/-0.5 respectively. No significant differences in the intensity of these perfusion defects were found. EDV both at rest and at stress was significantly higher in examination II as compared with the examination I study. Similar, but less pronounced changes of ESV were found. This study confirms other authors' observations on LV, EDV and LV, ESV and also that the percentage of asymptomatic DM1 patients having silent myocardial ischemia is high as was in all our patients. Nevertheless, in the current literature, we were unable to find a study similar to the present one, comparing basal and after four years LV functional GSPET data, in asymptomatic DM1 patients. In conclusion, myocardial perfusion GSPET was useful as a screening test in DM1 patients in showing four years after the basal study, prodromal signs of cardiovascular disease, especially increase of left ventricular volumes and silent myocardial ischemia, in these patients. Our research on the above protocol is being continued.