QT & RR variability spots the earliest autonomic deregulation in diabetes. Fading of vagal sino-atrial drive but not of sympathetic ventricular responsiveness to life challenges.

27 consecutive insulin-dependent diabetic patients (pts), under 50 years, with blood glucose controlled within normal limits and no significant or multiple cardiovascular/neurological complications in the lights of clinical tests, went through a protocol as follows: laiddown at relaxed rest for 10 min, then stood-up quietly for 7 min, and finally experienced a stress-interview for 10 min while supine. A thoracic ECG lead was digitized at I ms (Codas, Dataq Instr.), RR and QT intervals were software-detected, resampled at 500 ms, and Fourier-transformed over 3 min epochs to get auto-or cross-spectra. RR-by-QT mean square coherence detached the RR-independent fraction of QT low fequency (LF) spectral power, called idioventricular QT-LF. We detected autonomic impairment of three types (discriminant score = 92.31%), presumably differentiated upon the locus of lesion, using RR's basal variance and mean RR shortening when standing as follows: (I) RR shortening > 200 ms in 10 pts; (II) normal RR shortening but no RR variance in 4 pts; (III) stiff RR around 600 ms and no RR variance in 2 pts. The above pts have been excluded from further analysis. The remaining 11 pts with no such impairments (5M and 6F, 36.4 y +/- 4.4 SD, history of 6.0 y +/- 5.2) have been compared with 11 normal subjects in an age and gender-paired control group in two steps. Step 1: Preliminary MANOVA/ANOVA showed significant effects on the ensemble of spectral variables of every single factor (status: normal or patient group; intervention; gender) with no significant factor interactions. Significant effects of intervention or status on main RR spectral variables and on a few QT spectral variables were also documented. Step 2: Non-parametric tests showed that diabetics had (mildly to moderately) shorter mean RR, while their RR-LF was always significantly lower than those found in normals--a difference propagated to QT-LF but not to idioventricular QT-LF. In the intra-group there were similar responses to interventions except stress with respect to mean RR. Consistent reduction in RR-LF under moderate or no change in mean RR suggests vagal down- regulation that, judging by idioventricular QT-LF showing, goes perhaps before a similar process with sympathetic control of ventricles. This phase delay may introduce an early arrhythmic risk worth dealing with in secondary prevention.