Abnormal ECG-patterns in patients with acute and chronic cerebral processes are well known; the prognostic value, however, is still uncertain. Therefore, we examined 12 conventional ECG-leads retrospectively (at the day of admission to hospital) with respect to heart rate, occurrence of heart rhythm disturbances, and repolarization abnormalities in 131 patients (pts) with acute strokes and in 116 pts with cerebral tumors. Patients with atrial fibrillation or bundle branch blocks were excluded. In all pts the longest QT(c)-intervals (heart rate correction according to Bazett) were found in the precordial leads V2-V6 and Nehb D, A, I. Patients with strokes had the longest QT(c)-intervals: 418 +/- 43 ms (II)-445 +/- 55 ms (V5). The differences in healthy persons (n = 25) and pts with cerebral tumors were significant (p less-than-or-equal-to 0.01). Between the standard and precordial leads the differences in this group were also significant. The QT(c)-values in non-survivors were significantly longer (429 +/- 45 ms in lead I, 458 +/- 45 ms in V4) than in survivors (409 +/- 35 ms in lead I, 436 +/- 52 ms in Nehb A). Initially, unconscious pts (n = 22) also revealed significantly longer QT(c)-intervals (485 +/- 58 ms, Nehb D) than conscious pts (440 +/- 45 ms, lead V5). 78.6% of pts with strokes had QT(c)-values in at least one lead longer than 420 ms, and in 64%, we registered QT(c)-intervals > 440 ms. Significant differences were found between non-survivors (n = 56) and survivors (n = 75). The risk of dying was 2.78 fold higher in pts with at least one QT(c)-interval > 420 ms (n = 91% of pts), and 2.5 fold higher, if the maximal QT(c) interval was > 440 ms. Pts with cerebral tumors also had increased QT(c)-intervals: 398 +/- 48 ms (lead I) to 420 +/- 33 ms (V3), but the differences between survivors and non-survivors were not significant. Only pts with severe neurological disturbances (n = 76) had significantly longer QT(c)-intervals than pts with no or only mild neurological disturbances. Localization or histology of tumor had no influence on the length of QT(c)-intervals. All other investigated parameters including blood pressure were not different between pts who died and those who survived in both groups. We conclude that prolonged QT(c)-intervals with and without other repolarization abnormalities are signs of severe cerebral disturbances with secondary damage of the heart (autonomic imbalance, disseminated necroses of the myocardium, and that QT(c)-prolongations in at least one ECG lead should be more often considered in identifying risk patients with acute cerebral disorders.
