Dynamic QT/RR relationship in post-myocardial infarction patients with and without cardiac arrest.

OBJECTIVES: Changes in QT interval dynamicity may be associated with susceptibility to ventricular fibrillation (VF) after myocardial infarction (MI). We tested the hypothesis that dynamic QT/RR relationship might differ between post-MI patients with and without a history of VF. We also evaluated the influence of negative T-waves on the assessment of QT/RR relationship. DESIGN: We reviewed Holter recordings from 37 post-MI patients resuscitated from VF not associated with new MI (VF group) and 30 patients after MI without known sustained ventricular arrhythmias (control group). With an automated computerized program, we measured QT interval dynamicity as the mean QT/RR slope and as the maximal QT/RR slope determined at stable heart rates. RESULTS: The mean QT/RR slope was 0.20 ± 0.08 in control group and 0.15 ± 0.09 in VF group (p=0.01) whereas corresponding maximal QT/RR slope values were 0.42 ± 0.20 and 0.33 ± 0.18 (p=0.01), respectively. Thirteen control patients (43%) and 22 VF patients (59%) showed only negative or both positive and negative T-waves (p=0.45). Mean QT/RR slope values were similar irrespective of T-wave polarity whereas maximal QT/RR slopes were steeper in cases with both positive and negative T-waves. Cases showing T-waves of both positive and negative polarity exhibited greatest intersubject variability of both QT/RR slope values. CONCLUSIONS: Lower mean QT/RR slope may be associated with a risk of VF after MI. A detailed assessment and definition of differing T-wave polarities is essential in evaluating the QT/RR relation in post-MI patients.

Changing capacity of electrocardiographic ventricular repolarization in post-myocardial infarction patients with and without nonfatal cardiac arrest.

Prolonged and labile ventricular repolarization and decreased heart rate variability may be associated with susceptibility to ventricular fibrillation (VF) after myocardial infarction (MI). The response of ventricular repolarization related to abrupt heart rate changes may also be associated with arrhythmia vulnerability. We investigated whether diurnal maximal values or changing capacities of QT and T-wave peak to T-wave end (TPE) intervals are different in patients after MI with and without a history of VF. With an automated computerized program, Holter recordings from 29 patients after MI resuscitated from VF not associated with new MI (VF group) and 27 patients after MI without clinical ventricular arrhythmias (control group) were analyzed. Maximal QT and maximal TPE intervals were shorter in the VF group than in the control group. Patients with VF exhibited smaller capacity to change QT and TPE intervals, with differences between study groups being greatest at heart rates from 60 to 75 beats/min (p = 0.002 and 0.01, respectively). Capacity to change QT and TPE intervals correlated with vagally mediated measurements of heart rate variability (r from 0.35 to 0.46, p from 0.01 to <0.001, respectively). In conclusion, long maximal QT interval may not be the key factor exposing patients after MI to VF. Impaired capacity to change QT and TPE intervals seems to be associated with risk of VF after MI.

Effects of beta-blocker therapy on ventricular repolarization documented by 24-h electrocardiography in patients with type 1 long-QT syndrome.

OBJECTIVES: We tested the hypothesis that in long-QT syndrome (LQT) type 1 (LQT1), beta-blocker therapy may decrease both the diurnal maximal T-wave peak to T-wave end interval (TPE) and the maximal ratio between late and early T-wave peak amplitude (T2/T1 ratio), which are electrocardiographic counterparts of transmural dispersion of repolarization (TDR) and early afterdepolarizations (EA), respectively. BACKGROUND: Ventricular repolarization duration and increased TDR and EAs are the three electrophysiological components generating the high risk of ventricular arrhythmias and sudden death in the inherited LQT. In the most prevalent LQT1 form of LQT, treatment with beta-blockers reduces serious arrhythmia events dramatically without a known influence on QT interval duration. In experimental LQT1 models, beta-blockers decrease TDR and prevent EAs. METHODS: We reviewed 24-h electrocardiographic recordings obtained before and during the treatment with beta-blockers from 24 genotyped LQT1 patients to record maximal TPE intervals and T2/T1 ratios as well as maximal and rate-adapted QT intervals using a computer-assisted program. RESULTS: Treatment with beta-blockers decreased the maximal diurnal T2/T1 amplitude ratio from 3.0+/- 1.0 to 2.2 +/- 0.6 (p = 0.002). Beta-blockers also decreased both maximal TPE intervals and abrupt maximal QT intervals at heart rates higher than 85 beats/min, whereas QT intervals measured at steady-state conditions remained unchanged. CONCLUSIONS: Prevention of abrupt increases of electrocardiographic TDR, EA, and ventricular repolarization duration at elevated heart rates may explain the favorable clinical effects of beta-blockers in LQT1.