Effect of Premature Atrial Contraction on
QT Interval Duration in Patients with Previous
Myocardial Infarction and Ventricular Arrhythmias

K. Szydlo, M. Trusz-Gluza, A. Wnuk-Wojnar, K. Wita, and D. Urbanczyk

1^st Dept. of Cardiology, Silesian Medical Academy, Katowice, Poland

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1. Introduction

Many clinical trials from last two decades have shown that non-invasive risk factors can be very helpful in identifying of patients (pts) at high risk for sudden cardiac death (SCD). Special interest is focused on pts with history of myocardial infarction (MI) in whom risk stratification plays a crucial role e.g. in recommendation for the implantation of cardioverter-defibrillator (ICD). The QT interval duration, especially prolonged, is regarded as a one of the factors of higher risk of SCD and the malignant ventricular arrhythmias such as ventricular tachycardia (VT) or ventricular fibrillation (VF). The QT/RR relationship is still not clear. It is modifying by many factors such as heart rate (HR), sympatho-vagal activity or intrinsic state of myocardium in patients with the history of myocardial infarction (MI) (e.g. regional ischemia or ion channel activity in the region surrounding the scar). Changes in the heart rate are regarded as a most potent factor, which provides to the phenomenon of the QT adaptation- hysteresis lasting up to few minutes. But it was also shown during electrophysiological experiments that during stable sinus rhythm the prolongation of the QT interval could be observed even after one premature beat. That observation was made during ventricular stimulation, in which the lower was stimulation cycle the greater was following QT interval.

The purposes of study were to analyze if any changes of QT interval could be observed after premature atrial contraction (PAC) in postextrasystolic beats in patients (pts) with benign (No VT/VF) and malignant (VT/VF) arrhythmias, and if there are related to the prematurity of premature beat- PAC.

2.  Methods

The study population consisted of 80 pts with the history of MI (>30 days). There were: 40 pts with benign arrhythmia (No VT/VF) (25males, 58±7 yrs, EF- 45±7%, all treated with beta-blockers) and 40 pts with malignant ventricular arrhythmias (VT/VF) (all qualified to the implantation of ICD; 36 males, 57±11 yrs, EF- 42±11%, treated with amiodarone- 31 pts or beta-blockers- 9 pts). QT was calculated manually from the Holter recording's strips (one for each patient, always the same channel, between 9-12 a.m. during stable sinus rhythm 50-70 bpm, one sinus beat before and 4 after PAC). Duration of the coupling interval (CI), postextrasystolic pause (PP) were also measured with calculation of the premature index (PI). Both groups were divided into two subgroups: a cut-off point was established using the median value of PI in each group: for No VT/VF: Me= 0.65 and for VT/VF: Me= 0.68. The difference between QT of preceding (QT-1) and first sinus beat following (QT+1) PAC was also calculated- delta QT (dQT).

3.  Results

Table 1.   Basic ECG data of whole population.

*- p<0.01 for No VT/VF vs VT/VF

There were no significant differences in gender, ejection fraction or treatment between analysed groups and subgroups. Basic ECG parameters did not differ either. Patients with lower PI (<Me) were characterised by statistically higher QT duration after PAC in both No VT/VF and VT/VF subgroups, with the highest values in pts with VT/VF and with low PI. These subgroups (VT/VF<Me and VT/VF>Me) had also the highest increase of postextrasystolic QT duration (dQT). Significant augmentation of the QT duration in each study subgroup was observed only in the first sinus beat following PAC.

It may indicate that disturbances of the repolarization process could be observed even after PAC, when impulse propagation is orthodromic. These observations could be related to the intrinsic state of the myocardium with different electrophysiological properties in peri-scar region or greater disturbances in microvascular flow. Physiological propagation of the impulse may be responsible for the lower differences between study subgroups but the trend to higher values of QT duration in the VT/VF group with low PI is visible. The relationship between this fact and occurrence of malignant ventricular arrhythmias could be possible.

Table 2.   QT intervals in the study subgroups according to the median of PI (inter-group analysis).

*- p<0.01 for No VT/VF>Me vs VT/VF>Me

**- p<0.05 for No VT/VF<Me vs No VT/VF>Me and for VT/VF<Me vs VT/VF>Me

Table 3.   Comparison of QT duration of the sinus beat before PAC (QT-1) and preceding beats (QT+1 to QT+4) in study subgroups (p values are given).

	QT+1	QT+2	QT+3	QT+4
No VT/VF<Me	<0.001	ns	ns	ns
No VT/VF>Me	<0.01	ns	ns	ns
VT/VF<Me	<0.001	ns	ns	ns
VT/VF>Me	<0.001	ns	ns	ns

4.  Conclusion

Single PAC provokes prolongation of QT interval especially in patients with malignant ventricular arrhythmias and with low prematurity index. It may indicate greater disturbances of the repolarisation process in these patients which are unrelated to the physiological propagation of the impulse. Further investigation in this field is absolutely needed.