There is evidence from experimental studies that the time interval from the peak to the end of T-wave reflects the transmural dispersion in repolarization (electrical gradient) between myocardial "layers" (epicardial, M-cells, endocardial). Since Congenital Long QT Syndrome (LQTS) is considered to be classical disease or repolarisation abnormalities, we performed the present study to assess the transmural dispersion of repolarization in LQTS patients. The study group consisted of 17 patients: 7 LQTS pts and 10 pts from the control group. In each patient the 24-hour ECG recording was performed on magnetic tape. The interval from the peak to the end of the T-wave (TpTo) was automatically measured by Holter system during every hour as a measure of transmural dispersion of repolarisation. Thereafter the mean TpTo from 24-hours was calculated. In addition the spatial QT dispersion was measured from 12 lead ECG and 3 channel Holter tape as a difference between the shortest and the longest QT interval between leads. The values were compared between groups using the Anova test. TpTo was 79.6 +/- 9.6 ms (72-92 ms) in LQTS group and 62.4 +/- 7.5 ms (51-70) in the control group (p < 0.001). In LQTS group TpTo was significantly longer at night hours 72.5 +/- 2 when compared to day hours 87.4 +/- 8 (p < 0.01). The spatial QT dispersion was significantly higher in LQTS patients when compared to control, both in 12-lead standard and Holter ECG. Congenital long QT syndrome is associated with increase in both transmural and spatial dispersion of repolarization. The extent of prolongation of the terminal portion of QT in patients with congenital long QT syndrome is greater at night sleep hours compared to daily activity.

and the §Central Military Hospital Warsaw, Poland LUBINSKI, A., ET AL.: The Terminal Portion of the T Wave: A New Electrocardiographic Marker of Risk of Ventricular Arrhythmias. Experimental studies have shown that transmural dispersion of repolarization (DoR), defined as the difference in action potential duration between mid-myocardial M-cells, epicardial, and endocardial cells is reflected in the duration of the terminal portion of the T wave (TpTe) on the surface ECG. Since DoR is an important factor associated with the propensity for reentrant arrhyth mias, this study examined if TpTe may serve as a marker of risk of ventricular arrhythmias. Data from 18 patients with coronary artery disease and inducible sustained ventricular tachycardia (VT group) were compared with those of 16 survivors of myocardial infarction without inducible VT (control group). TpTe was automatically measured in each beat of 24-hour ECG recordings, and programmed ventricular stim ulation was performed in the antiarrhythmic drug-free state. TpTe was expressed as the absolute interval in milliseconds, and relative to the duration ofQTe (TpTe/QTe X 100%). TpTe duration was 74 ± 14 ms in the VT group versus 63 ± 16 ms in the control group (P < 0.004). The TpTe interval expressed as a per cent of the QT interval was 21 ± 4% in the VT group versus 17 ± 3% in the control group (P = 0.02). In patients with coronary artery disease, TpTe was longer in patients with, versus without, inducible VT. The results of this study support the hypothesis that TpTe reflects transmural dispersion of repolarization. (PACE 2000; 23[Pt. II]-.1957-1959 ventricular arrhythmias, dispersion of repolarization, T wave

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he traditional site for ventricular lead placement-the right ventricular apex (RVA), produces an abnormal pattern of ventricular depolarization, and there is growing evidence that pacing from this site is associated with detrimental functional and structural changes in the heart which might lead to an adverse clinical outcome. [1][2][3] These observations have increased interest in pacing at sites alternative to the RVA, mainly in the area of the right ventricular outflow tract (RVOT). It has been hypothesized that pacing in the RVOT, owing to its proximity to the His-bundle, results in a more physiological depolarization pattern and better hemodynamics and might reduce detrimental effects of long-term ventricular pacing. Results of a meta-analysis comparing RVA to RVOT pacing have suggested acute benefit from pacing at the RVOT. 4 However, poor definition of the outflow tract area and the non-randomized character of most trials confound the data. Longterm evaluation of the effects of chronic pacing are limited, although some mid-term observations show equivalency between apical and outflow tract pacing. 5,6 Other studies indicate that, in contrast to RVA, RVOT pacing preserves left ventricular (LV) function. 7 However, it is still not clear whether RVOT pacing provides better long-term outcome than RVA pacing.In this study we investigated RVOT pacing in comparison to RVA pacing in patients with standard indications for permanent ventricular pacing and preserved LV systolic function to determine whether RVOT pacing would provide better all-cause and cardiovascular survival. MethodsThe present study was a single-center randomized study performed in a tertiary care university hospital. The first patient was enrolled on 7 th September 1995 and the last patient on 24 th November 1997. After the 10-year follow-up visit the long-term survival in the studied population was evaluated. PatientsPatients were eligible for the study if they were at least 21 years old, had preserved LV ejection fraction (LVEF) There were no differences in the all-cause or cardiovascular mortality between the pacing sites after adjustment for age, gender, arterial hypertension, atrial fibrillation, New York Heart Association class and left ventricular end-diastolic diameter. Conclusions:The RVOT provides no additional benefit in terms of long-term survival over RVA pacing. (Circ J

Recently, multisite atrial pacing has been suggested as an alternative therapy to prevent recurrences of paroxysmal atrial fibrillation (PAF). A study was conducted to compare the acute effects of biatrial (BiA), left atrial (LA), and right atrial appendage (RAA) pacing on cardiac hemodynamics. In 14 patients with PAF and a BiA pacemaker (with leads in the RAA and coronary sinus), cardiac output (CO), right (RV) and left ventricular (LV) filling, RA-LA contraction delay [PA(m-t)] and the difference in A wave duration [Adif(m-p)] at the level of the mitral valve (Adurm) and pulmonary veins (Adurp) during RAA, BiA, and LA pacing were examined by echo-Doppler measurements. The atrial pacing site did not affect the CO. LA, but not BiA, pacing resulted in delayed RA contraction in comparison with RAA pacing with significant diminution of the RA contribution to RV filling. With LA pacing, the usual right-to-left atrial contraction sequence was reversed (PA(m-t): 8 +/- 7 ms control; 5 +/- 30 ms RAA; -10 +/- 21 ms BiA; -72 +/- 36 ms LA; LA versus control versus RAA and versus BiA, P < 0.001. LA and BiA pacing prolonged Adurp (LA 186 +/- 52 ms, BiA 180 +/- 45 ms, RAA 153 +/- 49 ms; LA and BiA vs RAA, P < 0.01). Thus Adurp exceeded Adurm [Adif (m-p): control 38 +/- 40 ms, RAA 7 +/- 42 ms, BiA -12 +/- 43 ms, LA -20 +/- 44 ms; control vs RAA, BiA, and LA; and RAA vs LA, P < 0.05]. The study showed that (1) the atrial pacing site has no influence on global cardiac performance; (2) the hemodynamic effect of BiA pacing is not superior to that of RAA pacing, and LA pacing can even be deleterious; (3) LA pacing reverses the usual right-to-left atrial contraction sequence and reduces the RA contribution to RV filling; (4) BiA and LA pacing prolong Adurp due to an altered activation pattern, decreased pulmonary venous return, or increased LA pressure.