Pacing-induced electrophysiological remodeling in hypertrophic obstructive cardiomyopathy--observations on cardiac memory.

BACKGROUND: Hypertrophic cardiomyopathy carries an increased risk for sudden cardiac death. While pacing therapy reduces the left ventricular outflow tract gradient and improves symptoms in a subgroup of hypertrophic obstructive cardiomyopathy (HOCM) patients, its electrophysiological consequences are unknown and were therefore assessed in this prospective study. METHODS AND RESULTS: Fifteen consecutive HOCM patients were studied and compared with 14 patients without HOCM paced because of sinus bradycardia. ECG intervals were measured before pacemaker implantation and after > or =3 months of DDD pacing in HOCM patients and > or =5 weeks in controls. Both groups showed similar ECG signs of cardiac memory development. In HOCM patients, with baseline QTc 447 +/- 33 ms, cardiac memory development was not associated with any significant changes in ECG intervals. In contrast, baseline repolarization in control patients was significantly prolonged by 6% (QTc 429 +/- 33 vs 454 +/- 46 ms; P < 0.05). Furthermore, in HOCM patients repolarization was 7% shorter during DDD pacing compared to sinus rhythm (JTc 329 +/- 25 vs 353 +/- 21 ms; P < 0.05), despite a significantly prolonged ventricular activation time (QRS duration 155 +/- 16 vs 91 +/- 9 ms; P < 0.01). CONCLUSIONS: Importantly, the development of cardiac memory-induced different repolarization responses depending on baseline structure and electrophysiology. In HOCM patients repolarization was shorter during right ventricular apical pacing than during normal activation despite prolonged activation time.

Transient proarrhythmic state following atrioventricular junction radiofrequency ablation: pathophysiologic mechanisms and recommendations for management.

The induction of complete heart block by radiofrequency ablation of the atrioventricular junction combined with pacemaker implantation has become an established therapy for rate control in patients with atrial fibrillation who are unresponsive to drugs. Reports of ventricular arrhythmias and sudden death after ablation have, however, raised concerns about safety. Ventricular arrhythmias are usually polymorphic and related to a phase of electrical instability due to an initial prolongation and then slow adaptation of repolarization caused by the change in heart rate and activation sequence. Structural heart disease, and other factors that predispose for the acquired long QT syndrome, seem to add to the risk. Ventricular activation and repolarization stabilize during the first week after the procedure. Routine pacing at 80 beats per minute during this phase is recommended, as well as in hospital monitoring for at least 48 hours. Patients with high-risk features for arrhythmias, such as congestive heart failure or impaired left ventricular function, may require pacing at higher rates. Adjustment of the pacing rate-although rarely below 70 beats per minute-is usually undertaken after a week in most patients, preferably after an electrocardiographic evaluation for repolarization abnormalities at the lower rate.

Repolarization measures and their relation to sex hormones in postmenopausal women with cardiovascular disease receiving hormone replacement therapy.

Women are more susceptible to the development of Torsades de Pointes ventricular tachycardia and have a longer heart rate-corrected QT interval than men. A causal role for estrogen has been implicated. The purpose of this study was to investigate if hormone replacement therapy (HRT) resulted in any changes in noninvasive depolarization and repolarization measurements, and to study their relation to circulating concentrations of sex hormones. Sixty postmenopausal women with cardiovascular disease (mean age 59 +/- 7 years; range 44 to 75) were randomized to receive oral conjugated estrogens, transdermal estradiol-17-beta (both with addition of progestins), or placebo. QRS, QT, and JT intervals and their dispersion on 12-lead electrocardiograms were analyzed at baseline, and after 6 and 12 treatment cycles of HRT. Blood samples for analyses of serum concentration of estrogens and androgens were obtained on the same occasions. Neither mean RR, QT, QTc, JT, and JTc intervals, nor QT and JT dispersion changed during treatment. There was a significant inverse relation between the mean JTc interval and the serum concentration of estradiol-17-beta, independent of age, testosterone levels, and abdominal obesity. There was also a significant inverse relation between the change in androstenedione levels and the change in QT interval (Spearman -0.35, p = 0.028) or JT interval (Spearman -0.41, p = 0.009) at 6 treatment cycles compared with baseline. In conclusion, treatment with oral conjugated estrogens or transdermal estradiol-17-beta combined with progestins did not alter depolarization or repolarization measurements. However, the inverse relation between repolarization and androgens fits with an effect of androgens on repolarization in postmenopausal women.

Transient proarrhythmic state following atrioventricular junctional radiofrequency ablation.

This study was designed to prospectively assess ventricular de- and repolarization by the QRS, QT, and JT intervals, and their dispersion in the 12-lead ECG during right ventricular pacing at 60, 70, and 80 beats/min during the first month after AV junctional RF ablation. Previous reports have found early polymorphic ventricular arrhythmia after RF AV junctional ablation. Our hypothesis was that there is a proarrhythmic state following this procedure, which depends on the paced rate and time after ablation. The analysis of the immediate changes was based on 17 patients (10 men) with a mean age of 64 years (SD 14) (range 38-82 years). A 12-lead ECG was recorded during right ventricular pacing at 60, 70, and 80 beats/min within 24 hours (day 1), between 24 and 48 hours (day 2), and 1 week after ablation (day 7). For analysis of changes beyond 1 week, 13 additional patients with a mean age of 73 years (SD 8) (range 62-90 years) were analyzed on days 1, 7, and 30. All intervals were measured with a digitizing table. The mean QRS duration shortened by 2.4% at 60 beats/min (P <0.01), and the mean QT and JT intervals shortened by 5-7% between days 1 and 7 (P < 0.001). The mean QT was 9% shorter and the mean JT interval was 13% shorter at 80 compared to 60 beats/min on day 1 (P < 0.001). QT dispersion was reduced by 13% when the stimulation rate was increasedfrom 60 to 80 beats/min on day 1 (P < 0.05). There were no significant changes beyond the first week. The study results point to the induction of a proarrhythmic state immediately after AV junctional RF ablation resolving during the first week. Repolarization shortened gradually between 80 and 60 beats/min to an extent that is suggestive of a clinically important antiarrhythmic effect at the higher rate, which was supported also by clinical experience.