Myocardial performance is reduced immediately prior to ventricular ectopy.

BACKGROUND: We recently demonstrated local voltage potentials indicating conduction impairment and block in the sinus beats preceding ventricular premature beats (VPBs) originating in the ventricular outflow tracts. OBJECTIVE: The purpose of this study was to test the hypothesis that impairment of impulse conduction would also lead to changes in the contractile performance of sinus beats preceding ventricular ectopy using Tissue Doppler echocardiography. METHODS: Twenty-three consecutive patients with VPBs were examined in the apical 4-chamber view with a frame rate of 150 Hz (GE VIVID VII). Eleven patients had no structural heart disease, 5 had dilated cardiomyopathy, 4 had ischemic heart disease, 2 had arrhythmogenic right ventricular dysplasia, and 1 had aortic stenosis. The ectopy originated in the ventricular outflow tracts in 15 patients and in the left ventricle 8. Eleven of the patients underwent radiofrequency ablation of the VPBs. RESULTS: Tissue Doppler imaging demonstrated a highly statistically significant decrease in myocardial performance in the last sinus beat before the VPB compared to earlier sinus beats. Thus, ejection time (time to peak end-systolic contraction) and peak systolic velocity shortened significantly (P <.001 for both) with a subsequent reduction in systolic shortening (end-systolic displacement; P <.001). CONCLUSION: Ventricular ectopy is preceded by a significant decrease in myocardial performance in the last sinus beat preceding VPBs as observed in consecutive patients with a broad variety of heart conditions pointing to a mutual underlying electrical mechanism (ie, localized conduction block confined to an area surrounding the ectopic pacemaker).

The role of local voltage potentials in outflow tract ectopy.

AIMS: Discrete, fragmented, local voltage potentials (LVPs) have been observed in electrograms recorded at the ablation site in patients undergoing radiofrequency ablation for arrhythmias originating in both the right and left ventricular outflow tract; however, the incidence and the significance of the LVP with respect to arrhythmogenesis is uncertain. METHODS AND RESULTS: We studied 25 patients with outflow tract arrhythmias referred for radiofrequency catheter ablation and recorded high-amplified intracardiac electrograms close to the site of origin of the arrhythmia. Ten patients undergoing ablation for supraventricular arrhythmias served as controls. During sinus rhythm, LVPs were recorded in 24 of the 25 patients, 10-85 ms (41 +/- 19 ms) after the onset of the QRS complex, duration 33 +/- 11 ms, voltage 2.0 +/- 1.5 mV. The same potential was recorded 10-52 ms (mean 37 +/- 11 ms) prior to the V potential in the ventricular premature beats. In 10 patients, ventricular parasystole was suggested by varying coupling intervals >100 ms, and fusion beats allowing for the estimation of the least common denominator of R-R intervals. In 23 of the 25 patients, the 12-lead electrocardiogram (ECG) and intracardiac contact mapping located the arrhythmias to an area of 3-4 cm(2) in the septal region of the right ventricular outflow tract; in two patients, the site of origin was in the left coronary cusp. Radiofrequency ablation carried out in 24 of the 25 patients was successful in 21 patients, and after successful ablation, the LVP could still be recorded in all these 21 patients. The LVP was not present in 10 controls. CONCLUSION: Local potentials are recorded close to the site of origin of ventricular ectopy in >90% of patients with idiopathic outflow tract ectopy and imply successful ablation. The potentials may reflect an area of depressed conductivity known to be a prerequisite for experimental ventricular ectopy including parasystole.

Phase 2 reentry in man.

BACKGROUND: Ventricular extrasystoles are characterized by a fixed coupling interval to the last QRST complex preceding it. OBJECTIVES: We hypothesized that this QRST complex differed from QRST complexes of other sinus beats not followed by ventricular extrasystoles. Further, we investigated whether phase 2 reentry, demonstrated in animal experiments to initiate ventricular extrasystoles, ventricular tachycardia, and ventricular fibrillation, also plays a role in humans. METHODS: We examined 18 patients with ventricular extrasystoles and/or ventricular tachycardia by signal averaging of the ECG (group A) or by single-beat analysis of intracardiac electrograms (group B). Group A consisted of six patients without structural heart disease and one patient with the Brugada syndrome. Six of the seven patients had right ventricular outflow tract ventricular extrasystoles. Group B consisted of 11 patients undergoing radiofrequency ablation. Eight of the 11 patients had right ventricular outflow tract extrasystoles. RESULTS: In six of the seven patients in group A, we demonstrated significant ST-elevation and/or T-wave changes in the sinus beat preceding ventricular extrasystoles compared with the second last sinus beat in one or more of the three orthogonal leads X, Y, and Z. In 9 of the 11 patients in group B, single-beat analysis of unipolar and bipolar electrograms recorded close to successful ablation sites demonstrated similar changes, that is, ST-elevation (median peak voltage gradient 150 muV, range 0-1,700) and T-wave changes in the sinus beat prior to ventricular ectopy. In addition, J-point elevation was demonstrated in several cases. In total, significant changes were demonstrated in 15 of the 18 patients studied (83%). CONCLUSION: J-point elevation, ST-elevation, and T-wave changes documented in the last sinus beat prior to ventricular extrasystoles are in agreement with phase 2 reentry, suggesting that this may be the responsible mechanism for ventricular extrasystoles and ventricular tachycardia/fibrillation. The phenomenon has been demonstrated in only animal experiments to date.