Relation of right ventricular pacing site to left ventricular mechanical synchrony.

Transvenous pacing leads are regularly placed in the right ventricular (RV) apex. Pediatric patients can develop myopathic changes after long-term RV apical pacing. Left ventricular (LV) mechanical dyssynchrony, estimated with echocardiography, may explain the acute decrease in LV function and long-term histopathologic changes. Ts-4w is an established echocardiographic measurement of LV synchrony, using tissue Doppler imaging (TDI). The purpose of this study was to determine whether TDI could identify acute changes in LV synchrony during pacing from different RV sites. We prospectively measured Ts-4w and Doppler-derived cardiac output after 5 minutes of pacing in 19 subjects undergoing catheter ablation. Each subject underwent pacing at 4 sites in random order: high right atrium, high RV septum (septal), RV outflow tract, and RV apex. Ts-4w was measured during sinus rhythm and each pacing protocol, with a value >65 ms defining mechanical dyssynchrony. Ts-4w during high right atrial (32.6 +/- 17.6 ms) and septal (28.9 +/- 10.9 ms) pacing were not different from sinus rhythm (39.5 +/- 15.5 ms). RV apex (85.7 +/- 18.4 ms) and RV outflow tract (84.2 +/- 20.4 ms) pacing induced mechanical dyssynchrony (p <0.0001). In conclusion, TDI demonstrated significant differences in LV synchrony related to pacing site. Ts-4w may be useful to determine ideal lead placement because it correlates with acutely improved hemodynamics.

Managed ventricular pacing in pediatric patients and patients with congenital heart disease.

Ventricular dyssynchrony induced by ventricular pacing (VP) may predispose patients to congestive heart failure. The detrimental effects of VP are directly related to the cumulative percentage of VP (Cum%VP). Managed VP (MVP) is a novel pacing algorithm developed to minimize unnecessary VP by uncoupling atrial pacing from VP. This retrospective analysis assessed the feasibility of using MVP in pediatric patients and patients with congenital heart disease (CHD). A multicenter review evaluated all pediatric patients <22 years old and older patients with CHD that had an implanted device using a MVP algorithm. Primary outcome variables were Cum%VP and adverse events. A subgroup analysis evaluated patients that had a DDD(R) pacemaker before a MVP device and compared Cum%VP before and after initiation of MVP. From 6 centers 62 patients (mean age 21.5 +/- 9.6 years) were included; 64% had CHD. With a MVP device, mean Cum%VP was 4.3 +/- 14.6% (range 0 to 83.7): Eleven patients were eligible for subgroup analysis. Compared with DDD(R), Cum%VP significantly decreased with MVP (67.1 +/- 29.4% vs 9.2 +/- 24.8%, p = 0.002). One MVP-related adverse event occurred; a patient with intermittent atrioventricular block had symptoms with frequent nonconducted atrial depolarizations and was reprogrammed to DDD. In conclusion, MVP can be used safely and can significantly reduce unnecessary VP in pediatric patients and patients with CHD.

Substrate characterization of ventricular tachycardia in a porcine model of tetralogy of Fallot using noncontact mapping.

BACKGROUND: Ventricular tachycardia (VT) in patients following tetralogy of Fallot (TOF) repair is challenging to map because of the presence of scar, patch material, and hemodynamic residua of surgery. This study investigates whether noncontact mapping can identify the arrhythmia substrate in a porcine model that involves a right ventricular outflow tract (RVOT) patch and either chronic volume or pressure load on the right ventricle. METHODS: Nine infant pigs (3-5 kg) underwent surgery involving an RVOT patch and creation of pulmonary insufficiency (PI, n = 4) or pulmonary stenosis (PS, n = 5). After a mean of 4.2 months, pigs underwent invasive electrophysiology studies (EPS) with noncontact mapping (Ensite, St. Jude Medical, St. Paul, MN USA) of the right ventricle. Automated, unipolar voltage maps (VM) were constructed during sinus rhythm. Threshold for substrate was set at -0.5 mV and incrementally adjusted to higher values until a contiguous region of low voltage was delineated. Programmed stimulation was performed to induce VT. VT activation was correlated to location of VM defined substrate. Three control pigs underwent EPS and VM. RESULTS: Free-wall RVOT substrate was identified in each of the model animals, correlating to location of the patch. The mean voltage threshold was -1.1 mV. VT was induced in 6/9 animals. Diastolic activation approximated the inferior or lateral border of the substrate in all animals. No RVOT substrate was identified in the control pigs. CONCLUSION: Automated voltage mapping of sinus beats identifies substrate for VT in a porcine model of TOF. Consistent diastolic activation of the substrate border was found during VT. Targeting this area may be useful in the ablation of VT after repair of TOF.