Open Access

Using guideline parameters for indication of cardiac resynchronization therapy (CRT), only about two thirds of the patients improve clinically. Unfortunately both, surface ECG and echo are uncertain to predict CRT response. To better characterize cardiac desynchronization in heart failure, interventricular (IVCD) and intra-leftventricular conduction delays (ILVCD) were measured by esophageal left ventricular electrogram (LVE). Recordings in 43 CRT patients (34m, 9f, age: 64.7 ± 9.5yrs) evidenced only weak correlation between IVCD and QRS of 0.53 and between ILVCD and QRS of 0.33. This demonstrated that QRS duration is not a reliable indicator of desynchronization. Therefore, the study resulted into development of LVE feature for a programmer with implant support device. It can be used interoperatively to guide the left ventricular electrode location in order to increase responder rate in CRT.

Introduction: Patient selection for cardiac resynchronization therapy (CRT) requires quantification of left ventricular conduction delay (LVCD). After implantation of biventricular pacing systems, individual AV delay (AVD) programming is essential to ensure hemodynamic response. To exclude adverse effects, AVD should exceed individual implant-related interatrial conduction times (IACT). As result of a pilot study, we proposed the development of a programmer-based transoesophageal left heart electrogram (LHE) recording to simplify both, LVCD and IACT measurement. This feature was implemented into the Biotronik ICS3000 programmer simultaneously with 3-channel surface ECG. Methods: A 5F oesophageal electrode was perorally applied in 44 heart failure CRT-D patients (34m, 10f, 65±8 yrs., QRS=162±21ms). In position of maximum left ventricular deflection, oesophageal LVCD was measured between onsets of QRS in surface ECG and oesophageal left ventricular deflection. Then, in position of maximum left atrial deflection (LA), IACT in VDD operation (As-LA) was calculated by difference between programmed AV delay and the measured interval from onset of left atrial deflection to ventricular stimulus in the oesophageal electrogram. IACT in DDD operation (Ap-LA) was measured between atrial stimulus and LA.. Results: LVCD of the CRT patients was characterized by a minimum of 47ms with mean of 69±23ms. As-LA and Ap-LA were found to be 41±23ms and 125±25ms, resp., at mean. In 7 patients (15,9%), IACT measurement in DDD operation uncovered adverse AVD if left in factory settings. In this cases, Ap-LA exceeded the factory AVD. In 6 patients (13,6%), IACT in VDD operation was less than or equal 10ms indicating the need for short AVD. Conclusion: Response to CRT requires distinct LVCD and AVD optimization. The ICS3000 oesophageal LHE feature can be utilized to measure LVCD in order to justify selection for CRT. IACT measurement simplifies AV delay optimization in patients with CRT systems irrespective of their make and model.

About 20% of those heart failure patients receiving cardiac resynchronization therapy (CRT) are in atrial fibrillation (AF). Current guidelines apply for patients in sinus rhythm only. Recent studies have shown again, that successful resynchronization is closely linked to a pre-existent ventricular desynchronization. In those studies, the interventricular conduction delay (IVCD) was determined prior to device implantation by ultrasound in patients with sinus rhythm (SR)only. In patients with AF this method ́s use is limited. To implement left-heart electrogram (LHE) into standard programmers and to simplify IVCD measurement in heart failure patients with AF, LHE was recorded in 11 AF patients with heart failure by Biotronik ICS3000 programmer via a15Hz Butterworth high-pass filter. Therefore, TOslim esophageal electrode (Dr. Osypka GmbH, Rheinfelden, Germany) was perorally applied and fixed in position of maximal left ventricular defection. IVCD was measured between onset of QRS in surface ECG and left ventricular defection (LV) in LHE. In addition, intra-left ventricular conduction delay (ILVCD) was measured as duration of LV in LHE. In all of the 11 AF patients, desynchronization was quantifiable by LHE. Mean QRS of 162 ± 27ms (120-206ms) was linked with IVCD of 62ms ± 27ms (37-98ms) and ILVCD of 110 ± 20ms (80-144ms), at mean. Correlation between IVCD and QRS was 0.39 (n. s.) with IVCD/QRS ratio of 0.38 ± 0.11 (0.22-0.81). A 15Hz high-pass filtered LHE feature of the Biotronik ICS3000 programmer is feasible to quantify ventricular dyssynchrony in heart failure patients with AF in order to clearly indicate implantation of CRT systems. As relations between QRS duration, IVCD and ILVCD considerably differ interindividually, the predictive values of IVCD, ILVCD and IVCD/QRS ratio for individual CRT response or non-response shall be identified in follow-up studies.

AV delay (AVD) optimization can improve hemodynamics and avoid nonresponding to cardiac resynchronization therapy (CRT). AVD can be approximated by the sum of the individual implant-related interatrial conduction interval and a mean electromechanical interval of about 50ms. We searched for methods to facilitate automatic, implant-based AV delay optimization. In 25 patients (19m, 6f, age: 65±8yrs.) with Medtronic Insync III Marquis CRT-D series systems and left ventricular electrode at lateral or posterolateral wall, we determined interatrial conduction intervals by telemetric left ventricular tip versus superior vena cava coil electrogram (LVCE). Compared with esophageal measurements, the duration of optimal AV delay by LVCE showed good correlation (k=0.98, p=0.01) with a difference of 1.5±4.9ms, only. Therefore, LVCE is feasible to determine interatrial conduction intervals in order to automate AV delay optimization in CRT-D pacing promising increased accuracy compared to other algorithms.