Transcoronary mapping of ventricular asynchrony due to left bundle branch block in a porcine model.

ABSTRACT

BACKGROUND: Optimal positioning of the left ventricular (LV) lead at the latest activated part of the left ventricle is one of the major challenges in implantation of cardiac resynchronization therapy (CRT) devices with respect to ascertaining an optimal resynchronization effect resulting in a high responder rate. In the present study, we evaluated the feasibility of transcoronary measurement of LV electrical activation by a coated guidewire in a porcine model. METHODS AND RESULTS: Transcoronary measurement of ventricular activation was performed in 16 pigs under general anesthesia. Left bundle branch block (LBBB) was induced by transvenous pacing in the right ventricular apex (RVA). A specially coated guidewire (Vision Wire; Biotronik) serving as the different electrode was positioned subsequently in the proximal and distal part of each coronary main vessel. A cutaneous skin patch electrode was placed at the back of the thorax of the animal to act as the indifferent electrode. Both electrodes were connected to a portable electrophysiology lab system (EP Tracer 38; CardioTek). Mean QRS width during transvenous right ventricular pacing was 83 ± 5 ms with a typical LBBB pattern. The measured time interval between the beginning of the QRS complex in the surface electrocardiogram (ECG) and the local signal derived from the tip of the guidewire (QRS-EGM) was 32 ± 9 ms in the distal ramus circumflex (RCX) coronary artery and 51 ± 6 ms in the proximal RCX, yielding a mean delay of 18 ± 8 ms within this vessel. In the left anterior descending (LAD) coronary artery, the local signal was 23 ± 10 ms in the distal part and 41 ± 10 ms in the proximal part of the vessel, with an identical mean delay of 18 ± 8 ms. The QRS-EGM interval within the right coronary artery (RCA) was 14 ± 8 ms in the distal part and 40 ± 9 ms in the proximal part of the vessel, resulting in a mean delay of 25 ± 7 ms. The delay between the activation of the distal RCA and the activation of the distal LAD and RCX was statistically significant (P<.001). Within the proximal guidewire positions, the latest electrical activation of the left ventricle during pacing-induced LBBB could be observed in the RCX with 51.4 ± 6.3 ms (P<.01). CONCLUSION: Transcoronary measurement of LV excitation by a specially coated guidewire is feasible and could confirm the electrical asynchrony induced by LBBB. Since coronary angiography is a mandatory part of the evaluation of patients for CRT implantation, a "transcoronary mapping procedure" can be easily performed, thereby evaluating the latest activated part of the left ventricle in advance of the implantation procedure, aiming to improve the responder rate in CRT therapy.