![]() Patients who were unable to give consent, or were clinically unstable, were excluded. Inclusion criteria for the CRT group were LBBB morphology on 12‐lead ECG with QRSd > 130 ms, EF < 35%, NYHA II–IV. Two groups of patients were recruited at a single tertiary cardiac center (Hammersmith Hospital, London, UK): (1) patients with LBBB and left ventricular impairment scheduled for biventricular pacemaker implantation with or without defibrillator function (2) a comparison group of patients with normal 12‐lead QRS morphology and narrow QRSd undergoing epicardial mapping for ventricular ectopy ablation, arrhythmia risk stratification, or recruited specifically as normal subjects. Therefore, although His‐CRT is a promising alternative to BVP, before proceeding to long‐term head‐to‐head randomized control trials it would be helpful to develop tools for improving patient selection and intra‐procedural targets: This can be particularly challenging in the presence of nonselective His bundle capture, which results in a pseudo‐delta wave as a result of local right ventricular myocardial capture at the lead tip.įurthermore, it is not known whether the reduction in activation times achieved with HBP is associated with restoration of the normal physiological ventricular activation pattern. These patients have the highest chance of successful resynchronization with HBP.Ī second challenge is that it is difficult, using the 12‐lead ECG, to quantify left ventricular resynchronization and therefore to determine whether the maximum potential resynchronization has been achieved: LVAT cannot be easily identified with the 12‐lead ECG. ![]() found, using intracardiac septal mapping, that conduction block within the left‐sided His fibers or proximal portion of the left bundle branch was present in 64% of patients with a 12‐lead ECG appearance of LBBB. The 12‐lead ECG is an imperfect tool for identifying the mechanism of conduction impairment. HBP is most likely to deliver ventricular resynchronization in patients with proximal conduction system disease. However, it does not appear to be possible to shorten ventricular activation time in all patients with 12‐lead ECG features of LBBB. His‐CRT can produce greater QRS duration (QRSd) shortening and LVAT reduction than BVP, which translate to larger improvements in acute hemodynamic function. His‐cardiac resynchronization therapy (His‐CRT) resynchronizes ventricular activation by overcoming proximal conduction system block, thereby activating the ventricles via the native His‐Purkinje system. His bundle pacing (HBP) has recently been proposed as a method for delivering more effective ventricular resynchronization than BVP. In fact, it produces only relatively modest reductions in ventricular activation time and results in nonphysiological ventricular activation patterns.Īs a result, there has been interest in the development of more effective CRT. However, BVP does not completely correct the disordered ventricular activation that occurs with LBBB. However, many patients treated with BVP continue to experience high symptom burdens and poor prognoses.īVP is thought to produce its beneficial effect by delivering more synchronous ventricular activation and shortening atrioventricular interval. ![]() ![]() Biventricular pacing (BVP) is the most widely used method for delivering CRT and has been shown to improve symptoms, clinical outcomes, and mortality. The aim of cardiac resynchronization therapy (CRT) is to correct this abnormality of electrical activation to improve cardiac function in patients with heart failure and LBBB. Left bundle branch block (LBBB) causes dyssynchronous ventricular activation.
0 Comments
Leave a Reply. |
Details
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |