TAVI is established as an option with reduced morbidity and mortality in high risk symptomatic patients unfit for open surgery
[10–14]. Considering the proximity of aortic valve annulus to conduction system, both open surgery and TAVI may impact on both AV node and His bundle conduction.
While complete AV block was reported in 5.7%, new LBBB occurred in 18% with an association to complete AV block, syncope, and sudden cardiac arrest at long term after open surgery
[15–17]. Risk factors for complete AV block after surgical aortic valve replacement include previous aortic regurgitation, myocardial infarction, pulmonary hypertension, and postoperative electrolyte imbalance
[16, 17], among ECG criteria right bundle branch block (RBBB) on surface ECG was the strongest predictor for pacemaker requirement
Although previous investigations report changes in surface-ECG after TAVI
[2, 10–14], our group was the first to describe intracardiac conduction abnormalities for better discrimination of new ECG changes on surface-ECG, and to predict critical conduction delays
. In our series, complete AV block was seen in 13.3%, while 8.9% suffered from type II second-degree AV block; thus, 22.2% of patients developed an indication for permanent pacemaker implantation corroborating previous findings
[10–14, 19–23]. Additionally, 28.9% patients received a pacemaker for new LBBB combined with a marked prolongation of the HV interval to ≥ 75 msec for primary prevention. Such indication may be debatable, but due to the lack of data and due to the novelty of TAVI in elderly patients with several comorbidities preventive pacemaker use appears justified
Jilaihawi et al. reported first that pacemaker requirement after TAVI correlates to left axis deviation at baseline, LBBB, baseline thickness of the native non-coronary cusp and to diastolic interventricular septal dimension > 17 mm
. Similarly, Piazza et al. revealed no prosthesis-related LBBB when the proximal end of the valve frame was positioned < 6.7 mm from the lower edge of the non-coronary cusp
. Degenerative calcification of the aortic and mitral annulus is probably a diffuse process, in which the cardiac conduction system is often involved and making it vulnerable to injury when exposed to mechanical compression by the nitinol frame of the CoreValve, which seems to completely expand within the first 7–10 days
. Differences to surgical aortic valve replacement might be due to the different techniques. In surgical approach the valve is replaced by another. Thus, the amount of conduction damage is predictable because the local trauma is nearly the same in all patients. However, in TAVI the amount of local damage is dependent of local calcification, the height of implantation in LVOT, the extend of trauma during index-procedure (balloon valvuloplasty, balloon-to-aortic annulus relation, post-TAVI dilatation) and from further aortic annulus geometry.
Our intracardiac measurements revealed that occurrence of first-degree AV block were predominantly due to prolongation of HV interval, which might be prognostically relevant
. We implanted pacemaker in patients with new LBBB and a HV prolongation to ≥ 75 msec in a somewhat liberal fashion in this patients with high comorbidity index. In contrast, our multivariate analysis revealed that only a PQ duration > 200 msec, a LBBB and a QRS duration > 120 msec immediately (within 60 minutes) after CoreValve implantation seem to predict critical AV conduction delay. Other baseline clinical and ECG parameters had no impact. The occurrence of above ECG findings soon after TAVI may reflect the extent of trauma from the procedure. Interestingly, the exact determination of both the amount of valve calcification and the height of implantation turned out to be non-reproducible although both parameters have been claimed to impact on conduction physiology
[10, 13]. For example, the Edwards SAPIEN valve, shorter and less likely to extend into the left ventricular outflow tract, is obviously associated with a lower rate of complete AV block (0-6%)
[25, 26]. As demonstrated by our results, we believe that regardless of favourable anatomy only the extent of trauma predict the occurrence of critical conduction delay after TAVI. According to our multivariate analysis HV prolongation ≥ 75 msec is not a predictor for pacemaker requirement. We have implanted since 2007 nearly 400 aortic valves. Our pacemaker rate was initially about 45%. This was due to the novelty of this technique and lack of information regarding the true indication for pacing. However, with further analysis of patients and improving implantation techniques (e.g. high implantation technique, no further post-TAVI balloon dilatation) our pacing rate decreased to 9-10%. Based on our data we decided not to perform routinely intracardiac measurements. The presence of a new left bundle branch block in case of normal AV conduction on surface ECG in not an indication for pacing. For clinical routine, a surface 12-lead ECG immediately (within 60 minutes) after the TAVI procedure may indicate the need for pacemaker without incremental information from intracardiac ECG recordings, the quantification of aortic valve calcification, septal thickness or height of implantation.