For ARVC patients, both missense and non-missense DSP mutations carry a high arrhythmic risk. Non-missense mutations are specifically associated with left-dominant forms. The presence of DSP non-missense mutations should alert to the likely development of LV dysfunction. These findings highlight the clinical relevance of genetic testing even after the clinical diagnosis of ARVC and the growing clinical impact of genetics.
Blood pressure measurement has a long history and a crucial role in clinical medicine. Manual measurement using a mercury sphygmomanometer and a stethoscope remains the Gold Standard. However, this technique is technically demanding and commonly leads to faulty values. Automatic devices have helped to improve and simplify the technical aspects, but a standardised procedure of obtaining comparable measurements remains problematic and may therefore limit their validity in clinical practice. This underlines the importance of less error-prone measurement methods such as ambulatory or home blood pressure measurements and automated office blood pressure measurements. These techniques may help to uncover patients with otherwise unrecognised or overestimated arterial hypertension. Additionally these techniques may yield a better prognostic value.
Background
Left bundle branch block (
LBBB
) is common after transcatheter aortic valve implantation (
TAVI
) and is an indicator of subsequent high‐grade atrioventricular block (
HAVB
). No standardized protocol is available to identify
LBBB
patients at risk for
HAVB
. The aim of the current study was to evaluate the safety and efficacy of an electrophysiology study tailored strategy in patients with
LBBB
after
TAVI
.
Methods and Results
We prospectively analyzed consecutive patients with
LBBB
after
TAVI
. An electrophysiology study was performed to measure the
HV
‐interval the day following
TAVI
. In patients with normal His‐ventricular (
HV
)‐interval ≤55 ms, a loop recorder was implanted (
ILR
‐group), whereas pacemaker implantation was performed in patients with prolonged
HV
‐interval >55 ms (
PM
‐group). The primary end point was occurrence of
HAVB
during a follow‐up of 12 months. Secondary end points were symptoms, hospitalizations, adverse events because of device implantation or electrophysiology study, and death. Of 373 patients screened after
TAVI
, 56 patients (82±6 years, 41% male) with
LBBB
were included.
HAVB
occurred in 4 of 41 patients (10%) in the
ILR
‐group and in 8 of 15 patients (53%) in the
PM
‐group (
P
<0.001). We did not identify other predictors for
HAVB
than the
HV
interval. The negative predictive value for the cut‐off of
HV
55 ms to detect
HAVB
was 90%. No
HAVB
‐related syncope occurred in the 2 groups.
Conclusions
An electrophysiology study tailored strategy to
LBBB
after
TAVI
with a cut‐off of
HV
>55 ms is a feasible and safe approach to stratify patients with regard to developing
HAVB
during a follow‐up of 12 months.
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