Introduction:
PICM is associated with a significantly increased risk of heart failure
hospitalization and all-cause mortality [1]. The incidence of
pacemaker induced cardiomyopathy PICM has been reported to be
approximately 10-15%, with increased risk in patients with a wide paced
QRS duration and a high right ventricular pacing burden
(>20%). The risk of PICM has also been suggested to be
higher in patients who are male, exhibit atrioventricular block as an
indication for PPM implantation, and have a previous history of
myocardial infarction, chronic kidney disease, and atrial fibrillation
[2 3]. Pacing mode has not been associated with an increased risk of
PICM. The reported incidence of PICM has also been dependent on how it
is defined in the given study. One recent meta-analysis of PICM
identified 15 unique definitions of PICM [1]. In that meta-analysis,
the pooled prevalence of PICM was 12%. The reported incidence is
highest when PICM is defined as a LVEF decrease of ≥10%. One recent
study showed that when PICM was defined as an LVEF reduction of ≥ 10%,
the reported incidence was 39% [4]. The most commonly used
definition of PICM is a ≥10% decrease in LVEF to an LVEF of
<50% [3]. This second definition is the most stringent
but also provides the highest degree of confidence that a cardiomyopathy
has developed as a result of pacing. In one recent study, the incidence
of PICM was shown to be significantly less with LPs compared to TVPs
[5]. However, robust data is lacking. Our study attempts to better
understand the impact of LPs on left ventricular function by assessing
pre and post implantation LVEF and how this is related to tricuspid
regurgitation, LP septal implantation location, and paced QRS duration.
The development of and worsening underlying tricuspid valve
regurgitation has also been shown in patients with both TVPs and LPs.
Implantation of TVPs leads to moderate to severe TVR in 14-29% of cases
and to worsening of baseline TVR in an even greater proportion of cases
[2 6-8]. The degree of TVR has been shown to increase with the
number of leads crossing the tricuspid valve, and the mechanisms of TVR
from pacemaker leads include valve obstruction caused by a lead placed
between leaflets, lead adherence due to fibrosis and scar formation to
the valve causing incomplete closure, lead entrapment in the tricuspid
valve apparatus, and valve perforation or laceration [6]. A recent
study containing 28 patients with a St. Jude Nanostim LP and 25 patients
with a Medtronic Micra LP showed worsening TVR by 1 or 2 gradations in
43% of patients [9]. The same study also showed that those with a
more septal compared to apical position were five times more prone to
worsening TVR. Potential pathophysiologic explanations of worsening TVR
after LP include direct interaction of the LP with tricuspid valve
apparatus, valve damage during implantation, and ventricular
dyssynchrony. However, the incidence of TVR attributable to LP
implantation in that study was unexpectedly high. Our study attempts to
better understand the impact of LPs on the frequency and severity of TVR
independent of and relative to septal location.