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.