In our study of patients we demonstrated the

In our study of 24 patients, we demonstrated the highly accurate identification of PVPs by using the HDMM. These findings aligned with several other studies applying high-density mapping catheters such as either the HDMM or other comparable basket catheters [9–11]. As confirmed by the study group of Neumann et al., as well as by our own study group, high-density guided mapping and ablation procedures not only lead to higher primary success rates, but also to excellent success rates in the follow-up period [8–10]. All procedures were carried out using a high-density mapping catheter and open-irrigated radiofrequency ablation. In contrast, the combination of such a high-density mapping catheter, like the HDMM, with ablation propertiesmerged into one catheter, the High Density Mesh Ablator (HDMA), didfail in the detection of PVI over time. High-resolution, mapping guided ablation led to an excellent initial acute success rate [15–17]. However, and as having been demonstrated by both Steinwender et al. and our own study, the favorable acute success rates initially demonstrated, had high AF relapse rates in the long term [18,19]. The thin electrodes of the HDMA, which are able to precisely map the PV-ostium, were not suitable to induce a durable ablation scar.
Study limitations
Conclusion
Conflict of interest
Introduction Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disease characterized pathologically by myocyte hypertrophy, myocyte disarray, fibrosis, and arteriolar remodeling [1]. HCM is also the most common cause of sudden cardiac death in young individuals [2]. Increased QT dispersion is considered a risk factor for sudden death in HCM [3–6]. The possible mechanisms underlying increased QT dispersion in HCM are ion channel [7] and gap junction remodeling [8], leading to increased MG 149 cost duration, decreased conduction velocity, and increased spatiotemporal dispersion of repolarization [9], which would manifest as QRS prolongation and increased QT dispersion on surface electrocardiogram (ECG). An important feature of HCM is inhomogeneity of the distribution of left ventricular (LV) hypertrophy, which has been shown to predispose to increased QT dispersion [10]. Another possible contributor to increased QT dispersion that has not been investigated is fibrosis. Fibrosis could slow impulse propagation and enhance dispersion of repolarization induced by hypertrophy. Gadolinium (Gd)-enhanced cardiac magnetic resonance (CMR) imaging permits non-invasive assessment of replacement fibrosis [11] and diffuse interstitial fibrosis [12–14], which are commonly seen in patients with HCM [15]. Gadolinium rapidly diffuses out of capillaries into the cardiac interstitium, but is unable to cross intact cell membranes. A greater volume of distribution combined with slower kinetics of Gd efflux from areas of interstitial and replacement fibrosis leads to higher amounts of Gd per unit volume in areas of fibrosis compared with the normal myocardium, which is detected by CMR imaging. In this study, we examined the relationship between fibrosis, dispersion of ventricular repolarization, and ventricular arrhythmias in patients with HCM. QTc dispersion on surface ECGs was used to assess dispersion of ventricular repolarization [16]. Diffuse interstitial fibrosis [17] and replacement fibrosis [14] (Fig. 1) were assessed by measuring post-contrast T1 relaxation time and late Gd enhancement (LGE), respectively, using CMR imaging.
Methods The study was approved by the Johns Hopkins Institutional Review Board (IRB# NA_00079621, last approval date 01-07-2013). Consecutive, unrelated adult patients who were seen in the Johns Hopkins HCM Clinic between 2009 and 2012 were retrospectively studied if they fulfilled the standard diagnostic criteria for HCM, namely left ventricular hypertrophy (maximum wall thickness ≥15mm) and/or septal-to-posterior free wall ratio > 1.3 by echocardiography, in the absence of other causes such as hypertension and/or valvular disease.