AimsSome authors recommend avoiding fusion with left ventricular (LV) intrinsic depolarization during cardiac resynchronization therapy (CRT). If fusion is still present during optimized biventricular (Biv) pacing and its long-term effects on the response to CRT are currently unknown. The aim of the study was to analyse the endocardial LV activation pattern induced by echocardiographically optimized Biv pacing and its influence on LV reverse remodelling.Methods and resultsContact electro-anatomical mapping was performed in 15 heart failure (HF) patients with left bundle branch block and echocardiographically optimized CRT (seven ischaemic aetiology, 64 ± 8 years, three women, New York Heart Association class 3 ± 0.4, LV ejection fraction 25 ± 5%). Left ventricular activation maps were performed in sinus rhythm (SR), during DDD right ventricular apical (RVA) and optimized Biv pacing. Fusion with intrinsic rhythm during pacing was considered when LV septal activation was produced at least partially by intrinsic depolarization, when compared with LV activation map during SR. Patients were considered responders to CRT if they had ≥10% reduction in LV end-systolic volume (LVESV) after 6 months of CRT. During SR, the LV breakthrough was mid-septal (n = 12), basal septum (n = 2), and apical (n = 1). During RVA pacing, LV breakthrough shifted apical in all patients. Right ventricular apical/Biv pacing proved fusion with intrinsic depolarization in 8 of 15 patients. The PR interval was shorter in patients with fusion RVA/Biv pacing (164 ± 24 vs. 234 ± 55 ms, P = 0.006). There was a trend for shorter LV activation time (LVat) in patients with fusion during RVA pacing (87 ± 33 vs. 113 ± 21 ms, P = 0.08) as well as during optimized Biv pacing (83 ± 18 vs. 104 ± 24 ms, P = 0.07), although LVat was similar in SR (100 ± 22 vs. 106 ± 20, P = NS). In patients with fusion, 6 months responder rate was significantly higher (100 vs. 28.5%, P < 0.007) as was the degree of LVESV reduction (39 ± 17 vs. 1.0 ± 14%, P < 0.001).ConclusionBiventricular pacing with fusion may substantially increase the structural responder rate probably by shortening LVat.
This paper presents a new diffeomorphic temporal registration algorithm and its application to motion and strain quantification from a temporal sequence of 3D images. The displacement field is computed by forward eulerian integration of a non-stationary velocity field. The originality of our approach resides in enforcing time consistency by representing the velocity field as a sum of continuous spatiotemporal B-Spline kernels. The accuracy of the developed diffeomorphic technique was first compared to a simple pairwise strategy on synthetic US images with known ground truth motion and with several noise levels, being the proposed algorithm more robust to noise than the pairwise case. Our algorithm was then applied to a database of cardiac 3D+t Ultrasound (US) images of the left ventricle acquired from eight healthy volunteers and three Cardiac Resynchronization Therapy (CRT) patients. On healthy cases, the measured regional strain curves provided uniform strain patterns over all myocardial segments in accordance with clinical literature. On CRT patients, the obtained normalization of the strain pattern after CRT agreed with clinical outcome for the three cases.
Abstract. In this paper, we propose a complete framework for the automatic detection and quantification of abnormal heart motion patterns using Statistical Atlases of Motion built from healthy populations. The method is illustrated on CRT patients with identified cardiac dyssynchrony and abnormal septal motion on 2D ultrasound (US) sequences. The use of the 2D US modality guarantees that the temporal resolution of the image sequences is high enough to work under a small displacements hypothesis. Under this assumption, the computed displacement fields can be directly considered as cardiac velocities. Comparison of subjects acquired with different spatiotemporal resolutions implies the reorientation and temporal normalization of velocity fields in a common space of coordinates. Statistics are then performed on the reoriented vector fields. Results show the ability of the method to correctly detect abnormal motion patterns and quantify their distance to normality. The use of local p-values for quantifying abnormal motion patterns is believed to be a promising strategy for computing new markers of cardiac dyssynchrony for better characterizing CRT candidates.
Background: This study sought to evaluate the clinical outcomes of patients treated with magnesium-based bioresorbable scaffolds (MgBRS) in the context of acute coronary syndromes (ACS) at long-term follow-up (24 months). The study also aims to investigate the MgBRS performance by angiography and the healing and bioresorption pattern by optical coherence tomography (OCT) at 18 months.
Methods:Between December 2016 and December 2018, a total of 90 patients admitted for ACS and treated with MgBRS (Magmaris, Biotronik AG, Bülach, Switzerland) were enrolled in a multicenter prospective study. Clinical follow-up was performed in all patients at 24 months and angiographic and OCT follow-up in 51.5% of patients at 18 months. Serial OCT was available in 33 patients (36.7%).Results: At a 2-year follow-up, 88.8% were free of symptoms, no cardiac death was reported, and the device-oriented composite event (DOCE): consisting of cardiac death, target vessel myocardial infarction, and target lesion revascularization (TLR) was 13.3%. Stent thrombosis and TLR were observed in 2.2 and 11.1%, respectively. Binary restenosis was observed in 21.7% of cases and in-stent late lumen loss was 0.61 ± 0.75 mm. By serial OCT imaging, the minimal lumen area was significantly reduced greater than 40% (from 6.12 ± 1.59 to 3.5 ± 1.55 mm2, p < .001).At follow-up, area stenosis was 44.33 ± 23.07% and half of the patients presented indiscernible struts. The principal observed mechanism of restenosis was scaffold collapse.Conclusions: At long-term follow-up, MgBRS implantation in ACS patients showed a high rate of DOCE, mainly caused by clinically driven TLR. MgBRS restenosis was caused by scaffold collapse in most of the cases.
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