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1.
J Interv Card Electrophysiol ; 66(8): 1867-1876, 2023 Nov.
Article in English | MEDLINE | ID: mdl-36763211

ABSTRACT

BACKGROUND OR PURPOSE: His bundle pacing (HBP) is the most physiological form of ventricular pacing. Few prospective studies have analyzed lead localization using imaging techniques and its relationship with electrical parameters and capture patterns. The objective of this study is to examine the correlation between electrical parameters and lead localization using three-dimensional transthoracic echocardiography (3D TTE). METHODS: This single-center, prospective, nonrandomized clinical research study (January 2018 to June 2020) included patients with an indication of permanent pacing, in whom 3D TTE was performed to define lead localization as supravalvular or subvalvular. RESULTS: A total of 92 patients were included: 56.5% of leads were supravalvular, and 43.5% were subvalvular, which resembles previous anatomic descriptions of autopsied hearts of His bundle localization within the triangle of Koch (ToK). R-wave sensing was higher when the His lead was localized subvalvular instead of supravalvular. His lead localization was not associated with HBP threshold or impedance differences, nor with the two different HBP patterns of capture, or with the ability of HBP to correct baseline BBB. The thresholds remained stable during follow-up visits, regardless of His lead localization. Higher R-wave sensing was observed during follow-up than at baseline, mainly in the subvalvular His leads. However, lead impedances in both positions decreased during follow-up. CONCLUSIONS: Lead localization in relation to the tricuspid valve did not influence the electrical performance of HBPs. Wide anatomical variations of the His bundle within the ToK explain our findings, reinforcing the idea that the technique for HBP should be fundamentally guided by electrophysiological and not anatomical parameters.

2.
Rev Esp Cardiol (Engl Ed) ; 75(6): 488-495, 2022 Jun.
Article in English, Spanish | MEDLINE | ID: mdl-34711514

ABSTRACT

INTRODUCTION AND OBJECTIVES: Hereditary transthyretin amyloidosis (hATTR) is a disease caused by mutations in the transthyretin gene that frequently shows cardiac involvement due to amyloid deposition in the myocardium. Our objective was to identify cardiac involvement in a Spanish cohort. METHODS: Retrospective multicenter study of patients diagnosed with hATTR with cardiac involvement from Spanish centers. We collected demographic, clinical, and genetic data. RESULTS: A total of 181 patients from 26 centers were included (65.2% men, with a median age at diagnosis of 62 years). The most frequent mutations were Val50Met (67.7%) and Val142Ile (12.4%). The main reason for consultation was extracardiac symptoms (69%), mainly neurological. The mean N-terminal pro-B-type natriuretic peptide level was 2145±3586 pg/mL. The most characteristic electrocardiogram findings were a pseudoinfarct pattern (25.9%) and atrioventricular block (25.3%). Mean ventricular thickness was 15.4±4.1mm. Longitudinal strain was reduced in basal segments by 29.4%. Late diffuse subendocardial enhancement was observed in 58.8%. Perugini grade 2 or 3 uptake was observed in 75% of scintigraphy scans. During follow-up, 24.9% of the patients were admitted for heart failure, 34.3% required a pacemaker, and 31.6% required a liver transplant. One third (32.5%) died during follow-up, mainly due to heart failure (28.8%). The presence of non-Val50Met mutations was associated with a worse prognosis. CONCLUSIONS: HATTR cardiac amyloidosis in Spain shows heterogeneous genetic and clinical involvement. The prognosis is poor, mainly due to cardiac complications. Consequently early diagnosis and treatment are vital.


Subject(s)
Amyloid Neuropathies, Familial , Cardiomyopathies , Heart Failure , Amyloid Neuropathies, Familial/diagnosis , Amyloid Neuropathies, Familial/epidemiology , Amyloid Neuropathies, Familial/genetics , Cardiomyopathies/diagnosis , Cardiomyopathies/epidemiology , Cardiomyopathies/genetics , Female , Heart Failure/complications , Humans , Male , Middle Aged , Prealbumin/genetics , Spain/epidemiology
3.
Europace ; 22(1): 125-132, 2020 01 01.
Article in English | MEDLINE | ID: mdl-31746996

ABSTRACT

AIMS: Permanent His bundle pacing (p-HBP) can correct intraventricular conduction disorders and could be an alternative to traditional cardiac resynchronization therapy (CRT) via the coronary sinus. We describe the short-term impact of HBP on left ventricular ejection fraction (LVEF) and improvement of left intraventricular synchrony. METHODS AND RESULTS: This prospective descriptive study, performed from January 2018 to February 2019, included patients with left bundle branch block (LBBB) and an CRT indication who were resynchronized by p-HBP. We used the Medtronic C315 His catheter or a combination of the CPS-Direct-Universal introducer, CPS-AIM™-Universal subselector (Abbot), and SelectSecure™ MRI-SureScan™ 3830 lead. Correction of the LBBB by HBP had been previously checked. At 1 month of follow-up, we analysed the quantification of LVEF and measurement of the delay of the septal wall with the posterior wall as a parameter of intraventricular synchrony. We included 48 patients with LBBB and an indication for CRT. With HBP, we corrected the LBBB in 81% of patients (n = 39), and we achieved cardiac resynchronization through permanent HBP in 92% of these patients (n = 36). Left ventricular ejection fraction and intraventricular mechanical resynchronization improved in all patients, which was demonstrated by echocardiography through the improvement of the delay of the septal wall with the posterior wall from 138 ms (range 131-151) to 41 ms (19-63). CONCLUSION: There is early improvement after p-HBP in LVEF and left ventricular electromechanical synchronization in patients with LBBB, heart failure, and an indication for CRT.


Subject(s)
Cardiac Resynchronization Therapy , Heart Failure , Bundle of His , Electrocardiography , Heart Failure/diagnosis , Heart Failure/therapy , Humans , Prospective Studies , Stroke Volume , Treatment Outcome , Ventricular Function, Left
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