RESUMEN
A dyssynchronous biventricular activation, which can be determined by left bundle branch block, chronic right ventricular pacing, frequent premature ventricular complexes, or pre-excitation, can cause a global abnormal contractility, thus leading to systolic dysfunction and left ventricular remodelling in a unique nosological entities: abnormal conduction-induced cardiomyopathies. In this clinical scenario, the mainstay therapy is eliminating or improving LV dyssynchrony, removing the trigger. This usually ensures the improvement and even recovery of cardiac geometry and left ventricular function, especially in the absence of genetic background. A multidisciplinary approach, integrating advanced multimodal imaging, is essential for the systematic aetiological definition and the subsequent evaluation and aetiology-guided therapies of patients and their families. This review aims to describe mechanisms, prevalence, risk factors, and diagnostic and therapeutic approach to the various abnormal conduction-induced cardiomyopathies, starting from reasonable certainties and then analysing the grey areas requiring further studies.
RESUMEN
Background: Strain imaging has been suggested as a tool to detect early left ventricular (LV) dysfunction due to frequent premature ventricular contractions (PVCs) in patients with preserved LV ejection fraction (EF). However, the progression of intraventricular dyssynchrony (IVD), radial, and circumferential strain (RS, CS) in PVC-cardiomyopathy (CM) are unknown. The aim of this study was to elucidate the progression patterns of CS, IVD, and electro-mechanical latency (EML) in PVC-CM. Methods and results: Pacemakers were implanted in 20 canines to reproduce ventricular bigeminy at 200ms (PVCs n = 11) for 12 weeks and compared to a sham group (n = 9). We obtained echocardiograms at baseline, 4-, 8- and 12-weeks. RS and CS were obtained at the LV mid-cavitary level. IVD was defined as the time between the earliest and latest peak RS. EML was defined as the time between the onset of QRS and the earliest peak RS. LVEF (62 ± 5 to 42 ± 7%, p < 0.01), CS (-18 ± 3 to -12 ± 3, p < 0.01), and EML (219 ± 37 to 283 ± 46ms, p = 0.02) changed significantly in the PVC group. Peak CS (-18 ± 3 to -14 ± 4, p = 0.02) and IVD (49 ± 31 to 122 ± 103, p = 0.05) had a significant change at 4-weeks despite preserved LVEF (51 ± 5%). IVD normalized while EML increased at weeks 8 and 12. Conclusion: Our findings consolidate the existing theory that changes in strain precede changes in LVEF in PVC-CM. While IVD becomes abnormal early in the development of PVC-CM, it pseudo-normalizes at advanced stages due to further increases in EML suggestive of cardiac contractility remodeling. These findings are consistent with recent published data where abnormal LV mechanics could be part of a substrate that can predispose to worse outcome in PVC-Cardiomyopathy.
RESUMEN
Despite being increasingly recognized as a specific disease, at the present time left bundle branch block (LBBB)-induced cardiomyopathy is neither formally included among unclassified cardiomyopathies nor among the acquired/non-genetic forms of dilated cardiomyopathy (DCM). Currently, a post-hoc diagnosis of LBBB-induced cardiomyopathy is possible when evaluating patients' response to cardiac resynchronization therapy (CRT). However, an early detection of a LBBB-induced cardiomyopathy could have significant clinical and therapeutic implications. Patients with the aforementioned form of dyssynchronopathy may benefit from early CRT and overall prognosis might be better as compared to patients with a primary muscle cell disorder (i.e. "true" DCM). The real underlying mechanisms, the possible genetic background as well as the early identification of this specific form of DCM remain largely unknown. In this review the complex relationship between LBBB and left ventricular non-ischaemic dysfunction is described. Furthermore, a multiparametric approach based on clinical, electrocardiographic and imaging red flags, is provided in order to allow an early detection of the LBBB-induced cardiomyopathy.
Asunto(s)
Bloqueo de Rama/complicaciones , Bloqueo de Rama/diagnóstico por imagen , Cardiomiopatías/diagnóstico por imagen , Cardiomiopatías/etiología , Bloqueo de Rama/fisiopatología , Terapia de Resincronización Cardíaca/métodos , Cardiomiopatías/fisiopatología , Ecocardiografía/métodos , Electrocardiografía/métodos , Humanos , Disfunción Ventricular Izquierda/diagnóstico por imagen , Disfunción Ventricular Izquierda/etiología , Disfunción Ventricular Izquierda/fisiopatologíaRESUMEN
Spontaneous resolution of non-rate-dependent left bundle branch block (LBBB) has been rarely reported. We present the case of a 74-year-old woman admitted with pulmonary edema, a newly diagnosed LBBB and severe left ventricular (LV) dysfunction. Five months later, the patient was asymptomatic, the ECG recording showed complete regression of the LBBB to narrow QRS and LV function completely recovered. However, at one-year follow-up LBBB reappeared together with mild LV dysfunction. Spontaneous resolution of LBBB may be responsible for LV electrical and mechanical reverse remodeling in dyssynchronopathies.
Asunto(s)
Remodelación Atrial/fisiología , Bloqueo de Rama/complicaciones , Bloqueo de Rama/fisiopatología , Electrocardiografía/métodos , Disfunción Ventricular Izquierda/complicaciones , Disfunción Ventricular Izquierda/fisiopatología , Anciano , Femenino , Estudios de Seguimiento , HumanosRESUMEN
Left bundle branch block (LBBB) is considered a marker of underlying structural cardiac disease. To determine whether LBBB is cause or consequence of deterioration of left ventricular (LV) function is difficult as both are often diagnosed concomitantly. We discuss a patient where reversal of LBBB and subsequent normalization of LV function was observed after 2 different therapies, first after start of heart failure medication, and years later after implantation of a cardiac resynchronization device. This indicates that LBBB per se may result in the development of non-ischemic cardiomyopathy and that LBBB resolution can lead to reverse remodeling in dyssynchronopathy.
Asunto(s)
Bloqueo de Rama/complicaciones , Bloqueo de Rama/prevención & control , Terapia de Resincronización Cardíaca/efectos adversos , Cardiomiopatías/diagnóstico , Cardiomiopatías/etiología , Disfunción Ventricular Izquierda/diagnóstico , Disfunción Ventricular Izquierda/etiología , Diagnóstico Diferencial , Electrocardiografía , Humanos , Masculino , Persona de Mediana EdadRESUMEN
BACKGROUND: In Boston Scientific dual-chamber devices, the RYTHMIQ algorithm aims to minimize right ventricular pacing. OBJECTIVE: We evaluated the performance of this algorithm determining (1) the appropriateness of the switch from the AAI(R) mode with backup VVI pacing to the DDD(R) mode in case of suspected loss of atrioventricular (AV) conduction and (2) the rate of recorded pacemaker-mediated tachycardia (PMT) when AV hysteresis searches for restored AV conduction. METHODS: In this multicenter study, we included 157 patients with a Boston Scientific dual-chamber device (40 pacemakers and 117 implantable cardioverter-defibrillators) without permanent AV conduction disorder and with the RYTHMIQ algorithm activated. We reviewed the last 10 remote monitoring-transmitted RYTHMIQ and PMT episodes. RESULTS: We analyzed 1266 episodes of switch in 142 patients (90%): 207 (16%) were appropriate and corresponded to loss of AV conduction, and 1059 (84%) were inappropriate, of which 701 (66%) were related to compensatory pause (premature atrial contraction, 7%; premature ventricular contraction, 597 (56%); or both, 27 (3%)) or to a premature ventricular contraction falling in the post-atrial pacing ventricular refractory period interval (219, 21%) and 94 (10%) were related to pacemaker dysfunction. One hundred fifty-four PMT episodes were diagnosed in 27 patients (17%). In 85 (69%) of correctly diagnosed episodes, the onset of PMT was directly related to the algorithm-related prolongation of the AV delay, promoting AV dissociation and retrograde conduction. CONCLUSION: This study highlights some of the limitations of the RYTHMIQ algorithm: high rate of inappropriate switch and high rate of induction of PMT. This may have clinical implications in terms of selection of patients and may suggest required changes in the algorithm architecture.