Risk of syncopal recurrences in patients treated with permanent pacing for bradyarrhythmic syncope: role of correlation between symptoms and electrocardiogram findings.

AIMS: To evaluate the risk of syncopal recurrences after pacemaker implantation in a population of patients with syncope of suspected bradyarrhythmic aetiology. METHODS AND RESULTS: Prospective, multicentre, observational registry enrolling 1364 consecutive patients undergoing pacemaker implantation for syncope of bradyarrhythmic aetiology (proven or presumed). Before pacemaker implantation, all patients underwent a cardiac work-up in order to establish the bradyarrhythmic aetiology of syncope. According to the results of the diagnostic work-up, patients were divided into three groups: Group A, patients in whom a syncope-electrocardiogram (ECG) correlation was established (n = 329, 24.1%); Group B, those in whom clinically significant bradyarrhythmias were detected without a documented syncope-ECG correlation (n = 877, 64.3%); and Group C, those in whom bradyarrhythmias were not detected and the bradyarrhythmic origin of syncope remained presumptive (n = 158, 11.6%). During a median follow-up of 50 months, 213 patients (15.6%) reported at least one syncopal recurrence. Patients in Groups B and C showed a significantly higher risk of syncopal recurrences than those in Group A [hazard ratios (HRs): 1.60 and 2.66, respectively, P < 0.05]. Failure to establish a syncope-ECG correlation during diagnostic work-up before pacemaker implantation was an independent predictor of syncopal recurrence on multivariate analysis (HR: 1.90; P = 0.002). CONCLUSION: In selecting patients with syncope of suspected bradyarrhythmic aetiology for pacemaker implantation, establishing a correlation between syncope and bradyarrhythmias maximizes the efficacy of pacing and reduces the risk of syncopal recurrences.

Causes of syncopal recurrences in patients treated with permanent pacing for bradyarrhythmic syncope: Findings from the SYNCOPACED registry.

BACKGROUND: Few studies have examined the causes of syncope/collapse recurrences in patients with a previously implanted pacemaker for bradyarrhythmic syncope. OBJECTIVE: The purpose of this study was to assess the causes of syncope/collapse recurrences after pacemaker implantation for bradyarrhythmic syncope in a large patient population. METHODS: The SYNCOpal recurrences in patients treated with permanent PACing for bradyarrhythmic syncope (SYNCOPACED) registry was a prospective multicenter observational registry enrolling 1364 consecutive patients undergoing pacemaker implantation for bradyarrhythmic syncope. During follow-up, the time to the first syncope/collapse recurrence was recorded. Patients with syncope/collapse recurrences underwent a predefined diagnostic workup aimed at establishing the mechanism of syncope/collapse. RESULTS: During a median follow-up of 50 months, 213 patients (15.6%) reported at least 1 syncope/collapse recurrence. The risk of syncope/collapse recurrence was highest in patients who underwent implantation for cardioinhibitory vasovagal syncope (26.4%), followed by unexplained syncope and chronic bifascicular block (21.5%), cardioinhibitory carotid sinus syndrome (17.2%), atrial fibrillation needing pacing (15.5%), atrioventricular block (13.6%), and sinus node disease (12.5%) (P = .017). The most frequent cause of syncope/collapse recurrence was reflex syncope (27.7%), followed by orthostatic hypotension (26.3%), pacemaker or lead malfunction (5.6%), structural cardiac disease (5.2%), and atrial and ventricular tachyarrhythmias (4.7% and 3.8%, respectively). In 26.8% of cases, the mechanism of syncope/collapse remained unexplained. CONCLUSION: In patients receiving a pacemaker for bradyarrhythmic syncope, reflex syncope and orthostatic hypotension are the most frequent mechanisms of syncope/collapse recurrence after implantation. Pacing system malfunction, structural cardiac diseases, and tachyarrhythmias are rare mechanisms. The mechanism remains unexplained in >25% of patients.

Atrial conduit function quantitation precardioversion predicts early arrhythmia recurrence in persistent atrial fibrillation patients.

AIMS: Atrial fibrillation incidence is increasing due to ageing population and electrical cardioversion (ECV) is overused because of atrial fibrillation recurrences. Study's aim was to evaluate value of novel three-dimensional echocardiographic-derived left atrial conduit (LAC) function quantification in predicting early atrial fibrillation recurrence after ECV. METHODS: We included 106 patients [74 (64-78) years] who underwent ECV for persistent nonvalvular atrial fibrillation. For all clinical data and simultaneous left atrial and left ventricular (LV) three-dimensional full-volume data sets were available before ECV. We computed LAC as: [(LV maximum - LV minimum) - (left atrial maximum - left atrial minimum) volume], expressed as % LV stroke volume. Atrial fibrillation recurrence was checked with Holter monitoring. RESULTS: One month after ECV 66 patients were in sinus rhythm and 40 experienced atrial fibrillation recurrence. Pre-ECV patients with atrial fibrillation recurrence showed higher LAC contribution to LV filling (P < 0.0001) and noninvasively estimated left atrial stiffness (P < 0.0001) compared with sinus rhythm patients. There were no other differences, neither in clinical characteristics nor in LV properties. At multivariate LAC (P < 0.001), left atrial stiffness (P = 0.002) and volume (P = 0.043) predicted early atrial fibrillation relapse, even when compared with other confounding factors. Receiver-operating characteristics area (ROC) analysis confirmed LAC as best atrial fibrillation recurrence predictor (0.84, P < 0.0001), cut-off value more than 54% exhibiting reasonable sensibility-specificity (76-75%). CONCLUSION: Atrial fibrillation makes LV filling dependent on reciprocation between left atrial reservoir/conduit phases. Our data suggest that LAC larger contribution to filling in persistent atrial fibrillation patients reflects left atrial and LV diastolic dysfunction, which skews atrio-ventricular interaction that leads to atrial fibrillation perpetuation, making LAC a powerful atrial fibrillation recurrence predictor after ECV.

Association between left atrial phasic conduit function and early atrial fibrillation recurrence in patients undergoing electrical cardioversion.

BACKGROUND: Diastolic dysfunction promotes atrial fibrillation (AF) inducing left atrial (LA) remodeling, with chamber dilation and fibrosis. Predominance of LA phasic conduit (LAC) function should reflect not only chamber alterations but also underlying left ventricular (LV) filling impairment. Thus, LAC was tested as possible predictor of early AF relapse after electrical cardioversion (EC). METHODS: 96 consecutive patients, who underwent EC for persistent non-valvular AF, were prospectively enrolled. Immediately after successful EC (3 h ± 15 min), an echocardiographic apical four-chamber view was acquired with transmitral velocities, annular tissue Doppler and simultaneous LV and LA three-dimensional full-volume datasets. Then, from LA-LV volumetric curves we computed LAC as: [(LV maximum - LV minimum) - (LA maximum - LA minimum) volume], expressed as % LV stroke volume. LA pump, immediately post-EC, was assumed and verified as being negligible. Sinus rhythm persistence at 1 month was checked with ECG-Holter monitoring. RESULTS: At 1 month 62 patients were in sinus rhythm and 34 in AF. AF patients presented pre-EC higher E/é values (p = 0.012), no major LA volume differences (p = NS), but a stiffer LV cavity (p = 0.012) for a comparable LV capacitance (p = 0.461). Conduit contributed more (p < 0.001) to LV stroke volume in AF subpopulation. Multiple regression revealed LAC as the most significant AF predictor (p = 0.013), even after correction for biometric characteristics and pharmacotherapy (p = 0.008). CONCLUSION: Our data suggest that LAC larger contribution to LV filling soon after EC reflects LA-LV stiffening, which skews atrioventricular interaction leading to AF perpetuation and makes conduit dominance a powerful predictor of early AF recurrence.

Association between rheumatic diseases and cancer: results from a clinical practice cohort study.

The association between cancer and immune-mediated rheumatic conditions is controversial, especially as far as polymyalgia rheumatica (PMR) is concerned. Furthermore, no clinical feature has been shown to be suggestive of a paraneoplastic rheumatic syndrome. With the present study, we aim to address both these issues. The study population comprised N = 1750 patients, including N = 100 with PMR, who attended our tertiary immuno-rheumatology clinic between January 1, 2005 and November 30, 2012. A rheumatic disease was deemed paraneoplastic if cancer had been diagnosed in the 2 years preceding or following its onset. The probability of a significant association between a specific rheumatic disease and cancer was evaluated by computing the odds ratio (OR): N = 702 patients with osteoarthritis serving as controls. Furthermore, clinical features distinguishing paraneoplastic rheumatic diseases were searched for by univariate and multivariate analysis. Sjogren's syndrome (SS) [OR 3.6 (CI 95% 1.7-7.5)], PMR (OR 5.1 CI 95% 2.9-8.9), dermatomyositis/polymyositis [OR 12.09 (CI 95% 2.6-55.8)] and vasculitis [OR 3.70 (CI 95% 1.81-7.52)] are associated with cancer. At multivariate analysis, older age is associated with cancer among SS patients (p = 0.03), while in the PMR group, older age, male gender, and ≥6 tender joints are independent predictors of paraneoplastic PMR (p < 0.0004). Cancer frequently either heralds or follows rheumatic manifestations, including PMR. Older age, male gender and a more extensive joint involvement should be considered red flags for paraneoplastic PMR.