Electrophysiological findings during atrial fibrillation reablation: Extending from pulmonary vein reconnection to sequential bipolar voltage map information.

BACKGROUND: Left atrial substrate modification targeting low voltage zones (LVZ) is an ablation strategy that-in addition to pulmonary vein (PV) isolation-tries to eliminate arrhythmogenic mechanisms harbored in such tissue. Electrophysiological findings at reablation include (a) PV reconnection, (b) reconnection over previous substrate ablation, and (c) de-novo LVZ. OBJECTIVE: To study, prevalence and contribution of these arrhythmogenic electrophysiological entities in patients with atrial fibrillation (AF) recurrences. METHODS: Consecutive patients with highly symptomatic AF undergoing index and reablation were included (n = 113). In all patients' PV reconnection, reconnection over previous substrate ablation and spontaneous de-novo LVZ were quantitatively assessed and integrated into an individual reablation strategy. Follow-up was based on continuous device monitoring. RESULTS: At re-do procedure, 45 out of 113 (39.8%) patients showed PV reconnection as the only electrophysiological abnormality. Reconduction over previous lines was the only electrophysiological abnormality in 8 out of 113 (7.1%) patients. Spontaneous de-novo LVZ was the only electrophysiological abnormality in 12 out of 113 (10.6%) patients. Combined findings of PV reconnection, line reconduction, and/or spontaneous de-novo LVZ were seen in 40 out of 113 (35.4%) patients. No detectable electrophysiological abnormality was observed in 8 out of 113 (7.1%) patients. In univariate analysis, none of the tested electrophysiological characteristics independently predicted the outcome after re-do. CONCLUSIONS: In patients undergoing reablation, we could show that reconduction over previous substrate ablation as well as the development of new low voltage areas are frequent findings besides classical PV reconnection-without a clear leading cause for recurrences. These findings impact reablation strategies as well as the strategic focus during index procedures.

Impaired Endothelial Function in Hereditary Angioedema During the Symptom-Free Period.

Introduction: The presence of coronary endothelial dysfunction was previously shown in Hereditary Angioedema (HAE) patients. The aim of our study was to evaluate the effect of HAE on systemic endothelial function and whether there was a relationship among endothelial function, asymmetric dimethylarginine (ADMA) -which is a strong inhibitor of nitric oxide synthesis-, and disease severity scores. Methods: Twenty-four HAE patients (18 females, aged 47.9 ± 2 years) without factors known to interfere with endothelial function were studied and compared with 24 healthy peers age- and gender-matched. Endothelial function was assessed by means of non-invasive finger plethysmography (reactive hyperaemia index: RHI) and ADMA levels by high-performance liquid chromatography. HAE severity scores have been calculated according to published literature. Results: In HAE patients RHI was lower (2.03 ± 0.46 vs. 2.82 ± 0.34, p < 0.0001) and ADMA higher (0.636 ± 7 vs. 585 ± 5 micromol/L, p < 0.01) than in controls. A statistically significant inverse correlation was revealed between RHI and patients' ADMA levels (r = -0.516, p = 0.009) as well as between RHI and patients' chronological age (r = -0.49, p = 0.015). A statistically significant correlation between RHI and ADMA was confirmed even when excluding the possible influence of cholesterol (r = -0.408, p = 0.048). No other significant correlations were found with the examined laboratory and clinical parameters (chronological age, age at disease onset, disease duration, severity scores, and gender). Conclusion: The dysfunction previously shown in HAE patients at the coronary arteries seems to involve the peripheral vessels as well, without a correlation with disease severity.

The reasons why cardiologists should consider prematurity at birth and intrauterine growth retardation among risk factors.

The survival percentage of infants born preterm has risen steadily worldwide thanks to the giant steps forward made in the field of perinatal (the period immediately after birth) and neonatal (the first 4 weeks of birth following delivery) medicine. However, prematurity at birth and consequent low birth weight still represent the major causes of neonatal morbidity and mortality. Infants born preterm are at high risk of developing neurological, ophthalmological, and gastrointestinal complications as well. Furthermore, extensive more recent epidemiological findings have demonstrated an increase in risk factors and a higher mortality rate due to cardiovascular causes in patients born preterm and/or with intrauterine growth restriction. The aim of this review is to provide scientific evidence about how the cardiovascular system may be negatively influenced by prematurity and by a low birth weight that should by rights be viewed as new cardiovascular risk factors. This condition is referred to as 'cardiovascular perinatal programming'. In the light of the above, an early, constant, and prolonged cardiovascular follow-up should be implemented in former preterm individuals.