Endocardial repolarization dispersion in BrS: A novel automatic algorithm for mapping activation recovery interval.

INTRODUCTION: Repolarization dispersion in the right ventricular outflow tract (RVOT) contributes to the type-1 electrocardiographic (ECG) phenotype of Brugada syndrome (BrS), while data on the significance and feasibility of mapping repolarization dispersion in BrS patients are scarce. Moreover, the role of endocardial repolarization dispersion in BrS is poorly investigated. We aimed to assess endocardial repolarization patterns through an automated calculation of activation recovery interval (ARI) estimated on unipolar electrograms (UEGs) in spontaneous type-1 BrS patients and controls; we also investigated the relation between ARI and right ventricle activation time (RVAT), and T-wave peak-to-end interval (Tpe) in BrS patients. METHODS: Patients underwent endocardial high-density electroanatomical mapping (HDEAM); BrS showing an overt type-1 ECG were defined as OType1, while those without (latent type-1 ECG and LType1) received ajmaline infusion. BrS patients only underwent programmed ventricular stimulation (PVS). Data were elaborated to obtain ARI corrected with the Bazett formula (ARIc), while RVAT was derived from activation maps. RESULTS: 39 BrS subjects (24 OType1 and 15 LTtype1) and 4 controls were enrolled. OType1 and post-ajmaline LType1 showed longer mean ARIc than controls (306 ± 27.3 ms and 333.3 ± 16.3 ms vs. 281.7 ± 10.3 ms, p = .05 and p < .001, respectively). Ajmaline induced a significant prolongation of ARIc compared to pre-ajmaline LTtype1 (333.3 ± 16.3 vs. 303.4 ± 20.7 ms, p < .001) and OType1 (306 ± 27.3 ms, p < .001). In patients with type-1 ECG (OTtype1 and post-ajmaline LType1) ARIc correlated with RVAT (r = .34, p = .04) and Tpec (r = .60, p < .001), especially in OType1 subjects (r = .55, p = .008 and r = .65 p < .001, respectively). CONCLUSION: ARIc mapping demonstrates increased endocardial repolarization dispersion in RVOT in BrS. Endocardial ARIc positively correlates with RVAT and Tpec, especially in OType1.

Correlational analysis of electroencephalographic and end-tidal carbon dioxide signals during breath-hold exercise.

The central mechanism of breathing control is not totally understood. Several studies evaluated the correlation between electroencephalographic (EEG) power spectra and respiratory signals by performing resting state tasks or adopting hypercapnic/hypoxic stimuli. The observation of brain activity during voluntary breath hold tasks, might be an useful approach to highlight the areas involved in mechanism of breath regulation. Nevertheless, studies of brain activity with EEG could present some limitations due to presence of severe artifacts. When artifact rejection methods, as independent component analysis, cannot reliably clean EEG data, it is necessary to exclude noisy segments. In this study, global field power in the delta band and end-tidal CO2 were derived from EEG and CO2 signals respectively in 4 healthy subjects during a breath-hold task. The cross correlation function between the two signals was estimated taking into account the presence of missing samples. The statistical significance of the correlation coefficients at different time lags was assessed using surrogate data. Some simulations are introduced to evaluate the effect of missing data on the correlational analysis and their results are discussed. Results obtained on subjects show a significant correlation between changes in EEG power in the delta band and end-tidal CO2. Moreover, the changes in end-tidal CO2 were found to precede those of global field power. These results might help to better understand the cortical mechanisms involved in the control of breathing.

[Recent knowledges on chemosensitivity to hypoxia and hypercapnia in cardiovascular disease]. / Recenti conoscenze sulla sensibilità chemocettiva ad ipossia ed ipercapnia in patologia cardiovascolare.

The pathophysiologic role of enhanced chemosensitivity to carbon dioxide and/or hypoxia has been underscored in several cardiovascular diseases, including heart failure. In the early stages of this syndrome, the chemoreflex acts as a compensatory mechanism. Later on, however, it contributes to sustain the sympathetic activation, with detrimental effects on cardiovascular function and prognosis.