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Background: It is known that autonomic nerve activity controls the sinus rate. However, the coupling between local nerve activity and electrical activation at the sinoatrial node (SAN) remains unclear. We hypothesized that we would be able to record nerve activity at the SAN to investigate if right stellate ganglion (RSG) activation can increase the local intrinsic nerve activity, accelerate sinus rate, and change the earliest activation sites.Methods: High-density mapping of the epicardial surface of the right atrium including the SAN was performed in 6 dogs during stimulation of the RSG and after RSG stellectomy. A radio transmitter was implanted into 3 additional dogs to record RSG and local nerve activity at the SAN.Results: Heart rate accelerated from 108±4 bpm at baseline to 125±7 bpm after RSG stimulation (P=0.001), and to 132±7 bpm after apamin injection (P<0.001). Both electrical RSG stimulation and apamin injection induced local nerve activity at the SAN with the average amplitudes of 3.60±0.72 and 3.86±0.56 μV, respectively. RSG stellectomy eliminated the local nerve activity and decreased the heart rate. In ambulatory dogs, local nerve activity at the SAN had a significantly higher average Pearson correlation to heart rate (0.72±0.02, P=0.001) than RSG nerve activity to HR (0.45±0.04, P=0.001).Conclusions: Local intrinsic nerve activity can be recorded at the SAN. Short bursts of these local nerve activities are present before each atrial activation during heart rate acceleration induced by stimulation of the RSG. [ABSTRACT FROM AUTHOR]

Background: Ventricular fibrillation (VF) during heart failure is characterized by stable reentrant spiral waves (rotors). Apamin-sensitive small-conductance calcium-activated potassium currents (IKAS) are heterogeneously upregulated in failing hearts. We hypothesized that IKAS influences the location and stability of rotors during VF.Methods and Results: Optical mapping was performed on 9 rabbit hearts with pacing-induced heart failure. The epicardial right ventricular and left ventricular surfaces were simultaneously mapped in a Langendorff preparation. At baseline and after apamin (100 nmol/L) infusion, the action potential duration (APD80) was determined, and VF was induced. Areas with a >50% increase in the maximum action potential duration (ΔAPD) after apamin infusion were considered to have a high IKAS distribution. At baseline, the distribution density of phase singularities during VF in high IKAS distribution areas was higher than in other areas (0.0035±0.0011 versus 0.0014±0.0010 phase singularities/pixel; P=0.004). In addition, high dominant frequencies also colocalized to high IKAS distribution areas (26.0 versus 17.9 Hz; P=0.003). These correlations were eliminated during VF after apamin infusion, as the number of phase singularities (17.2 versus 11.0; P=0.009) and dominant frequencies (22.1 versus 16.2 Hz; P=0.022) were all significantly decreased. In addition, reentrant spiral waves became unstable after apamin infusion, and the duration of VF decreased.Conclusions: The IKAS current influences the mechanism of VF in failing hearts as phase singularities, high dominant frequencies, and reentrant spiral waves all correlated to areas of high IKAS. Apamin eliminated this relationship and reduced VF vulnerability. [ABSTRACT FROM AUTHOR]

The article presents a study on whether inferior vena cava-inferior atrial ganglionated plexus nerve activity (IVC-IAGPNA) triggers ventricular rate (VR) control during atrial fibrillation (AF) in ambulatory dogs. IVC-IAGPNA is said to be invariably linked to VR reduction during AF. Right or left vagal nerve activity was related to VR reduction only when it coactivates with the IVC-IAGPNA. The vagal nerve that controls VR during AF may reportedly differ from that which controls sinus rhythm.

The article presents a study which hypothesized that unresponsiveness of superior sinoatrial node (SAN) to sympathetic stimulation is strongly linked with the development of symptomatic bradycardia in patients with atrial fibrillation (AF). A three-dimensional (3D) endocardial mapping in healthy controls and patients with AF were performed. The study concluded that superior SAN serves as the earliest activation site (EAS) during sympathetic stimulation in patients without AF.

The article presents the results of a study on the role of phase 2 and phase 3 early afterdepolarizations (EAD) in developing arrhythmias in intact heart tissue. According to the authors, coupling of cells with heterogeneous repolarization could extrinsically generate phase 3 EADs via electronic current flow. They indicate that low extracellular K can reduce acetylcholine-activated K and promote ventricular arrhythmias mediated by phase 3 EADs in acquired long-QT syndromes caused by acetylcholine-activated K blockade.

The authors comment on the study "Does Location of Epicardial Adipose Tissue (EAT) Correspond to Endocardial High Dominant Frequency (DF) or Complex Fractionated Atrial Electrogram Sites During Atrial Fibrillation (AF)?," by K. Nagashima and colleagues. The study revealed higher EAT volume and greater serum inflammatory biomarker levels in patients with persistent AF (PerAF) than in patients with paroxysmal AF (PAF). The location of high DF sites adjacent to EAT sites is also noted.

The author reflects on the study conducted by Kurotobi and colleagues on the number of arrhythmogenic foci in provocative atria with isoproterenol infusion in patients with persistent and permanent atrial fibrillation. He argues that the association between the number of foci in the development of atrial fibrillation is not clearly established and that it can be observed by the late phase-3 early after depolarization. He also presents some possible explanations to the said association.