scholarly journals Role of LVA Ca channels in norepinephrine-induced automatic activity in rat pulmonary vein myocardial sleeve

2020 ◽  
Vol 12 (2-4) ◽  
pp. 254
Author(s):  
C.O. Malecot
Author(s):  
Reina Tonegawa-Kuji ◽  
Kenichiro Yamagata ◽  
Kengo Kusano

Abstract Background  Cough-induced atrial tachycardia (AT) is extremely rare and its electrical origin remains largely unknown. Atrial tachycardias triggered by pharyngeal stimulation, such as swallowing or speech, appears to be more common and the majority of them originate from the superior vena cava or right superior pulmonary vein (PV). Only one case of swallow-triggered AT with right inferior pulmonary vein (RIPV) origin has been reported to date. Case summary  We present a case of a 41-year-old man with recurring episodes of AT in the daytime. He underwent electrophysiology study without sedation. Atrial tachycardia was not observed when the patient entered the examination room and could not be induced with conventional induction procedures. By having the patient cough periodically on purpose, transient AT with P-wave morphology similar to the clinical AT was consistently induced. Activation mapping of the AT revealed a centrifugal pattern with the earliest activity localized inside the RIPV. After successful radiofrequency isolation of the right PV, AT was no longer inducible. Discussion  In the rare case of cough-induced AT originating from the RIPV, the proximity of the inferior right ganglionated plexi (GP) suggests the role of GP in triggering tachycardia. This is the first report that demonstrates voluntary cough was used to induce AT. In such cases that induction of AT is difficult using conventional methods, having the patient cough may be an effective induction method that is easy to attempt.


2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P2320-P2320
Author(s):  
D. Vollmann ◽  
L. Luethje ◽  
J. Seegers ◽  
C. Sohns ◽  
S. Sossalla ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257050
Author(s):  
Nándor Szegedi ◽  
Zoltán Salló ◽  
Péter Perge ◽  
Katalin Piros ◽  
Vivien Klaudia Nagy ◽  
...  

Introduction Our pilot study aimed to evaluate the role of local impedance drop in lesion formation during pulmonary vein isolation with a novel contact force sensing ablation catheter that records local impedance as well and to find a local impedance cut-off value that predicts successful lesion formation. Materials and methods After completing point-by-point radiofrequency pulmonary vein isolation, the success of the applications was evaluated by pacing along the ablation line at 10 mA, 2 ms pulse width. Lesions were considered successful if loss of local capture was achieved. Results Out of 645 applications, 561 were successful and 84 were unsuccessful. Compared to the unsuccessful ablation points, the successful applications were shorter (p = 0.0429) and had a larger local impedance drop (p<0.0001). There was no difference between successful and unsuccessful applications in terms of mean contact force (p = 0.8571), force-time integral (p = 0.0699) and contact force range (p = 0.0519). The optimal cut-point for the local impedance drop indicating successful lesion formation was 21.80 Ohms on the anterior wall [AUC = 0.80 (0.75–0.86), p<0.0001], and 18.30 Ohms on the posterior wall [AUC = 0.77 (0.72–0.83), p<0.0001]. A local impedance drop larger than 21.80 Ohms on the anterior wall and 18.30 Ohms on the posterior wall was associated with an increased probability of effective lesion creation [OR = 11.21, 95%CI 4.22–29.81, p<0.0001; and OR = 7.91, 95%CI 3.77–16.57, p<0.0001, respectively]. Conclusion The measurement of the local impedance may predict optimal lesion formation. A local impedance drop > 21.80 Ohms on the anterior wall and > 18.30 Ohms on the posterior wall significantly increases the probability of creating a successful lesion.


2008 ◽  
Vol 22 (1) ◽  
pp. 167-168 ◽  
Author(s):  
Emanuele Catena ◽  
Roberto Paino ◽  
Stefano Fieschi ◽  
Alessandro Rinaldo ◽  
Filippo Milazzo ◽  
...  

2009 ◽  
Vol 297 (1) ◽  
pp. H102-H108 ◽  
Author(s):  
Nicolas Doisne ◽  
Véronique Maupoil ◽  
Pierre Cosnay ◽  
Ian Findlay

Ectopic activity in cardiac muscle within pulmonary veins (PVs) is associated with the onset and the maintenance of atrial fibrillation in humans. The mechanism underlying this ectopic activity is unknown. Here we investigate automatic activity generated by catecholaminergic stimulation in the rat PV. Intracellular microelectrodes were used to record electrical activity in isolated strips of rat PV and left atrium (LA). The resting cardiac muscle membrane potential was lower in PV [−70 ± 1 (SE) mV, n = 8] than in LA (−85 ± 1 mV, n = 8). No spontaneous activity was recorded in PV or LA under basal conditions. Norepinephrine (10−5 M) induced first a hyperpolarization (−8 ± 1 mV in PV, −3 ± 1 mV in LA, n = 8 for both) then a slowly developing depolarization (+21 ± 2 mV after 15 min in PV, +1 ± 2 mV in LA) of the resting membrane potential. Automatic activity occurred only in PV; it was triggered at approximately −50 mV, and it occurred as repetitive bursts of slow action potentials. The diastolic membrane potential increased during a burst and slowly depolarized between bursts. Automatic activity in the PV was blocked by either atenolol or prazosine, and it could be generated with a mixture of cirazoline and isoprenaline. In both tissues, cirazoline (10−6 M) induced a depolarization (+37 ± 2 mV in PV, n = 5; +5 ± 1 mV in LA, n = 5), and isoprenaline (10−7 M) evoked a hyperpolarization (−11 ± 3 mV in PV, n = 7; −3 ± 1 mV in LA, n = 6). The differences in membrane potential and reaction to adrenergic stimulation lead to automatic electrical activity occurring specifically in cardiac muscle in the PV.


2014 ◽  
Vol 44 (9) ◽  
pp. 1158-1168 ◽  
Author(s):  
Kevin Todd Dyer ◽  
Anthony Marcus Hlavacek ◽  
Felix Gabriel Meinel ◽  
Carlo Nicola De Cecco ◽  
Andrew Douglas McQuiston ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Hiroshige Yamabe ◽  
Hisanori Kanazawa ◽  
Tadashi Hoshiyama ◽  
Miwa Ito ◽  
Shozo Kaneko ◽  
...  

Background: It has been suggested rotor which is located within the pulmonary vein (PV) acted as the driving sources of atrial fibrillation (AF). However, it has never been confirmed whether or not the rotor exists within PV in human. Objectives: We analyzed the activation sequence within the PV during AF and examined how the PV acted as the driving sources of AF. Methods: Selective endocardial mapping of left superior PV (LSPV) was performed during AF in 11 paroxysmal AF patients using a non-contact mapping system (EnSite 3000). Presence of rotor activation was defined when the circular activation around the functional block line once completed its whole reentrant activation. We analyzed the relation between the pivoting activation and the rotor activation. To define the preferable site of rotor and pivoting activation, we also analyzed the relation between the location of rotor and pivoting activation and region of the complex fractionated electrogram (CFE) recording site. Results: Rotor activation was observed with a mean number of 4.6±3.6 times/sec. CFE was observed at the roof (n=5), ridge (n=11) and carina (n=7) of the proximal half of LSPV with a mean area of 9.1±3.4 cm2. The number of rotor activation observed at the CFE area was significantly higher than that at the non-CFE area (4.1±3.9 vs. 0.7±1.2 times/sec, p=0.025). Total frequency of pivoting activation was 37.0±14.7 times/sec. Pivoting activation involved in the rotor activation was significantly lower than that not involved in the rotor activation (8.8±8.1 vs. 27.7±15.8 times/sec, p=0.0116). Regarding the CFE area, pivoting activation involved in the rotor activation was also significantly lower than that not involved in the rotor activation (8.4±8.2 vs. 24.1±12.0 times/sec, p=0.0105). However, there was no difference between the frequencies of pivoting activation with and without rotor activation in the non-CFE area (1.0±2.0 vs. 3.6±6.1 times/sec, p=NS). Conclusions: Rotor activation was observed at the proximal portion of the LSPV coincided with the location of CFE area. However, most of pivoting activation was not involved in the rotor activation. These suggest that AF was driven by the other meandering propagation associated with frequent non-stable pivoting activation over the CFE area.


2006 ◽  
Vol 105 (2) ◽  
pp. 288-293 ◽  
Author(s):  
Yoshifumi Kawanabe ◽  
Tomoh Masaki ◽  
Nobuo Hashimoto

Object Endothelin 1 (ET-1) is a major cause of cerebral vasospasm after subarachnoid hemorrhage (SAH), and extracellular Ca++ influx plays an essential role in ET-1–induced vasospasm. The authors recently demonstrated that ET-1 activates two types of Ca++-permeable nonselective cation channels (designated NSCC-1 and NSCC-2) and a store-operated Ca++ channel (SOCC) in vascular smooth-muscle cells located in the basilar arteries (BAs) of rabbits. In the present study, they investigate the effects of phospholipase C (PLC) on ET-1–induced activation of these Ca++ channels and BA contraction by using the PLC inhibitor U73122. Methods To determine which Ca++ channels are activated via a PLC-dependent pathway, these investigators monitored the intracellular free Ca++ concentration ([Ca++]i). The role of PLC in ET-1–induced vascular contraction was examined by performing a tension study of rabbit BA rings. The U73122 inhibited the ET-1–induced transient increase in [Ca++]i, which resulted from mobilization of Ca++; from the intracellular store. Phospholipase C also inhibited ET-1–induced extracellular Ca++ influx through the SOCC and NSCC-2, but not through the NSCC-1. The U73122 inhibited the ET-1–induced contraction of the rabbit BA rings, which depended on extracellular Ca++ influx through the SOCC and NSCC-2. Conclusions These results indicate the following. 1) The SOCC and NSCC-2 are stimulated by ET-1 via a PLC-dependent cascade whereas NSCC-1 is stimulated via a PLC-independent cascade. 2) The PLC is involved in the ET-1–induced contraction of rabbit BA rings, which depends on extracellular Ca++ influx through the SOCC and NSCC-2.


2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Paolo D. Dallaglio ◽  
Timothy R. Betts ◽  
Matthew Ginks ◽  
Yaver Bashir ◽  
Ignasi Anguera ◽  
...  

The cornerstone of atrial fibrillation (AF) ablation is pulmonary vein isolation (PVI), which can be achieved in more than 95% of patients at the end of the procedure. However, AF recurrence rates remain high and are related to recovery of PV conduction. Adenosine testing is used to unmask dormant pulmonary vein conduction (DC). The aim of this study is to review the available literature addressing the role of adenosine testing and determine the impact of ablation at sites of PV reconnection on freedom from AF. Adenosine infusion, by restoring the excitability threshold, unmasks reversible injury that could lead to recovery of PV conduction. The studies included in this review suggest that adenosine is useful to unmask nontransmural lesions at risk of reconnection and that further ablation at sites of DC is associated with improvement in freedom from AF. Nevertheless it has been demonstrated that adenosine is not able to predict all veins at risk of later reconnection, which means that veins without DC are not necessarily at low risk. The role of the waiting period in the setting of adenosine testing has also been analyzed, suggesting that in the acute phase adenosine use should be accompanied by enough waiting time.


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