Effects of pituitary adenylate cyclase-activating polypeptide on canine atrial electrophysiology

2001 ◽  
Vol 281 (4) ◽  
pp. H1667-H1674 ◽  
Author(s):  
Masamichi Hirose ◽  
Zeng Leatmanoratn ◽  
Kenneth R. Laurita ◽  
Mark D. Carlson

We hypothesized that pituitary adenylate cyclase-activating polypeptide (PACAP) activates intracardiac postganglionic parasympathetic nerves and has a different effect than cervical vagal stimulation. We measured effective refractory period (ERP) and conduction velocity at four atrial sites [high right atrium (HRA), low right atrium (LRA), high left atrium (HLA), and low left atrium (LLA)] and minimum atrial fibrillation (AF) cycle length at 12 atrial sites during cervical vagal stimulation and after PACAP in 26 autonomically decentralized, open-chest, anesthetized dogs. PACAP shortened ERP to a similar extent at all four sites (HRA, 58 ± 2.0 ms; LRA, 60 ± 6.3 ms; HLA, 68 ± 11.5 ms; and LLA, 60 ± 8.3 ms). Low- and high-intensity vagal stimulation shortened ERP at the HRA, but not in the other atrial sites (low-intensity stimulation: HRA, 64 ± 4.0 ms; LRA, 126 ± 5.1 ms; HLA, 110 ± 9.5 ms; and LLA, 102 ± 11.5 ms; high-intensity stimulation: HRA, 58 ± 4.2 ms; and HLA, 101 ± 4.0 ms). Conduction velocity was not altered by any intervention. Minimum AF cycle length after PACAP was similar in both atria but was shorter in the right atrium than in the left atrium during vagal stimulation. After atropine administration, no interventions changed ERP. These results suggest that PACAP shortens atrial refractoriness uniformly in both atria through activation of intrinsic cardiac nerves, not all of which are activated by cervical vagal stimulation.

EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
V Sobota ◽  
A Van Hunnik ◽  
S Zeemering ◽  
G Gatta ◽  
D Opacic ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): ITN Networks PersonalizeAF: Personalized Therapies for Atrial Fibrillation. A Translational Approach, No. 860974; CATCH ME: Characterizing Atrial fibrillation by Translating its Causes into Health Modifiers in the Elderly, No. 633196; MAESTRIA: Machine Learning and Artificial Intelligence for Early Detection of Stroke and Atrial Fibrillation, No. 965286; AFib-TrainNet: EU Training Network on Novel Targets and Methods in Atrial Fibrillation, No. 675351 Netherlands Heart Foundation: CVON2014-09, RACE V Reappraisal of Atrial Fibrillation: Interaction between hyperCoagulability, Electrical remodeling, and Vascular Destabilization in the Progression of Atrial Fibrillation Background Few studies report on mechanisms leading to termination of atrial fibrillation (AF). Purpose To characterise electrophysiological parameters and conduction patterns during the transition from AF to sinus rhythm under various conditions of AF termination. Methods A retrospective evaluation of 6 goat studies was performed. AF was maintained for 3-4 weeks in 29 animals. Four animals were in SR. Unipolar electrograms were acquired with one 249-electrode array/atrium. Pharmacological termination of AF was evoked by various drugs; AP14145 (n = 5), PA6 (n = 7), XAF-1407 (n = 9) vernakalant (n = 8). In animals with sinus rhythm, AF was acutely induced and terminated spontaneously. Baseline AF and ≤3 recordings of the last 10 seconds preceding AF termination were analysed. Intervals with temporal continuous and periodic activity were distinguished in the recordings. AF cycle length (AFCL), conduction velocity and path length were determined for each interval. Results In total, 85 AF terminations were recorded. Switches between temporal continuous and periodic activity were seen frequently during AF. However, termination of AF was always preceded by a phase of periodic activity (PA). The final phase of PA persisted for a median number of 21 [IQR 10-28] cycles in the left atrium and somewhat shorter in the right atrium, Table 1. This final phase of PA was accompanied by a profound bi-atrial increase of AFCL, conduction velocity and path length and a disappearance of inter-atrial cycle length differences. Equipotent changes were not observed in the preceding PAs. During the final AF beats, the number of wave fronts were low, 1 or 2. Interestingly, 92% of the patterns during the last beats of AF involved the Bachmann’s bundle as main source of atrial conduction. Conclusion AF termination is preceded by an increased organisation of fibrillatory conduction, associated with abrupt prolongation of the path length. Propagation in atrial free walls regularly originated from the Bachmann’s bundle. These findings suggest that AF termination was not a random process but follows common spatiotemporal patterns. Final period of temporal organisation Left atrium Right atrium Final PA start Final PA end Final PA start Final PA end Af cycle length (ms) 163 ± 37 204 ± 50* 146 ± 44 207 ± 49* Conduction velocity (cm/s) 77 ± 15 96 ± 25* 83 ± 20 103 ± 24* Path Length (cm) 12.2 ± 2.7 19.3 ± 6.3* 12.0 ± 4.1 21.2 ± 6.4* Length of final periodic activity (beats) NA 21 [IQR 10-28] NA 15 [IQR 10- 25] Electrophysiological changes during the final period periodic activity (PA). Wilcoxon signed rank test. *p <0.05NA= not available


2002 ◽  
Vol 283 (3) ◽  
pp. H1244-H1252 ◽  
Author(s):  
Shengmei Zhou ◽  
Che-Ming Chang ◽  
Tsu-Juey Wu ◽  
Yasushi Miyauchi ◽  
Yuji Okuyama ◽  
...  

Repetitive rapid activities are present in the pulmonary veins (PVs) in dogs with pacing-induced sustained atrial fibrillation (AF). The mechanisms are unclear. We induced sustained (>48 h) AF by rapidly pacing the left atrium (LA) in six dogs. High-density computerized mapping was done in the PVs and atria. Results show repetitive focal activations in all dogs and in 12 of 18 mapped PVs. Activation originated from the middle of the PV and then propagated to the LA and distal PV with conduction blocks. The right atrium (RA) was usually activated by a single large wavefront. Mean AF cycle length in the PVs (left superior, 82 ± 6 ms; left inferior, 83 ± 6 ms; right inferior, 83 ± 4 ms) and LA posterior wall (87 ± 5 ms) were significantly ( P < 0.05) shorter than those in the LA anterior wall (92 ± 4 ms) and RA (107 ± 5 ms). PVs in normal dogs did not have focal activations during induced AF. No reentrant wavefronts were demonstrated in the PVs. We conclude that nonreentrant focal activations are present in the PVs in a canine model of pacing-induced sustained AF.


1991 ◽  
Vol 69 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Pierre L. Pagé ◽  
Hamid Hassanalizadeh ◽  
René Cardinal

The mechanism of atrial flutter and fibrillation induced by rapid pacing in 22 dogs with 3-day-old sterile pericarditis was investigated by computerized epicardial mapping of atrial activation before and after administration of agents known to modify atrial electrophysiologic properties: procainamide, isoproterenol, and electrical stimulation of the vagosympathetic trunks. Before the administration of any of these agents, a total of 30 episodes of sustained atrial flutter (> 1 min duration, monomorphic; regular cycle length, 127 ± 12 ms, mean ± SD) was induced in 15 out of 22 dogs and 9 episodes of unstable atrial flutter (duration, <1 min; cycle length, 129 ± 34 ms; monomorphic, alternating with fibrillation) were induced in the remaining 7 preparations. In the latter, administration of procainamide transformed unstable atrial flutter and atrial fibrillation to sustained atrial flutter (cycle length, 142 ± 33 ms; n = 9 episodes). During control atrial flutter, atrial maps displayed circus movement of excitation in the right atrial free wall with faster conduction parallel to the orientation of intra-atrial myocardial bundles. Vagal stimulation changed atrial flutter to atrial fibrillation in 32 of 73 trials; this was associated with acceleration of conduction in the lower right atrium, leading to fragmentation of the major wave front. Isoproterenol produced a 6–25% increase of the atrial rate in 6 out of 14 trials of atrial flutter and induced atrial fibrillation in 4. After procainamide, the reentrant pathway was lengthened and conduction was slowed further in the right atrium. Maps obtained during unstable atrial flutter showed incomplete circuits involving the right atrium. Following procainamide infusion, the area of functional dissociation or block was enlarged and a stable circus movement pattern, which was similar to the pattern seen in control atrial flutter, was established in the right atrium. We conclude that (1) the transitions among atrial fibrillation, atrial flutter, and sinus rhythm occur between different functional states of the same circus movement substratum primarily located in the lower right atrial free wall, and (2) the anisotropic conduction properties of the right atrium may contribute to these reentrant arrhythmias and may be potentiated by acute pericarditis.Key words: atrial flutter, atrial fibrillation, atrial mapping, antiarrhythmic drugs, vagal stimulation.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
I Marco Clement ◽  
R Eiros ◽  
R Dalmau ◽  
T Lopez ◽  
G Guzman ◽  
...  

Abstract Introduction The diagnosis of sinus venosus atrial septal defect (SVASD) is complex and requires special imaging. Surgery is the conventional treatment; however, transcatheter repair may become an attractive option. Case report A 60 year-old woman was admitted to the cardiology department with several episodes of paroxysmal atrial flutter, atrial fibrillation and atrioventricular nodal reentrant tachycardia. She reported a 10-year history of occasional palpitations which had not been studied. A transthoracic echocardiography revealed severe right ventricle dilatation and moderate dysfunction. Right volume overload appeared to be secondary to a superior SVASD with partial anomalous pulmonary venous drainage. A transesophageal echocardiography confirmed the diagnosis revealing a large SVASD of 16x12 mm (Figure A) with left-right shunt (Qp/Qs 2,2) and two right pulmonary veins draining into the right superior vena cava. Additionally, it demonstrated coronary sinus dilatation secondary to persistent left superior vena cava. CMR and cardiac CT showed right superior and middle pulmonary veins draining into the right superior vena cava 18 mm above the septal defect (Figures B and C). After discussion in clinical session, a percutaneous approach was planned to correct the septal defect and anomalous pulmonary drainage. For this purpose, anatomical data obtained from CMR and CT was needed to plan the procedure. During the intervention two stents graft were deployed in the right superior vena cava. The distal stent was flared at the septal defect level so as to occlude it while redirecting the anomalous pulmonary venous flow to the left atrium (Figure D). Control CT confirmed the complete occlusion of the SVASD without residual communication from pulmonary veins to the right superior vena cava or the right atrium (Figure E). Anomalous right superior and middle pulmonary veins drained into the left atrium below the stents. Transthoracic echocardiographies showed progressive reduction of right atrium and ventricle dilatation. The patient also underwent successful ablation of atrial flutter and intranodal tachycardia. She is currently asymptomatic, without dyspnea or arrhythmic recurrences. Conclusions In this case, multimodality imaging played a key role in every stage of the clinical process. First, it provided the diagnosis and enabled an accurate understanding of the patient’s anatomy, particularly of the anomalous pulmonary venous connections. Secondly, it allowed a transcatheter approach by supplying essential information to guide the procedure. Finally, it assessed the effectiveness of the intervention and the improvement in cardiac hemodynamics during follow-up. Abstract P649 Figure.


2021 ◽  
pp. 28-31
Author(s):  
Inkar Sagatov ◽  
Nurzhan Dosmailov

The article describes the types of correction of the supracardial form of abnormal drainage of the pulmonary veins. One of the methods of correcting this defect is the Warden operation, which includes: after sternotomy, connection of artificial circulation, cardioplegia, the superior vena cava is cut off, the proximal end is sutured. Next, a right atriotomy is performed, an anastomosis is formed using an autopericardial patch between the abnormal drainage and the left atrium through the ASD. Then an anastomosis is formed between the auricle of the right atrium and the distal end of the superior vena cava. As a result, blood from the abnormal pulmonary veins begins to drain into the left atrium through the ASD.


1993 ◽  
Vol 2 (1) ◽  
pp. 72-80 ◽  
Author(s):  
LL Kee ◽  
JS Simonson ◽  
NA Stotts ◽  
P Skov ◽  
NB Schiller

BACKGROUND: The phlebostatic axis--the junction of the fourth intercostal space and the midpoint of the anterior-posterior diameter--has been accepted as a reliable external reference point for the mid-right and mid-left atrium. Acceptance of this reference point is based upon research conducted in 1945 that measured venous pressures in the hands of subjects positioned with the head of the bed raised to different levels. The validity of this reference point for intracardiac pressure measurements in supine or laterally positioned patients has not been established. PURPOSE: To determine the validity of the phlebostatic axis in the supine and lateral positions. METHODS: To determine validity in the supine position, we compared the distance from the phlebostatic axis to a fixed external point (the bed surface) and the distance from the right and left atria in the supine position to this same fixed external point. The distances from the right and left atria to the bed surface were determined with echocardiography and were used as the standard for the proper position of external reference points. To determine the validity of the phlebostatic axis in lateral positions, we compared the distances from the right atrium and left atrium to the bed surface in the supine position with those distances in different lateral positions. RESULTS: We analyzed the data of 25 normal, healthy subjects. The study findings show that the phlebostatic axis is a valid reference point for the right atrium, and the phlebostatic axis and midanterior-posterior diameter are valid reference points for the left atrium in the supine position. However, neither is a valid external reference point in the lateral positions. Pressure measurements obtained when patients are in the lateral positions are not accurate. There remains a need to develop valid methods of accurate pressure measurements in various body positions.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S M Binno ◽  
L Moderato ◽  
G Pastorini ◽  
B Matrone ◽  
D Aschieri ◽  
...  

Abstract We report a case of a 83-year-old female, who had an admission for dyspnea. Laboratory showed D-dimer 1000 ng/ml, haemoglobin 12.4 mg/dL, CPR 0.08mg/dl whereas on Arterial Blood Gas test she had hypoxia with respiratory alkalosis. In view of suspected pulmonary embolism, she underwent Thoracic Computed Tomography scan that excluded it. During the stay the patient seemed more symptomatic while in standing position(with SpO2s 89% while supine plunging to 50% while standing): ABGs were performed both standing (reservoir 15 l/min pH 7.50, pO2 37.2 mmHg, pCO2 37.1 mmHg, HCO3 28.9 mmol/l) and recumbent position (reservoir 15 l/min pH 7.47, pO2 65.5 mmHg, pCO2 35.1 mmHg, HCO3 25.6 mmol), showing a difference of 28 mmHg. Subsequently the patient underwent v/p pulmonary scintigraphy: no signs of pulmonary embolism though it revealed a multiple focus of capitation Tc-99m macro aggregated albumin in brain, thyroid and kidneys (IMG top), compatible for veno-arterial shunt. Trans-esophageal echocardiography (TOE) revealed a massive stretched patent foramen ovale (PFO) with continuous right-to-left shunting through the atria. The bubble test (IMG bottom) confirmed the presence of patency along with sudden passage of microbubbles through the foramen. Qp/Qs = 0.8, due to volume overload in the left atrium from the right atrium. The imaging along with clinical scenario confirmed the suspected diagnosis of platypnea-orthodeoxia, finding the patent foramen ovale as the anatomical cause. Platypnea-orthodeoxia syndrome is a clinical condition characterized by dyspnea. Typically blood oxygen saturation declines with standing position while it resolves with recumbent. The classification entails 3 groups: intracardiac shunting (most common presentation), pulmonary shunting, ventilation-perfusion mismatch. Presence of multiple focus of albumin macroaggregates outside the lungs in v/p scintigraphy examination is suggestive for veno-arteriuous shunt: without shunt, normally all the albumin aggregates are hampered in the lungs’ field. Images in bottom are taken in sequence from a single acquisition during the TOE, in one single cardiac beat. Here is depicted the evidence of the PFO, the influx of bubbles in the right atrium and the instantaneous and massive shunt of the bubbles across the interatrial septum, in the left atrium. Usually the diagnosis is performed within 55 years old: it is interesting how late the diagnosis occurred in this patient with such resounding clinical manifestation. Top Scintigraphy with ventilation and perfusion lung scan sequences. Next, scintigraphy with capitation of Tc-99m macro aggregated albumin in brain, thyroid and kidneys. Bottom, Transesophageal echocardiogram: images taken within the same heart beat proving right-to-left passage of bubble across the septum. Abstract P1317 Figure. Scintigraphy and Transesophageal echo


1976 ◽  
Vol 231 (3) ◽  
pp. 781-785 ◽  
Author(s):  
OM Brown

The distribution of acetylcholine (ACh) in the cat heart was investigated by a pyrolysis-gas chromatography (PGC) method. The hearts were dissected into various regions and homogenized in acetonitrile in the presence of propionylcholine, internal standard. Following extraction with toluene and hexane, the choline esters were precipitated as the enneaiodide complex. The isolated choline esters were analyzed by PGC, and the peak corresponding to ACh was quantified. The compound extracted from heart tissue that eluted with the retention time of authentic ACh was identified by mass spectrometry as dimethylaminoethylacetate, the pyrolysis product of ACh. ACh concentrations were found to be higher in the atria than the ventricles. In both the atria and the ventricles, a higher content of ACh was found in the right than the left portions: right ventricle, 5.0 compared to left ventricle, 2.0 nmol/g; and right atrium, 16.8 compared to left atrium, 11.3 nmol/g. Some cats were subjected to a bilateral cervical vagotomy 3 wk before removal and analysis of heart tissue. Hearts from vagotomized cats contained less ACh than controls in the right ventricle (-31%), right atrium (-54%), SA node (-42%), and papillary muscle (-53%), but no decreases were found in the left ventricle, left atrium, or interventricular septum.


2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Szilvia Herczeg ◽  
Joseph Galvin ◽  
John J. Keaney ◽  
Edward Keelan ◽  
Roger Byrne ◽  
...  

Introduction. Growing evidence suggests that fibrotic changes can be observed in atrial fibrillation (AF) in both atria. Quantification of the scar burden during electroanatomical mapping might have important therapeutic and prognostic consequences. However, as the current invasive treatment of AF is focused on the left atrium (LA), the role of the right atrium (RA) is less well understood. We aimed to characterize the clinical determinates of the RA low-voltage burden and its relation to the LA scaring. Methods. We have included 36 patients who underwent catheter ablation for AF in a prospective observational study. In addition to LA mapping and ablation, high-density RA bipolar voltage maps (HD-EAM) were also reconstructed. The extent of the diseased RA tissue (≤0.5 mV) was quantified using the voltage histogram analysis tool (CARTO®3, Biosense Webster). Results. The percentage of RA diseased tissue burden was significantly higher in patients with a CHA2DS2-VASc score ≥ 2 p=0.0305, higher indexed LA volume on the CTA scan and on the HD‐EAM (p=0.0223 and p=0.0064, respectively), or higher indexed RA volume on the HD‐EAM p=0.0026. High RA diseased tissue burden predicted the presence of high LA diseased tissue burden (OR = 7.1, CI (95%): 1.3–38.9, p=0.0145), and there was a significant correlation of the same (r = 0.6461, p<0.0001). Conclusions. Determining the extent of the right atrial low-voltage burden might give useful clinical information. According to our results, the diseased tissue burden correlates well between the two atria: the right atrium mirrors the left atrium.


1983 ◽  
Vol 244 (1) ◽  
pp. H102-H108 ◽  
Author(s):  
J. X. Thomas ◽  
W. C. Randall

Autonomic innervation of the atrioventricular (AV) junction modulates conduction of the cardiac impulse, the sympathetic nerves facilitating and parasympathetic nerves impeding conduction. Experiments assessed the relative importance of parasympathetic vs. sympathetic control by pharmacologic blockade with atropine (0.2 mg/kg) or propranolol (1.0 mg/kg) while pacing the right atrium (100-400 beats/min) in normal, conscious resting dogs and in dogs that had undergone chronic, intrapericardial cardiac denervation. Maximum pacing rate with 1:1 atrioventricular conduction was termed Rmax. Control Rmax at rest was 125.69 +/- 9.49 beats/min and was slightly reduced after propranolol to 118.28 +/- 10.98 (P = 0.043). After atropine, Rmax was significantly increased to 344 beats/min. Propranolol and atropine together resulted in an Rmax of 308 beats/min, which was significantly less than after atropine alone. Rmax in cardiac-denervated dogs was 301 beats/min, which was not significantly different from that following total pharmacologic blockade. In conscious, resting, unsedated dogs, the upper limit of AV nodal conduction is associated with the level of parasympathetic rather than sympathetic tone; during exercise the sympathetics assume greater importance.


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