scholarly journals Endocardial late potentials recorded during sinus rhythm in man: Incidence in different cardiac disease states

1988 ◽  
Vol 11 (3) ◽  
pp. 164-174 ◽  
Author(s):  
K.-P. Bethge ◽  
B.-D. Gonska ◽  
H. Kreuzer ◽  
R. Kühn ◽  
G. Sauthoff ◽  
...  
1983 ◽  
pp. 767-772 ◽  
Author(s):  
R. A. Jauemig ◽  
J. Senges ◽  
W. Lengfelder ◽  
I. Rizos ◽  
Ellen Hoffmann ◽  
...  

EP Europace ◽  
2017 ◽  
Vol 19 (suppl_3) ◽  
pp. iii232-iii232
Author(s):  
S. Magnani ◽  
F. Calore ◽  
CM. Barbaro ◽  
G. D'angelo ◽  
C. Bisceglia ◽  
...  

2012 ◽  
Vol 303 (9) ◽  
pp. R950-R958 ◽  
Author(s):  
Jean C. Hardwick ◽  
E. Marie Southerland ◽  
Allison E. Girasole ◽  
Shannon E. Ryan ◽  
Sara Negrotto ◽  
...  

Chronic heart disease induces remodeling of cardiac tissue and associated neuronal components. Treatment of chronic heart disease often involves pharmacological blockade of adrenergic receptors. This study examined the specific changes in neuronal sensitivity of guinea pig intrinsic cardiac neurons to autonomic modulators in animals with chronic cardiac disease, in the presence or absence of adrenergic blockage. Myocardial infarction (MI) was produced by ligature of the coronary artery and associated vein on the dorsal surface of the heart. Pressure overload (PO) was induced by a banding of the descending dorsal aorta (∼20% constriction). Animals were allowed to recover for 2 wk and then implanted with an osmotic pump (Alzet) containing either timolol (2 mg·kg−1·day−1) or vehicle, for a total of 6–7 wk of drug treatment. At termination, intracellular recordings from individual neurons in whole mounts of the cardiac plexus were used to assess changes in physiological responses. Timolol treatment did not inhibit the increased sensitivity to norepinephrine seen in both MI and PO animals, but it did inhibit the stimulatory effects of angiotensin II on the norepinephrine-induced increases in neuronal excitability. Timolol treatment also inhibited the increase in synaptically evoked action potentials observed in PO animals with stimulation of fiber tract bundles. These results demonstrate that β-adrenergic blockade can inhibit specific aspects of remodeling within the intrinsic cardiac plexus. In addition, this effect was preferentially observed with active cardiac disease states, indicating that the β-receptors were more influential on remodeling during dynamic disease progression.


2014 ◽  
Vol 30 (4) ◽  
pp. 320-322
Author(s):  
Shiro Nakahara ◽  
Yuichi Hori ◽  
Sayuki Kobayashi ◽  
Naofumi Tsukada ◽  
Yoshihiko Sakai ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Vincent Y See ◽  
Jessica Fugate ◽  
Gagandeep Gurm ◽  
Dawn Ament ◽  
Timm-Michael Dickfeld ◽  
...  

Background: Soluble ST2 (sST2) is a decoy receptor that modulates the anti-hypertrophic and anti-fibrotic IL-33/ST2 pathway. sST2 is associated with adverse prognosis in HF and ACS; both states are associated with cardiac injury. However, sST2 levels are also increased in non-cardiac disease. To determine the extent of cardiac production of sST2 both chronically and after acute myocardial injury, we measured fractional cardiac production of sST2 compared to the cardiac specific injury marker high sensitive (hs) cTnT before and after elective cardiac ablation. Methods: Twenty-three patients undergoing ablation of atrial fibrillation were enrolled [Caucasian 22 (96%); Male 17 (74%); Age 57.7±10.4 years; eGFR 58.7 ± 0.6 mL/min/1.73m2). Of the 23, 15 (65%) had paroxysmal atrial fibrillation. At baseline, 14 (61%) were in sinus rhythm. Samples were obtained from the radial artery and coronary sinus (CS) pre- and post-ablation. sST2 was measured by the Presage assay. Post ablation samples were measured 201±44 minutes after the first ablation. Results: At baseline, in contrast to cTnT, there was no cardiac production of sST2. Both arterial and CS levels of sST2 increased after ablation but not nearly to the extent of cTnT. No net cardiac production of sST2 was noted (Table). Conclusion: Cardiac production of sST2 is not observed at baseline. Systemic sST2 levels modestly increase following acute myocardial injury. Despite direct myocardial injury, no cardiac production of sST2 is observed. The source of sST2 is extra-cardiac both chronically and after acute injury.


EP Europace ◽  
2020 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
N Srinivasan ◽  
J Garcia ◽  
R J Schilling ◽  
S Ahsan ◽  
G Babu ◽  
...  

Abstract Introduction Activation and entrainment mapping of VT remains the gold standard for identifying critical sites for ablation of VT, however, this method is limited by poorly tolerated or non-sustained VT. Several substrate guided approaches have been developed, however, outcomes when comparing both methods are similar and overall success can be as low as 47%. A key element in facilitating VT is the presence of dynamic changes within the substrate which may not be evident during sinus rhythm substrate mapping, but may form a critical aspect of the tachycardia mechanism when conduction velocity slows dynamically and tissue refractory periods lengthen. These are rarely studied as part of clinical VT mapping.  Purpose This study aimed to investigate dynamic substrate changes to local abnormal ventricular activity (LAVA) and late potentials (LP), in relation to critical sites for VT ablation using high resolution mapping of the ventricle with the HD Grid (Abbott, Inc, USA), during short coupled singe extra stimuli from the right ventricle (RV) (Barts Sense Protocol), designed to invoke conduction delay. We hypothesized that the dynamic functional late potential mapping would improve the identification of critical substrate and ablation of these regions would improve outcomes.  Methods Thirty patients (age 67 +/- 9yrs, 27Male) underwent ablation. Mean ejection fraction was 25% (+/- 10%). Mapping was performed with the AdvisorTM HD Grid multipolar catheter. A bipolar voltage map was obtained during sinus rhythm (SR) and RV Sensed Protocol (SP) single extra pacing. SR and SP late potential (LP) and local abnormal ventricular activity (LAVA) maps were made and compared with critical sites for ablation, defined as sites of best entrainment or pace mapping. Ablation was then performed to critical sites and LP/LAVA identified by the SP. Results At a median follow up of 10 months 90% of patients were free from symptomatic ATP or ICD shocks. The median area of late potentials across the 30 patients during sinus rhythm was 6.4mm2 during sinus rhythm mapping and 19.3mm2 during sense protocol pacing (p = 0.001). The functional unmasking of LP and LAVA was seen in 26 patients and showed good correlation to critical regions of the VT circuit (sites of best entrainment or pace map). In 24 patients functionally unmasked late potentials were located within 10mm of critical regions within the mapped VT circuit, with a median distance of 8.5mm, compared to 7 patients during sinus rhythm mapping with a median distance of 22mm (p= <0.001). Figure 1 demonstrates and example of the SP, where increased functional LP are seen along the mapped VT isthmus.  Conclusion Functional LP and LAVA can be unmasked by the sense protocol enabling better delineation of critical regions for VT ablation which may not be visible during sinus rhythm. This unique delineation of functional substrate changes combined with activation or pacemapping may improve outcomes. Abstract Figure 1


Heart Rhythm ◽  
2021 ◽  
Vol 18 (8) ◽  
pp. S421
Author(s):  
Satish K. Misra ◽  
Catherine E. Markert ◽  
Andrew P. Quigley ◽  
Jonathan Ims ◽  
Rohit Mehta ◽  
...  

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