scholarly journals Right ventricular arrhythmogenesis in failing human heart: the role of conduction and repolarization remodeling

2012 ◽  
Vol 303 (12) ◽  
pp. H1426-H1434 ◽  
Author(s):  
Qing Lou ◽  
Deborah L. Janks ◽  
Katherine M. Holzem ◽  
Di Lang ◽  
Birce Onal ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Human Heart ◽  
Field Of View ◽  
Mapping Data ◽  
Human Heart Failure ◽  
Dispersion Of Repolarization ◽  
Cycle Lengths ◽  
Rapid Pacing ◽  
The Right

Increased dispersion of repolarization has been suggested to underlie increased arrhythmogenesis in human heart failure (HF). However, no detailed repolarization mapping data were available to support the presence of increased dispersion of repolarization in failing human heart. In the present study, we aimed to determine the existence of enhanced repolarization dispersion in the right ventricular (RV) endocardium from failing human heart and examine its association with arrhythmia inducibility. RV free wall preparations were dissected from five failing and five nonfailing human hearts, cannulated and coronary perfused. RV endocardium was optically mapped from an ∼6.3 × 6.3 cm2 field of view. Action potential duration (APD), dispersion of APD, and conduction velocity (CV) were quantified for basic cycle lengths (BCL) ranging from 2,000 ms to the functional refractory period. We found that RV APD was significantly prolonged within the failing group compared with the nonfailing group (560 ± 44 vs. 448 ± 39 ms, at BCL = 2,000 ms, P < 0.05). Dispersion of APD was increased in three failing hearts (161 ± 5 vs. 86 ± 19 ms, at BCL = 2,000 ms). APD alternans were induced by rapid pacing in these same three failing hearts. CV was significantly reduced in the failing group compared with the nonfailing group (81 ± 11 vs. 98 ± 8 cm/s, at BCL = 2,000 ms). Arrhythmias could be induced in two failing hearts exhibiting an abnormally steep CV restitution and increased dispersion of repolarization due to APD alternans. Dispersion of repolarization is enhanced across the RV endocardium in the failing human heart. This dispersion, together with APD alternans and abnormal CV restitution, could be responsible for the arrhythmia susceptibility in human HF.

scholarly journals ISCHEMIC VERSUS NON-ISCHEMIC RIGHT VENTRICULAR TRANSCRIPTOME IN END-STAGE HUMAN HEART FAILURE

2014 ◽  
Vol 63 (12) ◽  
pp. A921
Author(s):  
Thomas Gerard Di Salvo ◽  
Cristi Galindo ◽  
Yan Guo ◽  
Yan Ru Su ◽  
Tarek bsi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Human Heart ◽  
Human Heart Failure ◽  
End Stage

scholarly journals Simulation and Mechanistic Investigation of the Arrhythmogenic Role of the Late Sodium Current in Human Heart Failure

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e32659 ◽  
Author(s):  
Beatriz Trenor ◽  
Karen Cardona ◽  
Juan F. Gomez ◽  
Sridharan Rajamani ◽  
Jose M. Ferrero ◽  
...  
Keyword(s):  
Heart Failure ◽  
Human Heart ◽  
Sodium Current ◽  
Human Heart Failure ◽  
Late Sodium Current ◽  
Mechanistic Investigation

Abstract 14985: Presence of Repolarization Gradients Reverses Post-infarct Ventricular Tachycardia Exit and Entrance Sites in Personalized Digital Hearts

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Eric Sung ◽  
Adityo Prakosa ◽  
Natalia Trayanova
Keyword(s):  
Border Zone ◽  
Non Invasive ◽  
Cycle Lengths ◽  
Rapid Pacing ◽  
Vt Ablation ◽  
Right Ventricular Apex ◽  
The Right ◽  
Ventricular Tachycardias ◽  
Infarct Border Zone ◽  
Infarct Border

Introduction: Post-infarct ventricular tachycardias (VT) arise due to structural remodeling (scarring). Physiological repolarization gradients (apicobasal and transmural) exist in the human heart, but the effects on post-infarct VT dynamics are unknown. Hypothesis: We hypothesized that incorporation of repolarization gradients in personalized digital hearts of post-infarct patients impacts VT exit sites without altering the location of the VTs. Methods: 3D late-gadolinium enhanced CMR images were acquired from 7 post-infarct patients. Personalized image-based computational heart models (digital hearts) representing scar and infarct border zone distributions were constructed. Apicobasal (AB) and transmural (TM) repolarization gradients were incorporated using a validated method (Fig A). VTs were induced at baseline (no repolarization gradient) via rapid pacing in the right ventricular apex, using two pacing cycle lengths, mimicking non-invasive programmed stimulation. Pacing protocols that induced baseline VTs were repeated under AB and TM conditions. Results: Ten VTs were induced in baseline digital hearts. 8 AB VTs and 8 TM VTs were induced; the remaining 2 VTs for both AB and TM digital hearts could not be induced. 5/8 induced AB VTs had VT exit sites matching baseline VT exit sites; the remaining 3/8 AB VTs had reversed VT exit and entrance sites from the corresponding baseline VTs (Fig B, VT 1 & 2). 4/8 induced TM VTs had exit sites that matched those at baseline; the remaining TM VTs had exit and entrance sites reversed from those of baseline VTs (Fig B, VT 1, 2 & 3). All 8 AB VTs and 8 TM VTs had the same location as corresponding baseline VTs. Conclusion: AB and TM repolarization gradients can act to reverse VT entrance and exit sites without changing VT location. Thus, incorporation of physiological repolarization gradients into personalized digital hearts may not impact VT ablation targeting but may affect accurate prediction of VT exit or entrance sites.

Recurrent appearance of protective zones after an unsuccessful defibrillation shock

1996 ◽  
Vol 271 (4) ◽  
pp. H1491-H1497 ◽  
Author(s):  
C. Hwang ◽  
W. Fan ◽  
P. S. Chen
Keyword(s):  
Right Ventricular ◽  
Energy Requirement ◽  
Right Ventricular Outflow Tract ◽  
Posterior Wall ◽  
Ventricular Outflow Tract ◽  
Specific Time ◽  
Time Intervals ◽  
Cycle Lengths ◽  
Right Ventricular Apex ◽  
The Right

This study was designed to test the hypothesis that protective zones appear recurrently at the initiation of ventricular fibrillation (VF) and that when shocks are delivered during protective zones, there can be a decrease in the defibrillation energy requirement. A total of 12 open-chest dogs were studied. Six dogs were included in protocol 1. After eight baseline pacing stimuli (S1) with cycle lengths of 300 ms, a strong premature stimulus (S2) (73 +/- 10 mA) was given to induce VF. In subsequent episodes, a second strong premature stimulus (S3) was given at progressively longer S2-S3 intervals in 20-ms increments. In protocol 2, we delivered unsuccessful defibrillation shocks via a transvenous defibrillation electrode placed in the right ventricular apex of six dogs. A second shock was then delivered to patch electrodes on the right ventricular outflow tract and the posterior wall of the left ventricle. The results of protocol 1 showed that the S3 terminated reentry and prevented VF only when it occurred at specific time intervals after the S2 (the protective zones). These protective zones appear recurrently up to 375 ms after the onset of VF. The results of protocol 2 showed that the total energy required for successful defibrillation was dependent on the interval between the first and second shocks. Intervals favoring effective defibrillation (protective zones) appeared recurrently for up to 280 ms after the first shock. When the second shock was delivered during a protective zone, the defibrillation energy requirement was decreased by up to 23% (from 13.1 +/- 2.0 to 10.1 +/- 1.8 J, P < 0.003). However, when the shock was delivered outside the protective zone, a significant increase in the defibrillation energy requirement was observed. We conclude that protective zones appear recurrently at the onset of VF and after unsuccessful defibrillation shocks.

scholarly journals Right ventricular cyclic nucleotide signaling is decreased in hyperoxia-induced pulmonary hypertension in neonatal mice

2015 ◽  
Vol 308 (12) ◽  
pp. H1575-H1582 ◽  
Author(s):  
Rachel P. Heilman ◽  
Megan B. Lagoski ◽  
Keng Jin Lee ◽  
Joann M. Taylor ◽  
Gina A. Kim ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Premature Infants ◽  
Ventricular Hypertrophy ◽  
Neonatal Mouse ◽  
Pulmonary Vasculature ◽  
The Right ◽  
Phosphodiesterase 5 ◽  
Expression And Activity

Pulmonary hypertension (PH) and right ventricular hypertrophy (RVH) affect 25–35% of premature infants with significant bronchopulmonary dysplasia (BPD), increasing morbidity and mortality. We sought to determine the role of phosphodiesterase 5 (PDE5) in the right ventricle (RV) and left ventricle (LV) in a hyperoxia-induced neonatal mouse model of PH and RVH. After birth, C57BL/6 mice were placed in room air (RA) or 75% O2 (CH) for 14 days to induce PH and RVH. Mice were euthanized at 14 days or recovered in RA for 14 days or 42 days prior to euthanasia at 28 or 56 days of age. Some pups received sildenafil or vehicle (3 mg·kg−1·dose−1 sc) every other day from P0. RVH was assessed by Fulton's index [RV wt/(LV + septum) wt]. PDE5 protein expression was analyzed via Western blot, PDE5 activity was measured by commercially available assay, and cGMP was measured by enzyme-linked immunoassay. Hyperoxia induced RVH in mice after 14 days, and RVH did not resolve until 56 days of age. Hyperoxia increased PDE5 expression and activity in RV, but not LV + S, after 14 days. PDE5 expression normalized by 28 days of age, but PDE5 activity did not normalize until 56 days of age. Sildenafil given during hyperoxia prevented RVH, decreased RV PDE5 activity, and increased RV cGMP levels. Mice with cardiac-specific overexpression of PDE5 had increased RVH in RA. These findings suggest normal RV PDE5 function is disrupted by hyperoxia, and elevated PDE5 contributes to RVH and remodeling. Therefore, in addition to impacting the pulmonary vasculature, sildenafil also targets PDE5 in the neonatal mouse RV and decreases RVH.

Role of the Cardiac Renin-Angiotensin System in Human Heart Failure

1995 ◽  
pp. 279-283 ◽  
Author(s):  
Martin Paul ◽  
Philippe Stock ◽  
Matthias Langheinrich ◽  
Lutz Liefeldt ◽  
Gilbert Schönfelder ◽  
...  
Keyword(s):  
Heart Failure ◽  
Human Heart ◽  
Renin Angiotensin System ◽  
Human Heart Failure ◽  
Angiotensin System ◽  
Renin Angiotensin
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