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1,066 results on '"Jalife, José"'

301. Atrial Septopulmonary Bundle of the Posterior Left Atrium Provides a Substrate for Atrial Fibrillation Initiation in a Model of Vagally Mediated Pulmonary Vein Tachycardia of the Structurally Normal Heart

Author

Klos, Matthew, primary, Calvo, David, additional, Yamazaki, Masatoshi, additional, Zlochiver, Sharon, additional, Mironov, Sergey, additional, Cabrera, José-Angel, additional, Sanchez-Quintana, Damian, additional, Jalife, José, additional, Berenfeld, Omer, additional, and Kalifa, Jérôme, additional

Published
2008
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306. Arrhythmogenic Mechanisms in a Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Cerrone, Marina, primary, Noujaim, Sami F., additional, Tolkacheva, Elena G., additional, Talkachou, Arkadzi, additional, O’Connell, Ryan, additional, Berenfeld, Omer, additional, Anumonwo, Justus, additional, Pandit, Sandeep V., additional, Vikstrom, Karen, additional, Napolitano, Carlo, additional, Priori, Silvia G., additional, and Jalife, José, additional

Published
2007
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307. Spatial Distribution of Fibrosis Governs Fibrillation Wave Dynamics in the Posterior Left Atrium During Heart Failure

Author

Tanaka, Kazuhiko, primary, Zlochiver, Sharon, additional, Vikstrom, Karen. L., additional, Yamazaki, Masatoshi, additional, Moreno, Javier, additional, Klos, Matthew, additional, Zaitsev, Alexey. V., additional, Vaidyanathan, Ravi, additional, Auerbach, David S., additional, Landas, Steve, additional, Guiraudon, Gérard, additional, Jalife, José, additional, Berenfeld, Omer, additional, and Kalifa, Jérôme, additional

Published
2007
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311. Optical mapping of Langendorff-perfused human hearts: establishing a model for the study of ventricular fibrillation in humans

Author

Nanthakumar, Kumaraswamy, primary, Jalife, José, additional, Massé, Stéphane, additional, Downar, Eugene, additional, Pop, Mihaela, additional, Asta, John, additional, Ross, Heather, additional, Rao, Vivek, additional, Mironov, Sergey, additional, Sevaptsidis, Elias, additional, Rogers, Jack, additional, Wright, Graham, additional, and Dhopeshwarkar, Rajesh, additional

Published
2007
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316. Ventricular Tachycardia and Early Fibrillation in Patients With Brugada Syndrome and Ischemic Cardiomyopathy Show Predictable Frequency-Phase Properties on the Precordial ECG Consistent With the Respective Arrhythmogenic Substrate.

Author

Calvo, David, Atienza, Felipe, Saiz, Javier, Martínez, Laura, Ávila, Pablo, Rubín, José, Herreros, Benito, Arenal, Ángel, Fernández, Javier García, Ferrer, Ana, Sebastián, Rafael, Camblor, Pablo Martínez, Jalife, José, Berenfeld, Omer, García-Fernández, Javier, and Martínez-Camblor, Pablo

Subjects
ELECTROCARDIOGRAPHY, HEART function tests, CARDIOMYOPATHIES, RESEARCH funding, VENTRICULAR fibrillation, VENTRICULAR tachycardia, BRUGADA syndrome
Abstract

Background: Ventricular fibrillation (VF) has been proposed to be maintained by localized high-frequency sources. We tested whether spectral-phase analysis of the precordial ECG enabled identification of periodic activation patterns generated by such sources.Methods and Results: Precordial ECGs were recorded from 15 ischemic cardiomyopathy and 15 Brugada syndrome (type 1 ECG) patients during induced VF and analyzed in the frequency-phase domain. Despite temporal variability, induced VF episodes lasting 19.6±7.9 s displayed distinctly high power at a common frequency (shared frequency, 5.7±1.1 Hz) in all leads about half of the time. In patients with Brugada syndrome, phase analysis of shared frequency showed a V1-V6 sequence as would be expected from patients displaying a type 1 ECG pattern (P<0.001). Hilbert-based phases confirmed that the most stable sequence over the whole VF duration was V1-V6. Analysis of shared frequency in ischemic cardiomyopathy patients with anteroseptal (n=4), apical (n=3), and inferolateral (n=4) myocardial infarction displayed a sequence starting at V1-V2, V3-V4, and V5-V6, respectively, consistent with an activation origin at the scar location (P=0.005). Sequences correlated with the Hilbert-based phase analysis (P<0.001). Posterior infarction (n=4) displayed no specific sequence. On paired comparison, phase sequences during monomorphic ventricular tachycardia correlated moderately with VF (P<0.001). Moreover, there was a dominant frequency gradient from precordial leads facing the scar region to the contralateral leads (5.8±0.8 versus 5.4±1.1 Hz; P=0.004).Conclusions: Noninvasive analysis of ventricular tachycardia and early VF in patients with Brugada syndrome and ischemic cardiomyopathy shows a predictable sequence in the frequency-phase domain, consistent with anatomic location of the arrhythmogenic substrate. [ABSTRACT FROM AUTHOR]

Published
2015
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317. Atrial remodeling, fibrosis, and atrial fibrillation.

Author

Jalife, José and Kaur, Kuljeet

Subjects
*ATRIAL fibrillation, *VENTRICULAR remodeling, *FIBROSIS, *ARRHYTHMIA, *ELECTROPHYSIOLOGY, *INFLAMMATION
Abstract

The fundamental mechanisms governing the perpetuation of atrial fibrillation (AF), the most common arrhythmia seen in clinical practice, are poorly understood, which explains in part why AF prevention and treatment remain suboptimal. Although some clinical parameters have been identified as predicting a transition from paroxysmal to persistent AF in some patients, the molecular, electrophysiological, and inflammation changes leading to such a progression have not been described in detail. Oxidative stress, atrial dilatation, calcium overload, inflammation, microRNAs, and myofibroblast activation are all thought to be involved in AF-induced atrial remodeling. However, it is unknown to what extent and at which time points such alterations influence the remodeling process that perpetuates AF. Here we postulate a working model that might open new pathways for future investigation into mechanisms of AF perpetuation. We start from the premise that the progression to AF perpetuation is the result of interplay among manifold signaling pathways with differing kinetics. Some such pathways have relatively fast kinetics (e.g., oxidative stress-mediated shortening of refractory period); others likely depend on molecular processes with slower kinetics (e.g., transcriptional changes in myocyte ion channel protein expression mediated through inflammation and fibroblast activation). We stress the need to fully understand the relationships among such pathways should one hope to identify novel, truly effective targets for AF therapy and prevention. [ABSTRACT FROM AUTHOR]

Published
2015
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318. Scn1b deletion leads to increased tetrodotoxin-sensitive sodium current, altered intracellular calcium homeostasis and arrhythmias in murine hearts.

Author

Lin, Xianming, O'Malley, Heather, Chen, Chunling, Auerbach, David, Foster, Monique, Shekhar, Akshay, Zhang, Mingliang, Coetzee, William, Jalife, José, Fishman, Glenn I., Isom, Lori, and Delmar, Mario

Subjects
SODIUM channels regulation, BRUGADA syndrome, ARRHYTHMIA, CALCIUM channels, EPILEPSY research
Abstract

Key points Na+ current ( INa) results from the integrated function of a molecular aggregate (the voltage-gated Na+ channel complex) that includes the β subunit family., Mutations or rare variants in Scn1b (encoding the β1 and β1B subunits) have been associated with various inherited arrhythmogenic syndromes, including Brugada syndrome and sudden unexpected death in patients with epilepsy., We used Scn1b null mice to understand better the relation between Scn1b expression, and cardiac electrical function., Loss of Scn1b caused, among other effects, increased amplitude of tetrodotoxin-sensitive INa, delayed after-depolarizations, triggered beats, delayed Ca2+ transients, frequent spontaneous calcium release events and increased susceptibility to polymorphic ventricular arrhythmias. Most alterations in Ca2+ homeostasis were prevented by 100 n m tetrodotoxin., We propose that life-threatening arrhythmias in patients with mutations in Scn1b, a gene classically defined as ancillary to the Na+ channel α subunit, can be partly consequent to disrupted intracellular Ca2+ homeostasis., Abstract Na+ current ( INa) is determined not only by the properties of the pore-forming voltage-gated Na+ channel (VGSC) α subunit, but also by the integrated function of a molecular aggregate (the VGSC complex) that includes the VGSC β subunit family. Mutations or rare variants in Scn1b (encoding the β1 and β1B subunits) have been associated with various inherited arrhythmogenic syndromes, including cases of Brugada syndrome and sudden unexpected death in patients with epilepsy. Here, we have used Scn1b null mouse models to understand better the relation between Scn1b expression, and cardiac electrical function. Using a combination of macropatch and scanning ion conductance microscopy we show that loss of Scn1b in juvenile null animals resulted in increased tetrodotoxin-sensitive INa but only in the cell midsection, even before full T-tubule formation; the latter occurred concurrent with increased message abundance for the neuronal Scn3a mRNA, suggesting increased abundance of tetrodotoxin-sensitive NaV1.3 protein and yet its exclusion from the region of the intercalated disc. Ventricular myocytes from cardiac-specific adult Scn1b null animals showed increased Scn3a message, prolonged action potential repolarization, presence of delayed after-depolarizations and triggered beats, delayed Ca2+ transients and frequent spontaneous Ca2+ release events and at the whole heart level, increased susceptibility to polymorphic ventricular arrhythmias. Most alterations in Ca2+ homeostasis were prevented by 100 n m tetrodotoxin. Our results suggest that life-threatening arrhythmias in patients with mutations in Scn1b, a gene classically defined as ancillary to the Na+ channel α subunit, can be partly consequent to disrupted intracellular Ca2+ homeostasis in ventricular myocytes. [ABSTRACT FROM AUTHOR]

Published
2015
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320. Activation of Inward Rectifier Potassium Channels Accelerates Atrial Fibrillation in Humans

Author

Atienza, Felipe, primary, Almendral, Jesús, additional, Moreno, Javier, additional, Vaidyanathan, Ravi, additional, Talkachou, Arkazdi, additional, Kalifa, Jérôme, additional, Arenal, Angel, additional, Villacastín, Julian P., additional, Torrecilla, Esteban G., additional, Sánchez, Ana, additional, Ploutz-Snyder, Robert, additional, Jalife, José, additional, and Berenfeld, Omer, additional

Published
2006
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324. Mechanisms of Wave Fractionation at Boundaries of High-Frequency Excitation in the Posterior Left Atrium of the Isolated Sheep Heart During Atrial Fibrillation

Author

Kalifa, Jérôme, primary, Tanaka, Kazuhiko, additional, Zaitsev, Alexey V., additional, Warren, Mark, additional, Vaidyanathan, Ravi, additional, Auerbach, David, additional, Pandit, Sandeep, additional, Vikstrom, Karen L., additional, Ploutz-Snyder, Robert, additional, Talkachou, Arkadzi, additional, Atienza, Felipe, additional, Guiraudon, Gérard, additional, Jalife, José, additional, and Berenfeld, Omer, additional

Published
2006
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327. Spectral Analysis Identifies Sites of High-Frequency Activity Maintaining Atrial Fibrillation in Humans

Author

Sanders, Prashanthan, primary, Berenfeld, Omer, additional, Hocini, Mélèze, additional, Jaïs, Pierre, additional, Vaidyanathan, Ravi, additional, Hsu, Li-Fern, additional, Garrigue, Stéphane, additional, Takahashi, Yoshihide, additional, Rotter, Martin, additional, Sacher, Fréderic, additional, Scavée, Christophe, additional, Ploutz-Snyder, Robert, additional, Jalife, José, additional, and Haïssaguerre, Michel, additional

Published
2005
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333. Heart failure results in reduced rate and increased variability of wave patterns at the posterior wall of the fibrillating left atrium of the sheep heart

Author

Tanaka, Kazuhiko, primary, Kalifa, Jérôme, additional, Auerbach, David, additional, Moreno, Javier, additional, Warren, Mark, additional, Vaidyanathan, Ravi, additional, Zaitsev, Alexey V., additional, Berenfeld, Omer, additional, Guiraudon, Gérard M., additional, and Jalife, José, additional

Published
2005
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334. Prolongation of atrial fibrillation cycle length during catheter ablation at sites of maximal dominant frequency

Author

Sanders, Prashanthan, primary, Berenfeld, Omer, additional, Takahashi, Yoshihide, additional, Vaidyanathan, Ravi, additional, Hocini, Mélèze, additional, Jaïs, Pierre, additional, Garrigue, Stéphane, additional, Hsu, Li-Fern, additional, Rotter, Martin, additional, Rostock, Thomas, additional, Sacher, Fréderic, additional, Nalliah, Chrishan J., additional, Jalife, José, additional, and Haïssaguerre, Michel, additional

Published
2005
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336. A Novel Form of Short QT Syndrome (SQT3) Is Caused by a Mutation in the KCNJ2 Gene

Author

Priori, Silvia G., primary, Pandit, Sandeep V., additional, Rivolta, Ilaria, additional, Berenfeld, Omer, additional, Ronchetti, Elena, additional, Dhamoon, Amit, additional, Napolitano, Carlo, additional, Anumonwo, Justus, additional, di Barletta, Marina Raffaele, additional, Gudapakkam, Smitha, additional, Bosi, Giuliano, additional, Stramba-Badiale, Marco, additional, and Jalife, José, additional

Published
2005
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339. From Mouse to Whale

Author

Noujaim, Sami F., primary, Lucca, Elena, additional, Muñoz, Viviana, additional, Persaud, Dharmendra, additional, Berenfeld, Omer, additional, Meijler, Frits L., additional, and Jalife, José, additional

Published
2004
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