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152. MicroRNA-26 governs profibrillatory inward-rectifier potassium current changes in atrial fibrillation

Author

Luo, Xiaobin, Pan, Zhenwei, Shan, Hongli, Xiao, Jiening, Sun, Xuelin, Wang, Ning, Lin, Huixian, Xiao, Ling, Maguy, Ange, Qi, Xiao-Yan, Li, Yue, Gao, Xu, Dong, Deli, Zhang, Yong, Bai, Yunlong, Ai, Jing, Sun, Lihua, Lu, Hang, Luo, Xiao-Yan, Wang, Zhiguo, Lu, Yanjie, Yang, Baofeng, and Nattel, Stanley

Subjects
Atrial fibrillation -- Prognosis -- Care and treatment, MicroRNA -- Physiological aspects, Health care industry
Abstract

Atrial fibrillation (AF) is a highly prevalent arrhythmia with pronounced morbidity and mortality. Inward-rectifier [K.sup.+] current ([I.sub.K1]) is believed to be an important regulator of reentrant-spiral dynamics and a major [...]

Published
2013
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155. Contributors

Author

Abriel, Hugues, primary, Adkisson, Wayne O., additional, Agullo-Pascual, Esperanza, additional, Ajijola, Olujimi A., additional, Al-Ahmad, Amin, additional, Alli, Oluseun, additional, Altman, Robert K., additional, Anter, Elad, additional, Antzelevitch, Charles, additional, Anumonwo, Justus M.B., additional, Armaganijan, Luciana, additional, Ashikaga, Hiroshi, additional, Atienza, Felipe, additional, Avula, Uma Mahesh R., additional, Backx, Peter H., additional, Balse, Elise, additional, Barrett, Conor D., additional, Benditt, David G., additional, Berenfeld, Omer, additional, Bers, Donald M., additional, Berul, Charles I., additional, Blank, A. Christian, additional, Bloise, Raffaella, additional, Bogun, Frank Matthias, additional, Borggrefe, Martin, additional, Boyle, Noel G., additional, Breithardt, Günter, additional, Brini, Marisa, additional, Brink, Peter R., additional, Brugada, Josep, additional, Brugada, Pau, additional, Brugada, Pedro, additional, Brugada, Ramon, additional, Brugada, Victoria, additional, Buch, Eric, additional, Bukauskas, Feliksas F., additional, Burkhardt, J. David, additional, Bursac, Nenad, additional, Calkins, Hugh, additional, Callans, David J., additional, Campuzano, Oscar, additional, Caples, Sean M., additional, Carafoli, Ernesto, additional, Castellanos, Augustin, additional, Catterall, William, additional, Cerrone, Marina, additional, Chen, Lan S., additional, Chen, Lei, additional, Chen, Peng-Sheng, additional, Chin, Ashley, additional, Chugh, Aman, additional, Cohen, Ira S., additional, Connolly, Stuart J., additional, Constantino, Jason, additional, Crotti, Lia, additional, Cuoco, Frank A., additional, Curtis, Anne B., additional, Damiano, Ralph J., additional, Darbar, Dawood, additional, Das, Mithilesh K., additional, Delmar, Mario, additional, Delpón, Eva, additional, Di Biase, Luigi, additional, Dixit, Sanjay, additional, Dobrev, Dobromir, additional, Dosdall, Derek J., additional, Dyer, John W., additional, Eckardt, Lars, additional, Edwards, Andrew G., additional, Efimov, Igor R., additional, Ellenbogen, Kenneth A., additional, Ellinor, Patrick T., additional, Entcheva, Emilia, additional, Estes, N.A. Mark, additional, Fischmeister, Rodolphe, additional, Fisher, John D., additional, Fishman, Glenn I., additional, Frankel, David S., additional, Franz, Michael R., additional, Friedman, Paul A., additional, Froelicher, Victor F., additional, Gami, Apoor S., additional, George, Alfred L., additional, Gerstenfeld, Edward P., additional, Gold, Michael R., additional, Goldberger, Jeffrey J., additional, Grandi, Eleonora, additional, Gray, Richard A., additional, Groh, William J., additional, Grubb, Blair P., additional, Haissaguerre, Michel, additional, Hake, Johan, additional, Halperin, Henry R., additional, Harris, Louise, additional, Hatem, Stéphane, additional, Hayes, David L., additional, Hocini, Meleze, additional, Hohnloser, Stefan H., additional, Holmes, David Richard, additional, Hoshijima, Masahiko, additional, Hu, Yuxuan, additional, Hund, Thomas J., additional, Hutchinson, Mathew D., additional, Hwang, Hye Jin, additional, Ideker, Raymond E., additional, Ilkhanoff, Leonard, additional, Ingles, Jodie, additional, Jackman, Warren M., additional, Jais, Pierre, additional, Jalife, José, additional, Jhun, Bong Sook, additional, John, Roy M., additional, Jongbloed, Monique, additional, Josephson, Mark E., additional, Kadish, Alan H., additional, Kalifa, Jérôme, additional, Kalman, Jonathan M., additional, Kamp, Timothy J., additional, Kanj, Mohamed Hani, additional, Karabin, Beverly, additional, Kass, Robert S., additional, Katritsis, Demosthenes G., additional, Kaur, Kuljeet, additional, Kim, Jong J., additional, Kirchhof, Paulus, additional, Kléber, André G., additional, Klein, George J., additional, Kohl, Peter, additional, Kolandaivelu, Aravindan, additional, Krahn, Andrew D., additional, Krumerman, Andrew, additional, Kumar, Saurabh, additional, Kuck, Karl-Heinz, additional, Lakatta, Edward G., additional, Latchamsetty, Rakesh, additional, Lau, Dennis H., additional, Lerman, Bruce B., additional, Leroy, Jérôme, additional, Lewis, William R., additional, Lin, Shien-Fong, additional, Link, Mark S., additional, Liu, Christopher F., additional, Lockwood, Deborah J., additional, Loh, Peter, additional, Lopatin, Anatoli N., additional, Lopshire, John C., additional, Lubitz, Steven A., additional, Madias, Christopher, additional, Mahajan, Aman, additional, Makielski, Jonathan C., additional, Malik, Marek, additional, Maltsev, Victor A., additional, Marchlinski, Francis E., additional, Marelli, Ariane J., additional, Markowitz, Steven M., additional, Maron, Barry J., additional, Martens, Jeffrey R., additional, Marx, Steven O., additional, McCulloch, Andrew D., additional, Metzner, Andreas, additional, Michailova, Anuska P., additional, Miller, John Michael, additional, Milstein, Michelle Lynne, additional, Mohler, Peter, additional, Morady, Fred, additional, Myerburg, Robert J., additional, Nakagawa, Hiroshi, additional, Napolitano, Carlo, additional, Narayan, Sanjiv M., additional, Natale, Andrea, additional, Nattel, Stanley, additional, Nazarian, Saman, additional, Nerbonne, Jeanne M., additional, Ng, Fu Siong, additional, Nogami, Akihiko, additional, Noujaim, Sami F., additional, Olshansky, Brian, additional, Oral, Hakan, additional, O-Uchi, Jin, additional, Ouyang, Feifan, additional, Ozcan, Cevher, additional, Packer, Douglas L., additional, Pahlm, Olle, additional, Pandit, Sandeep V., additional, Park, David S., additional, Pitt, Geoffrey S., additional, Po, Sunny S., additional, Priori, Silvia G., additional, Rappel, Wouter-Jan, additional, Reddy, Vivek Y., additional, Robertson, Jason O., additional, Robinson, Richard B., additional, Roden, Dan M., additional, Rose, Robert A., additional, Rosen, Michael R., additional, Rosso, Raphael, additional, Rudy, Yoram, additional, Ruskin, Jeremy N., additional, Sabbah, Hani N., additional, Sachse, Frank B., additional, Saint, Lindsey L., additional, Saiz, Javier, additional, Sánchez-Chapula, José A., additional, Sanders, Prashanthan, additional, Sanguinetti, Michael C., additional, Santangeli, Pasquale, additional, Sarquella-Brugada, Georgia, additional, Satin, Jonathan, additional, Schalij, Martin Jan, additional, Scherlag, Benjamin J., additional, Schimpf, Rainer, additional, Schmidt, Georg, additional, Schwartz, Peter J., additional, Semsarian, Christopher, additional, Shah, Ashok J., additional, Shaw, Robin, additional, Sheu, Shey Shing, additional, Shivkumar, Kalyanam, additional, Skanes, Allan C., additional, Somers, Virend K., additional, Stambler, Bruce S., additional, Stein, Adam B., additional, Stevenson, Lynne Warner, additional, Stevenson, William G., additional, Sun, Jian, additional, Sutton, Richard, additional, Sweeney, Michael O., additional, Swerdlow, Charles, additional, Tamargo, Juan, additional, Tandri, Harikrishna, additional, Tawil, Rabi, additional, Tedrow, Usha, additional, Terrenoire, Cecile, additional, Tobón, Catalina, additional, Towbin, Jeffrey A., additional, Trayanova, Natalia A., additional, Tristani-Firouzi, Martin, additional, Trohman, Richard G., additional, Tseng, Zian H., additional, Turakhia, Mintu P., additional, Vaidyanathan, Ravi, additional, Valdivia, Héctor H., additional, Valiunas, Virginijus, additional, van der Heyden, Marcel A.G., additional, van der Werf, Christian, additional, Van, George F., additional, Vaseghi, Marmar, additional, Veltmann, Christian, additional, Vetter, Victoria L., additional, Viskin, Sami, additional, Voigt, Niels, additional, Vos, Marc A., additional, Wagner, Galen S., additional, Wang, Paul J., additional, Weerasooriya, Rukshen, additional, Wilde, Arthur A.M., additional, Wilkoff, Bruce L., additional, Wissner, Erik, additional, Woo, Y. Joseph, additional, Yamazaki, Masatoshi, additional, Yang, Felix, additional, Yaniv, Yael, additional, Yap, Sing-Chien, additional, Yee, Raymond, additional, Zarzoso, Manuel, additional, Zeppenfeld, Katja, additional, and Zipes, Douglas P., additional

Published
2014
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158. 2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design: A report of the Heart Rhythm Society (HRS) Task Force on Catheter and Surgical Ablation of Atrial Fibrillation. Developed in partnership with the European Heart Rhythm Association (EHRA), a registered branch of the European Society of Cardiology (ESC) and the European Cardiac Arrhythmia Society (ECAS); and in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), the Asia Pacific Heart Rhythm Society (APHRS), and the Society of Thoracic Surgeons (STS). Endorsed by the governing bodies of the American College of Cardiology Foundation, the American Heart Association, the European Cardiac Arrhythmia Society, the European Heart Rhythm Association, the Society of Thoracic Surgeons, the Asia Pacific Heart Rhythm Society, and the Heart Rhythm Society

Author

Calkins, Hugh, Kuck, Karl Heinz, Cappato, Riccardo, Brugada, Josep, Camm, A. John, Chen, Shih-Ann, Crijns, Harry J.G., Damiano, Ralph J., Jr., Davies, D. Wyn, DiMarco, John, Edgerton, James, Ellenbogen, Kenneth, Ezekowitz, Michael D., Haines, David E., Haissaguerre, Michel, Hindricks, Gerhard, Iesaka, Yoshito, Jackman, Warren, Jalife, Jose, Jais, Pierre, Kalman, Jonathan, Keane, David, Kim, Young-Hoon, Kirchhof, Paulus, Klein, George, Kottkamp, Hans, Kumagai, Koichiro, Lindsay, Bruce D., Mansour, Moussa, Marchlinski, Francis E., McCarthy, Patrick M., Mont, J. Lluis, Morady, Fred, Nademanee, Koonlawee, Nakagawa, Hiroshi, Natale, Andrea, Nattel, Stanley, Packer, Douglas L., Pappone, Carlo, Prystowsky, Eric, Raviele, Antonio, Reddy, Vivek, Ruskin, Jeremy N., Shemin, Richard J., Tsao, Hsuan-Ming, Wilber, David, Calkins, Hugh, Kuck, Karl Heinz, Cappato, Riccardo, Chen, Shih-Ann, Prystowsky, Eric N., Kuck, Karl Heinz, Natale, Andrea, Haines, David E., Marchlinski, Francis E., Calkins, Hugh, Davies, D. Wyn, Lindsay, Bruce D., Damiano, Ralph, Jr., Packer, Douglas L., Brugada, Josep, Camm, A. John, Crijns, Harry J.G., DiMarco, John, Edgerton, James, Ellenbogen, Kenneth, Ezekowitz, Michael D., Haissaguerre, Michel, Hindricks, Gerhard, Iesaka, Yoshito, Jackman, Warren M., Jais, Pierre, Jalife, José, Kalman, Jonathan, Keane, David, Kim, Young-Hoon, Kirchhof, Paulus, Klein, George, Kottkamp, Hans, Kumagai, Koichiro, Mansour, Moussa, Marchlinski, Francis, McCarthy, Patrick, Mont, J. Lluis, Morady, Fred, Nademanee, Koonlawee, Nakagawa, Hiroshi, Nattel, Stanley, Pappone, Carlo, Raviele, Antonio, Reddy, Vivek, Ruskin, Jeremy N., Shemin, Richard J., Tsao, Hsuan-Ming, Wilber, David, Ad, Niv, Cummings, Jennifer, Gillinov, A. Mark, Heidbuchel, Hein, January, Craig, Lip, Gregory, Markowitz, Steven, Nair, Mohan, Ovsyshcher, I. Eli, Pak, Hui-Nam, Tsuchiya, Takeshi, Shah, Dipen, Siong, Teo Wee, and Vardas, Panos E.

Published
2012
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164. Does gut microbiota affect atrial rhythm? Causalities and speculations

Author

Linz, Dominik, Gawałko, Monika, Sanders, Prashanthan, Penders, John, Li, Na, Nattel, Stanley, Dobrev, Dobromir, Linz, Dominik, Gawałko, Monika, Sanders, Prashanthan, Penders, John, Li, Na, Nattel, Stanley, and Dobrev, Dobromir

Abstract

Dietary intake has been shown to change the composition of gut microbiota and some changes in microbiota (dysbiosis) have been linked to diabetes, hypertension, and obesity, which are established risk factors for atrial fibrillation (AF). In addition, intestinal dysbiosis generates microbiota-derived bioactive metabolites that might exert proarrhythmic actions. Although emerging preclinical investigations and clinical observational cohort studies suggest a possible role of gut dysbiosis in AF promotion, the exact mechanisms through which dysbiosis contributes to AF remain unclear. This Viewpoint article briefly reviews evidence suggesting that abnormalities in the intestinal microbiota play an important and little-recognized role in the pathophysiology of AF and that an improved understanding of this role may open up new possibilities in the management of AF.

Published
2021

165. Chronic obstructive pulmonary disease and atrial fibrillation an interdisciplinary perspective

Author

Simons, Sami O., Elliott, Adrian, Sastry, Manuel, Hendriks, Jeroen M., Arzt, Michael, Rienstra, Michiel, Kalman, Jonathan M., Heidbuchel, Hein, Nattel, Stanley, Wesseling, Geertjan, Schotten, Ulrich, van Gelder, Isabelle C., Franssen, Frits M. E., Sanders, Prashanthan, Crijns, Harry J. G. M., Linz, Dominik, Simons, Sami O., Elliott, Adrian, Sastry, Manuel, Hendriks, Jeroen M., Arzt, Michael, Rienstra, Michiel, Kalman, Jonathan M., Heidbuchel, Hein, Nattel, Stanley, Wesseling, Geertjan, Schotten, Ulrich, van Gelder, Isabelle C., Franssen, Frits M. E., Sanders, Prashanthan, Crijns, Harry J. G. M., and Linz, Dominik

Abstract

Chronic obstructive pulmonary disease (COPD) is highly prevalent among patients with atrial fibrillation (AF), shares common risk factors, and adds to the overall morbidity and mortality in this population. Additionally, it may promote AF and impair treatment efficacy. The prevalence of COPD in AF patients is high and is estimated to be similar to 25%. Diagnosis and treatment of COPD in AF patients requires a close interdisciplinary collaboration between the electrophysiologist/cardiologist and pulmonologist. Differential diagnosis may be challenging, especially in elderly and smoking patients complaining of unspecific symptoms such as dyspnoea and fatigue. Routine evaluation of lung function and determination of natriuretic peptides and echocardiography may be reasonable to detect COPD and heart failure as contributing causes of dyspnoea. Acute exacerbation of COPD transiently increases AF risk due to hypoxia-mediated mechanisms, inflammation, increased use of beta-2 agonists, and autonomic changes. Observational data suggest that COPD promotes AF progression, increases AF recurrence after cardioversion, and reduces the efficacy of catheter-based antiarrhythmic therapy. However, it remains unclear whether treatment of COPD improves AF outcomes and which metric should be used to determine COPD severity and guide treatment in AF patients. Data from non-randomized studies suggest that COPD is associated with increased AF recurrence after electrical cardioversion and catheter ablation. Future prospective cohort studies in AF patients are needed to confirm the relationship between COPD and AF, the benefits of treatment of either COPD or AF in this population, and to clarify the need and cost-effectiveness of routine COPD screening.

Published
2021

168. 2012 HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial design

Author

Calkins, Hugh, Kuck, Karl Heinz, Cappato, Riccardo, Brugada, Josep, Camm, A. John, Chen, Shih-Ann, Crijns, Harry J. G., Damiano, Jr., Ralph J., Davies, D. Wyn, DiMarco, John, Edgerton, James, Ellenbogen, Kenneth, Ezekowitz, Michael D., Haines, David E., Haissaguerre, Michel, Hindricks, Gerhard, Iesaka, Yoshito, Jackman, Warren, Jalife, Jose, Jais, Pierre, Kalman, Jonathan, Keane, David, Kim, Young-Hoon, Kirchhof, Paulus, Klein, George, Kottkamp, Hans, Kumagai, Koichiro, Lindsay, Bruce D., Mansour, Moussa, Marchlinski, Francis E., McCarthy, Patrick M., Mont, J. Lluis, Morady, Fred, Nademanee, Koonlawee, Nakagawa, Hiroshi, Natale, Andrea, Nattel, Stanley, Packer, Douglas L., Pappone, Carlo, Prystowsky, Eric, Raviele, Antonio, Reddy, Vivek, Ruskin, Jeremy N., Shemin, Richard J., Tsao, Hsuan-Ming, and Wilber, David

Published
2012
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172. Recent advances in the molecular pathophysiology of atrial fibrillation

Author

Wakili, Reza, Voigt, Niels, Kaab, Stefan, Dobrev, Dobromir, and Nattel, Stanley

Subjects
Atrial fibrillation -- Genetic aspects -- Development and progression -- Research -- Risk factors, Single nucleotide polymorphisms -- Research -- Genetic aspects, Health care industry
Abstract

Atrial fibrillation (AF) is an extremely common cardiac rhythm disorder that causes substantial morbidity and contributes to mortality. The mechanisms underlying AF are complex, involving both increased spontaneous ectopic firing of atrial cells and impulse reentry through atrial tissue. Over the past ten years, there has been enormous progress in understanding the underlying molecular pathobiology. This article reviews the basic mechanisms and molecular processes causing AF. We discuss the ways in which cardiac disease states, extracardiac factors, and abnormal genetic control lead to the arrhythmia. We conclude with a discussion of the potential therapeutic implications that might arise from an improved mechanistic understanding., Introduction Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, and its prevalence is increasing with aging of the population (1). Normal cardiac rhythm shows regular rhythm initiation in [...]

Published
2011
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183. SEX DIFFERENCES IN SYMPTOM REPORTING AMONGST ATRIAL FIBRILLATION ABLATION PATIENTS: A SUB-STUDY OF THE ADENOSINE FOLLOWING PULMONARY VEIN ISOLATION TO TARGET DORMANT CONDUCTION ELIMINATION (ADVICE) TRIAL

Author

D'Aronco, Laura, primary, Samuel, Michelle, additional, Khairy, Paul, additional, Andrade, Jason, additional, Novak, Paul, additional, Verma, Atul, additional, Veenhuyzen, George, additional, Rivard, Lena, additional, Guerra, Peter G., additional, Dubuc, Marc, additional, Thibault, Bernard, additional, Dyrda, Katia, additional, Tadros, Rafik, additional, Cadrin-Tourigny, Julia, additional, Aguilar, Martin, additional, Raymond-Paquin, Alexandre, additional, Talajic, Mario, additional, Levesque, Sylvie, additional, Roy, Denis, additional, Tardif, Jean Claude, additional, Nattel, Stanley, additional, and Macle, Laurent, additional

Published
2021
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191. Mechanisms of atrial fibrillation termination by rapidly unbinding [Na.sup.+] channel blockers: insights from mathematical models and experimental correlates

Author

Comtois, Philippe, Sakabe, Masao, Vigmond, Edward J., Munoz, Mauricio, Texier, Anne, Shiroshita-Takeshita, Akiko, and Nattel, Stanley

Subjects
Action potentials (Electrophysiology) -- Evaluation, Arrhythmia -- Models, Arrhythmia -- Drug therapy, Arrhythmia -- Development and progression, Ion channels -- Properties, Mathematical models -- Usage, Biological sciences
Abstract

Atrial fibrillation (AF) is the most common sustained clinical arrhythmia and is a problem of growing proportions. Recent studies have increased interest in fast-unbinding [Na.sup.+] channel blockers like vernakalant (RSD1235) and ranolazine for AF therapy, but the mechanism of efficacy is poorly understood. To study how fast-unbinding [I.sub.Na] blockers affect AF, we developed realistic mathematical models of state-dependent [Na.sup.+] channel block, using a lidocaine model as a prototype, and studied the effects on simulated cholinergic AF in two-and three-dimensional atrial substrates. We then compared the results with in vivo effects of lidocaine on vagotonic AF in dogs. Lidocaine action was modeled with the Hondeghem-Katzung modulatedreceptor theory and maximum affinity for activated [Na.sup.+] channels. Lidocaine produced frequency-dependent [Na.sup.+] channel blocking and conduction slowing effects and terminated AF in both two- and three-dimensional models with concentration-dependent efficacy (maximum ~89% at 60 [micro]M). AF termination was not related to increases in wavelength, which tended to decrease with the drug, but rather to decreased source [Na.sup.+] current in the face of large ACh-sensitive [K.sup.+] current-related sinks, leading to the destabilization of primary generator rotors and a great reduction in wavebreak, which caused primary rotor annihilations in the absence of secondary rotors to resume generator activity. Lidocaine also reduced the variability and maximum values of the dominant frequency distribution during AF. Qualitatively similar results were obtained in vivo for lidocaine effects on vagal AF in dogs, with an efficacy of 86% at 2 mg/kg iv, as well as with simulations using the guarded-receptor model of lidocaine action. These results provide new insights into the mechanisms by which rapidly unbinding class I antiarrhythmic agents, a class including several novel compounds of considerable promise, terminate AF. state-dependent channel; cardiac action potential; antiarrhythmic drug therapy; computer simulations; heart arrhythmia models

Published
2008

193. Differential interactions of [Na.sup.+] channel toxins with T-type [Ca.sup.2+] channels

Author

Sun, Hui, Varela, Diego, Chartier, Denis, Ruben, Peter C., Nattel, Stanley, Zamponi, Gerald W., and Leblanc, Normand

Subjects
Sodium channels -- Properties, Sodium channels -- Structure, Calcium channels -- Properties, Calcium channels -- Structure, Evolution -- Research, Heart -- Properties, Heart -- Natural history, Biological sciences, Health
Abstract

Two types of voltage-dependent [Ca.sup.2+] channels have been identified in heart: high ([I.sub.CaL]) and low ([I.sub.CaT]) voltage-activated [Ca.sup.2+] channels. In guinea pig ventricular myocytes, low voltage-activated inward current consists of [I.sub.CaT] and a tetrodotoxin (TTX)-sensitive [I.sub.Ca] component ([I.sub.Ca(TTX)]). In this study, we reexamined the nature of low-threshold [I.sub.Ca] in dog atrium, as well as whether it is affected by [Na.sup.+] channel toxins. [Ca.sup.2+] currents were recorded using the whole-cell patch clamp technique. In the absence of external [Na.sup.+], a transient inward current activated near -50 mV, peaked at -30 mV, and reversed around +40 mV (HP = -90 mV). It was unaffected by 30 [micro]M TTX or micromolar concentrations of external [Na.sup.+], but was inhibited by 50 [micro]M [Ni.sup.2+] (by ~90%) or 5 [micro]M mibefradil (by ~50%), consistent with the reported properties of [I.sub.CaT]. Addition of 30 [micro]M TTX in the presence of [Ni.sup.2+] increased the current approximately fourfold (41% of control), and shifted the dose-response curve of [Ni.sup.2+] block to the right ([IC.sub.50] from 7.6 to 30 [micro]M). Saxitoxin (STX) at 1 [micro]M abolished the current left in 50 [micro]M [Ni.sup.2+]. In the absence of [Ni.sup.2+], STX potently blocked [I.sub.CaT] ([EC.sub.50] = 185 nM) and modestly reduced [I.sub.CaL] ([EC.sub.50] = 1.6 [micro]M). While TTX produced no direct effect on [I.sub.CaT] elicited by expression of h[Ca.sub.v] 3.1 and h[Ca.sub.v]3.2 in HEK-293 cells, it significantly attenuated the block of this current by [Ni.sup.2+] ([IC.sub.50] increased to 550 [micro]M [Ni.sup.2+] for [Ca.sub.v]3.1 and 15 [micro]M [Ni.sup.2+] for [Ca.sub.v]3.2); in contrast, 30 [micro]M TTX directly inhibited h[Ca.sub.v]3.3-induced [I.sub.CaT] and the addition of 750 [micro]M [Ni.sup.2+] to the TTX-containing medium led to greater block of the current that was not significantly different than that produced by [Ni.sup.2+] alone. 1 [micro]M STX directly inhibited [Ca.sub.v]3.1-, [Ca.sub.v]3.2-, and [Ca.sub.v]3.3-mediated [I.sub.CaT] but did not enhance the ability of [Ni.sup.2+] to block these currents. These findings provide important new implications for our understanding of structure-function relationships of [I.sub.CaT] in heart, and further extend the hypothesis of a parallel evolution of [Na.sup.+] and [Ca.sup.2+] channels from an ancestor with common structural motifs.

Published
2008

194. Arrhythmogenic ion-channel remodeling in the heart: heart failure, myocardial infarction, and atrial fibrillation

Author

Nattel, Stanley, Maguy, Ange, Le Bouter, Sabrina, and Yeh, Yung-Hsin

Subjects
Heart attack -- Research, Ion channels -- Research -- Models, Congestive heart failure -- Research, Atrial fibrillation -- Research, Biological sciences, Health, Models, Research
Abstract

I. Introduction A. Channel function as a regulated phenomenon B. Regional considerations II. Remodeling of Ionic Currents Associated With Cardiac Disease: Congestive Heart Failure A. Significance and arrhythmic consequences B. [...]

Published
2007

195. Pulmonary Vein Stenosis After Atrial Fibrillation Ablation: Insights From the ADVICE Trial.

Author

UCL - SSS/IREC/CARD - Pôle de recherche cardiovasculaire, UCL - (SLuc) Service de pathologie cardiovasculaire, Samuel, Michelle, Khairy, Paul, Mongeon, François-Pierre, Andrade, Jason G, Gomes, Sophie, Galvan, Zurine, Weerasooriya, Rukshen, Novak, Paul, Nault, Isabelle, Arentz, Thomas, Deisenhofer, Isabel, Veenhuyzen, George D, Jaïs, Pierre, Parkash, Ratika, Verma, Atul, Menon, Syamkumar, Puererfellner, Helmut, Scavee, Christophe, Talajic, Mario, Guerra, Peter G, Rivard, Lena, Dubuc, Marc, Dyrda, Katia, Thibault, Bernard, Mondesert, Blandine, Tadros, Rafik, Cadrin-Tourigny, Julia, Aguilar, Martin, Tardif, Jean-Claude, Levesque, Sylvie, Roy, Denis, Nattel, Stanley, Macle, Laurent, UCL - SSS/IREC/CARD - Pôle de recherche cardiovasculaire, UCL - (SLuc) Service de pathologie cardiovasculaire, Samuel, Michelle, Khairy, Paul, Mongeon, François-Pierre, Andrade, Jason G, Gomes, Sophie, Galvan, Zurine, Weerasooriya, Rukshen, Novak, Paul, Nault, Isabelle, Arentz, Thomas, Deisenhofer, Isabel, Veenhuyzen, George D, Jaïs, Pierre, Parkash, Ratika, Verma, Atul, Menon, Syamkumar, Puererfellner, Helmut, Scavee, Christophe, Talajic, Mario, Guerra, Peter G, Rivard, Lena, Dubuc, Marc, Dyrda, Katia, Thibault, Bernard, Mondesert, Blandine, Tadros, Rafik, Cadrin-Tourigny, Julia, Aguilar, Martin, Tardif, Jean-Claude, Levesque, Sylvie, Roy, Denis, Nattel, Stanley, and Macle, Laurent

Abstract

BACKGROUND: Pulmonary vein (PV) stenosis is a complication of atrial fibrillation (AF) ablation. The incidence of PV stenosis after routine post-ablation imaging remains unclear and is limited to single-centre studies. Our objective was to determine the incidence and predictors of PV stenosis following circumferential radiofrequency ablation in the multicentre Adenosine Following Pulmonary Vein Isolation to Target Dormant Conduction Elimination (ADVICE) trial. METHODS: Patients with symptomatic AF underwent circumferential radiofrequency ablation in one of 13 trial centres. Computed tomographic (CTA) or magnetic resonance (MRA) angiography was performed before ablation and 90 days after ablation. Two blinded reviewers measured PV diameters and areas. PVs with stenosis were classified as severe (> 70%), moderate (50%-70%), or mild (< 50%). Predictors of PV stenosis were identified by means of multivariable logistic regression. RESULTS: A total of 197 patients (median age 59.5 years, 29.4% women) were included in this substudy. PV stenosis was identified in 41 patients (20.8%) and 47 (8.2%) of 573 ablated PVs. PV stenosis was classified as mild in 42 PVs (7.3%) and moderate in 5 PVs (0.9%). No PVs had severe stenosis. Both cross-sectional area and diameter yielded similar classifications for severity of PV stenosis. Diabetes was associated with a statistically significant increased risk of PV stenosis (OR 4.91, 95% CI 1.45-16.66). CONCLUSIONS: In the first systematic multicentre evaluation of post-ablation PV stenosis, no patient acquired severe PV stenosis. Although the results are encouraging for the safety of AF ablation, 20.8% of patients had mild or moderate PV stenosis, in which the long-term effects are unknown.

Published
2020

196. Contributors

Author

Fox, Keith A.A., primary, Gersh, Bernard J., additional, Gotto, Antonio M., additional, Horowitz, John D., additional, Kaplan, Norman M., additional, Krum, Henry, additional, Meier, Juris J., additional, Nattel, Stanley, additional, Opie, Lionel H., additional, Pfeffer, Marc A., additional, Sliwa, Karen, additional, Teerlink, John R., additional, Victor, Ronald G., additional, and White, Harvey D., additional

Published
2013
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200. Comparison of [Ca.sup.2+]-handling properties of canine pulmonary vein and left atrial cardiomyocytes

Author

Coutu, Pierre, Chartier, Denis, and Nattel, Stanley

Subjects
Heart cells -- Research, Arrhythmia -- Risk factors, Arrhythmia -- Physiological aspects, Biological sciences
Abstract

Cardiac tissue in the pulmonary vein sleeves plays an important role in clinical atrial fibrillation. Mechanisms leading to pulmonary vein activity in atrial fibrillation remain unclear. Indirect experimental evidence points to pulmonary vein [Ca.sup.2+] handling as a potential culprit, but there are no direct studies of pulmonary vein cardiomyocyte [Ca.sup.2+] handling in the literature. We used the [Ca.sup.2+]-sensitive dye indo-1 AM to study [Ca.sup.2+] handling in isolated canine pulmonary vein and left atrial myocytes. Results were obtained at 35[degrees]C and room temperature in cells from control dogs and in cardiomyocytes from dogs subjected to 7-day rapid atrial pacing. We found that basic [Ca.sup.2+]-transient properties (amplitude: 186 [+ or -] 28 vs. 216 [+ or -] 25 nM; stimulus to half-decay time: 192 [+ or -] 9 vs. 192 [+ or -] 9 ms; atria vs. pulmonary vein, respectively, at 1 Hz), beat-to-beat regularity, propensity to alternans, [beta]-adrenergic response (amplitude increase at 0.4 Hz: 96 [+ or -] 52 vs. 129 + 61%), number of spontaneous [Ca.sup.2+]-transient events after [Ca.sup.2+] loading (in normal Tyrode: 0.9 [+ or -] 0.2 vs. 1.3 [+ or -] 0.2; with 1 [micro]M isoproterenol: 7.6 [+ or -] 0.3 vs. 5.1 [+ or -] 1.8 events/min), and caffeine-induced [Ca.sup.2+]-transient amplitudes were not significantly different between atrial and pulmonary vein cardiomyocytes. In an arrhythmia-promoting model (dogs subjected to 7-day atrial tachypacing), [Ca.sup.2+]-transient amplitude and kinetics were the same in cells from both pulmonary veins and atrium. In conclusion, the similar [Ca.sup.2+]-handling properties of canine pulmonary vein and left atrial cardiomyocytes that we observed do not support the hypothesis that intrinsic [Ca.sup.2+]-handling differences account for the role of pulmonary veins in atrial fibrillation. arrhythmia; heart rhythm disorders; ion transport; supraventricular arrhythmia

Published
2006

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