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4. Sleep apnea screening instrument evaluation and novel model development and validation in the paroxysmal atrial fibrillation population

Author

Anna M. May, Lu Wang, Deborah H. Kwon, David R. Van Wagoner, Mina K. Chung, Jarrod E. Dalton, and Reena Mehra

Subjects
Obstructive sleep apnea, Atrial fibrillation, Screening, STOP-BANG, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Standard sleep apnea (SA) screening instruments perform suboptimally in the atrial fibrillation (AF) population. We evaluated and optimized common OSA screening tools in the AF population. Participants of the Sleep Apnea and Atrial Fibrillation Biomarkers and Electrophysiologic Atrial Triggers (SAFEBEAT, NCT02576587) age (±5 years)-, sex-, body mass index (BMI ± 5 kg/m2)-matched case control study (n = 150 each group) completed concurrent questionnaires and overnight polysomnography. Models based on STOP, STOP-BANG, Berlin, NoSAS and Epworth Sleepiness Scale and also models with STOP-BANG predictors with resting heart rate or left atrial volume were constructed. “Best subset” analysis was used to select a predictor subset for evaluation. We assessed test performance for two outcome thresholds: apnea-hypopnea index (AHI) ≥ 5 and AHI ≥ 15. Paroxysmal AF participants were: 61.3 ± 12.1 years, BMI = 31.2 ± 6.6 kg/m2 with median AHI = 11.8(IQR: 3.8, 24.5); 65 (43.3%) with AHI ≥ 15. Only STOP and STOP-BANG did not perform worse in AF relative to controls. For AHI ≥ 15, STOP-BANG (AUC 0.71, 95%CI:0.55–0.85) did not perform as well as NABS – a composite of neck circumference, age, and BMI as continuous variables and snoring (AUC 0.88, 95%CI:0.76–0.96). Optimal model for AHI ≥ 15 was NABS (sensitivity = 45%, specificity = 97%). For AHI ≥ 5, NABS was also the best performing (AUC 0.82, 95%CI:0.68–0.92, sensitivity = 78%, specificity = 67%). We identify a novel, short-item SA screening instrument for use in paroxysmal AF, i.e. NABS, with improved discriminative ability compared to commonly-used instruments. Further validation studies are needed to assess utility in other AF subtypes.Trial registration: clinicaltrials.gov NCT02576587.

Published
2020
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5. Electrical Remodeling and Chronic Atrial Fibrillation

Author

David R. Van Wagoner

Subjects
medicine.medical_specialty, business.industry, Clinical course, Atrial fibrillation, medicine.disease, Pathophysiology, Muscle hypertrophy, Older patients, Fibrosis, Internal medicine, medicine, Cardiology, Chronic atrial fibrillation, Electrical Remodeling, sense organs, skin and connective tissue diseases, business
Abstract

Atrial fibrillation (AF) is a disease primarily affecting older patients, and its clinical course is often progressive. Although initial episodes are typically transient and self-terminating, with time episodes tend to increase in duration, sometimes becoming persistent. This progression from paroxysmal AF to persistent and then permanent AF involves both structural changes in the atria (with respect to the degree of dilatation, trabeculation, fibrosis, fatty infiltration, etc.), as well as biochemical changes in the individual atrial myocytes (e.g., hypertrophy or changes in ion channel density or distribution). This pathophysiologic adaptation of the atria to the fibrillatory rhythm has been broadly termed remodeling . More specifically, the changes primarily affecting the excitability and electrical activity of the atrial myocytes have been termed electrophysiologic remodeling , and the changes in chamber size, collagen deposition, and gross tissue structure have been termed structural remodeling . This chapter focuses on recent studies defining the electrophysiologic remodeling evident in human AF and in relevant experimental models and on some of the molecular mechanisms underlying these changes. Historical aspects of electrophysiologic remodeling in human AF have been discussed in recent reviews. 1 2

Published
2004

6. Contributors

Author

MICHAEL J. ACKERMAN, FELIPE AGUEL, CESAR ALBERTE-LISTA, MATTHIAS ANTZ, CHARLES ANTZELEVITCH, JUSTUS M.B. ANUMONWO, RISHI ARORA, PETER H. BACKX, JEFFREY R. BALSER, KAREN BECKMAN, DAVID G. BENDITT, EDWARD J. BERBARI, OMER BERENFELD, DONALD M. BERS, ERIC C. BEYER, MARTIN BIEL, NEIL E. BOWLES, MARK R. BOYETT, JOSEP BRUGADA, PEDRO BRUGADA, RAMON BRUGADA, NENAD BURSAC, ALFRED E. BUXTON, MICHAEL E. CAIN, HUGH CALKINS, DAVID J. CALLANS, RICCARDO CAPPATO, SHEILA J. CARROLL, AGUSTIN CASTELLANOS, LAN S. CHEN, PENG-SHENG CHEN, SHIN-ANN CHEN, XIONGWEN CHEN, DAVID E. CLAPHAM, JACQUES CLÉMENTY, HARRY J. CRIJNS, EMILE G. DAOUD, MITHILESH K. DAS, MARIO DELMAR, DARIO DIFRANCESCO, JOHN P. DIMARCO, HALINA DOBRZYNSKI, HEATHER S. DUFFY, IGOR R. EFIMOV, JOACHIM R. EHRLICH, NABIL EL-SHERIF, KENNETH A. ELLENBOGEN, ANDREW E. EPSTEIN, CENGIZ ERMIS, SABINE ERNST, N. A. MARK ESTES, VLADIMIR G. FAST, VADIM V. FEDOROV, GUY FONTAINE, SARA FORESTI, PAUL FORNES, ROBERT FRANK, MICHAEL R. FRANZ, JOSEPH M. GALVIN, ALAN GARFINKEL, ANNE M. GILLIS, MICHAEL R. GOLD, JEFFREY GOLDBERGER, RICHARD A. GRAY, WOLFRAM GRIMM, WILLIAM J. GROH, DAVID E. HAINES, MICHEL HAÏSSAGUERRE, CARLOS HARO, DAVID L. HAYES, VOLODYA HAYRAPETYAN, JEAN-LOUIS HEBERT, CRAIG S. HENRIQUEZ, STEFAN HERRMANN, GERHARD HINDRICKS, MÉLÈZE HOCINI, FRANZ HOFMANN, STEFAN H. HOHNLOSER, HARUO HONJO, STEVEN R. HOUSER, LARRY V. HRYSHKO, EDWARD W. HSU, JIAN HUANG, JEAN-SÉBASTIEN HULOT, GARY D. HUTCHINS, RAYMOND E. IDEKER, ALBERTO INTERIAN, SEI IWAI, WARREN M. JACKMAN, PIERRE JAÏS, JOSÉ JALIFE, CRAIG T. JANUARY, CHRISTOPHER R. JOHNSON, MARK E. JOSEPHSON, XAVIER JOUVEN, ALAN H. KADISH, JONATHAN M. KALMAN, TIMOTHY J. KAMP, ROBERT S. KASS, HAROLD L. KENNEDY, RICHARD E. KERBER, ANANT KHOSITSETH, MICHAEL J. KILBORN, ANDRÉ G. KLÉBER, GEORGE J. KLEIN, BRADLEY P. KNIGHT, ITSUO KODAMA, HANS KOTTKAMP, ANDREW D. KRAHN, JAN P. KUCERA, KARL-HEINZ KUCK, JOHN D. KUGLER, CHI TAI KUO, JUNKO KUROKAWA, MAX J. LAB, WEN TER LAI, CLAIRE LARSON, KENNETH R. LAURITA, RALPH LAZZARA, BRUCE B. LERMAN, DEBORAH L. LERNER, SAMUEL LÉVY, RONALD A. LI, DAVID LIN, DEBORAH LOCKWOOD, BARRY LONDON, FEI LÜ, ANDREAS LUDWIG, JONATHAN C. MAKIELSKI, MAREK MALIK, EDUARDO MARBÁN, FRANCIS E. MARCHLINSKI, VIAS MARKIDES, STEVEN M. MARKOWITZ, BARRY J. MARON, AGUSTÍN D. MARTÍNEZ, MARK A. MCGUIRE, GERHARD MEISSNER, WILLIAM M. MILES, JOHN M. MILLER, MICHAEL A. MILLER, SUNEET MITTAL, FEDERICO MOLEIRO, SVEN MOOSMANG, FRED MORADY, ALONSO P. MORENO, ARTHUR J. MOSS, ROBERT J. MYERBURG, HIROSHI NAKAGAWA, CARLO NAPOLITANO, STANLEY NATTEL, JEANNE M. NERBONNE, VLADIMIR P. NIKOLSKI, JEFFREY E. OLGIN, HAKAN ORAL, KENICHIRO OTOMO, GAVIN Y. OUDIT, FEIFAN OUYANG, PIERRE L. PAGÉ, CARLO PAPPONE, EUGENE PATTERSON, ARKADY M. PERTSOV, NICHOLAS S. PETERS, ROBERT W. PETERS, SILVIA G. PRIORI, CATHERINE PROST-SQUARCIONI, ERIC N. PRYSTOWSKI, BONNIE B. PUNSKE, ZHILIN QU, RAFAEL J. RAMIREZ, ILARIA RIVOLTA, RICHARD B. ROBINSON, DAN M. RODEN, STEPHAN ROHR, SALVATORE ROSANIO, MICHAEL R. ROSEN, DAVID S. ROSENBAUM, LEONID V. ROSENSHTRAUKH, BRADLEY J. ROTH, YORAM RUDY, JEREMY N. RUSKIN, FREDERICK SACHS, JEFFREY E. SAFFITZ, PRASHANTHAN SANDERS, MICHAEL C. SANGUINETTI, NADIR SAOUDI, BENJAMIN J. SCHERLAG, PETER J. SCHWARTZ, DAVID SCHWARTZMAN, OLIVER R. SEGAL, DIPEN C. SHAH, OLEG F. SHARIFOV, KALYANAM SHIVKUMAR, JEFFREY SIMMONS, BRAMAH N. SINGH, ALLAN C. SKANES, TIMOTHY W. SMITH, KYOKO SOEJIMA, PAUL L. SORGEN, DAVID C. SPRAY, MIDUTURU SRINIVAS, KENNETH M. STEIN, SUSAN F. STEINBERG, WILLIAM G. STEVENSON, JULIANE STIEBER, MARCO STRAMBA-BADIALE, S. ADAM STRICKBERGER, RUEY J. SUNG, MICHAEL O. SWEENEY, CHARLES D. SWERDLOW, BRUNO TACCARDI, STEVEN M. TAFFET, CHING-TAI TAI, DANIEL THOMAS, GORDON F. TOMASELLI, FERNANDO TONDATO, JEFFREY A. TOWBIN, JOSEPH V. TRANQUILLO, NATALIA A. TRAYANOVA, JOHN K. TRIEDMAN, MARTIN TRISTANI-FIROUZI, CHIN-FENG TSAI, LESLIE TUNG, GIOIA TURITTO, GEORGE F. VAN HARE, DAVID R. VAN WAGONER, MARC A. VOS, GREGORY P. WALCOTT, ALBERT L. WALDO, ZULU WANG, KENNETH M. WEINBERG, DAVID WEINSTEIN, MARCEL WELLNER, BRUCE L. WILKOFF, MARK A. WOOD, JIANYI WU, JIASHIN WU, D. GEORGE WYSE, KATHRYN A. YAMADA, BIN YE, RAYMOND YEE, ALEXEY V. ZAITSEV, WOJCIECH ZAREBA, GUOQIANG ZHONG, and DOUGLAS P. ZIPES

Published
2004

7. Contributors

Author

Jun-ichi Abe, Hugues Abriel, Eric A. Accili, Daniel Acosta, Lee F. Allen, Tara J. Allen, Charles Antzelevitch, Hiroki Aoki, Jeffrey L. Ardell, Makoto Arita, Morton F. Arnsdorf, John A. Auchampach, Shmuel Banai, Jacques Barhanin, M. Baruscotti, Brian M. Bennett, Bradford C. Berk, Donald M. Bers, Marvin Boluyt, Mulugu V. Brahmajothi, Eugene Braunwald, Alexander Burashnikov, Donald L. Campbell, D.J. Chambers, Frédéric Charron, Vijay S. Chauhan, Guoxiang Chu, Michael V. Cohen, Humbert De Smedt, Naranjan S. Dhalla, D. DiFrancesco, James M. Downey, Milou D. Drici, Guy Droogmans, Istvan Edes, Masao Endoh, Denis Escande, Michael S. Forbes, Akikazu Fujita, Tetsushi Furukawa, A. Marquis Gacy, Antony Galione, S. David Gertz, Augustus O. Grant, Christopher D. Hardin, Robert D. Harvey, Armin Haunstetter, D.J. Hearse, Gerd Heusch, Yuji Hirano, Masayasu Hiraoka, Franz Hofmann, Masatsugu Hori, Steven R. Houser, Joseph R. Hume, Seigo Izumo, Arshad Jahangir, Aleksandar Jovanovic, Sofija Jovanovic, Paul F. Kantor, Gary J. Kargacin, Robert S. Kass, Seiko Kawano, Junko Kimura, Masafumi Kitakaze, Kenji Kitamura, Evangelia G. Kranias, Iftikhar J. Kullo, Yoshihisa Kurachi, Adi Kurgan, Lubica Lacinová, Edward G. Lakatta, Amir Lerman, Andrew P. Levy, Jon W. Lomasney, Gary D. Lopaschuk, Benedict R. Lucchesi, Jane A. Madden, Jonathan C. Makielski, Ali J. Marian, Jure Marijic, Donald H. Maurice, William G. Mayhan, Gerhard Meissner, Ludwig Missiaen, Michael J. Morales, A. Moroni, Mariko Nakamura, Mona Nemer, Jeanne M. Nerbonne, Thomas Netticadan, Bernd Nilius, Katsushige Ono, Lionel H. Opie, Jan B. Parys, Richard J. Paul, Amir Pelleg, Carmen M. Perez-Terzic, Valentino Piacentino, Jan J. Piek, Giovanni M. Pitari, M. Pucéat, Stevan Rakovic, Ilaria Rivolta, Robert Roberts, Richard B. Robinson, Rosita J. Rodriguez, Michael R. Rosen, Yoram Rudy, Nancy J. Rusch, Manjot S. Sandhu, Jutta Schaper, Wolfgang Schaper, Win-Kuang Shen, Maria Siebes, Robert D. Simari, R. John Solaro, Jos A.E. Spaan, Nicholas Sperelakis, David C. Spray, Miduturu Srinivas, Susan F. Steinberg, Joseph R. Stimers, Harold C. Strauss, Sylvia O. Suadicani, Masanori Sunagawa, James Surapisitchat, Masayuki Tanemoto, Rana M. Temsah, Derek Terrar, Andre Terzic, Noritsuga Tohse, Ligia Toro, Helmut A. Tritthart, David R. Van Wagoner, Guy Vassort, Monique J. Vink, Gordon M. Wahler, Scott A. Waldman, Michael P. Walsh, Shimin Wang, Stephanie H. Wilson, Rui-Ping Xiao, Jun Yamazaki, Chen Yan, Hisashi Yokoshiki, and Ying-Ying Zhou

Published
2001

8. Molecular Mechanisms of Atrial Fibrillation

Author

Jeanne M. Nerbonne and David R. Van Wagoner

Subjects
Mitochondrial enlargement, medicine.medical_specialty, business.industry, Connexin, Atrial fibrillation, Interstitial fibrosis, medicine.disease, Electrophysiology, Internal medicine, Cardiology, Medicine, Verapamil, Channel blocker, sense organs, skin and connective tissue diseases, business, Calcium overload, medicine.drug
Abstract

This chapter focuses on the molecular mechanisms underlying the electrophysiological changes evident in atrial fibrillation (AF). AF is the most prevalent arrhythmia in the Western world, with an incidence that increases significantly with age, and it is characterized by disorganized, high rate atrial electrical activity. Structural changes in AF occur at several levels, including myocyte hypertrophy; ultrastructural changes, such as loss of fibrillar structure, myolysis, and mitochondrial enlargement; changes in the number and order of connexin junctions; and in the degree of interstitial fibrosis and fatty infiltration. When high rate electrical activity persists, the atria undergo a significant but still poorly characterized functional change leading to longer term reductions in I Ca(L) , I TO , APD, and ERP. These changes can be blocked by prior administration of verapamil, which suggests that calcium entry and subsequent calcium overload are primary causes of this rapid change in ERP. In addition, there are slower and longer lasting reductions in the ERP associated with longer episodes of AF. These, too, can be significantly blunted by the pre-administration of a Ca 2+ channel blocker. With respect to the chronology of the major electrophysiological changes, calcium overload is likely to be the primary factor mediating the long-term electrophysiological remodeling associated with AF.

Published
2001

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