© 1999 American Heart Association, Inc.
Cellular Biology |
Atrial L-Type Ca2+ Currents and Human Atrial Fibrillation
From the Department of Cardiology (D.R.V.W., M.L.) and Kaufman Center for Heart Failure and Department of Cardiothoracic Surgery (P.M.M.), The Cleveland Clinic Foundation, Cleveland, Ohio; Department of Biochemistry (A.L.P., S.S.R.), Purdue University, West Lafayette, Ind; and Department of Molecular Biology and Pharmacology (J.M.N.), Washington University School of Medicine, St. Louis, Mo.
Correspondence to David R. Van Wagoner, PhD, Dept of Cardiology, FF10, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195. E-mail vanwagd{at}ccf.org
Abstract—Chronic atrial fibrillation (AF) is characterized by decreased atrial contractility, shortened action potential duration, and decreased accommodation of action potential duration to changes in activation rate. Studies on experimental animal models of AF implicate a reduction in L-type Ca2+ current (ICa) density in these changes. To evaluate the effect of AF on human ICa, we compared ICa in atrial myocytes isolated from 42 patients in normal sinus rhythm at the time of cardiac surgery with that of 11 chronic AF patients. ICa was significantly reduced in the myocytes of patients with chronic AF (mean -3.35±0.5 pA/pF versus -9.13±1.0 pA/pF in the controls), with no difference between groups in the voltage dependence of activation or steady-state inactivation. Although ICa was lower in myocytes from the chronic AF patients, their response to maximal ß-adrenergic stimulation was not impaired. Postoperative AF frequently follows cardiac surgery. Half of the patients in the control group (19/38) of this study experienced postoperative AF. Whereas chronic AF is characterized by reduced atrial ICa, the patients with the greatest ICa had an increased incidence of postoperative AF, independent of patient age or diagnosis. This observation is consistent with the concept that calcium overload may be an important factor in the initiation of AF. The reduction in functional ICa density in myocytes from the atria of chronic AF patients may thus be an adaptive response to the arrhythmia-induced calcium overload.
Key Words: atrial fibrillation • postoperative atrial fibrillation • Ca2+ channel • ß-adrenergic antagonist • cardiac surgery
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U. Schotten, J. Ausma, C. Stellbrink, I. Sabatschus, M. Vogel, D. Frechen, F. Schoendube, P. Hanrath, and M. A. Allessie Cellular Mechanisms of Depressed Atrial Contractility in Patients With Chronic Atrial Fibrillation Circulation, February 6, 2001; 103(5): 691 - 698. [Abstract] [Full Text] [PDF]
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M. A. Allessie, P. A. Boyden, A. J. Camm, A. G. Kleber, M. J. Lab, M. J. Legato, M. R. Rosen, P. J. Schwartz, P. M. Spooner, D. R. Van Wagoner, et al. Pathophysiology and Prevention of Atrial Fibrillation Circulation, February 6, 2001; 103(5): 769 - 777. [Full Text] [PDF]
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F. Lombardi, A. Colombo, B. Basilico, R. Ravaglia, M. Garbin, D. Vergani, P. M. Battezzati, and C. Fiorentini Heart rate variability and early recurrence of atrial fibrillation after electrical cardioversion J. Am. Coll. Cardiol., January 1, 2001; 37(1): 157 - 162. [Abstract] [Full Text] [PDF]
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T. J. Kamp and J. W. Hell Regulation of Cardiac L-Type Calcium Channels by Protein Kinase A and Protein Kinase C Circ. Res., December 8, 2000; 87(12): 1095 - 1102. [Abstract] [Full Text] [PDF]
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 C.-C. Shieh, M. Coghlan, J. P. Sullivan, and M. Gopalakrishnan Potassium Channels: Molecular Defects, Diseases, and Therapeutic Opportunities Pharmacol. Rev., December 1, 2000; 52(4): 557 - 594. [Abstract] [Full Text] [PDF]
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S. Nattel and D. Li Ionic Remodeling in the Heart : Pathophysiological Significance and New Therapeutic Opportunities for Atrial Fibrillation Circ. Res., September 15, 2000; 87(6): 440 - 447. [Abstract] [Full Text] [PDF]
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 C.J. Garratt and S.P. Fynn Atrial electrical remodelling and atrial fibrillation QJM, September 1, 2000; 93(9): 563 - 565. [Full Text] [PDF]
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S. Nattel Ionic Determinants of Atrial Fibrillation and Ca2+ Channel Abnormalities : Cause, Consequence, or Innocent Bystander? Circ. Res., September 3, 1999; 85(5): 473 - 476. [Full Text] [PDF]
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C. Boixel, W. Gonzalez, L. Louedec, and S. N. Hatem Mechanisms of L-Type Ca2+ Current Downregulation in Rat Atrial Myocytes During Heart Failure Circ. Res., September 28, 2001; 89(7): 607 - 613. [Abstract] [Full Text] [PDF]
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M. K. Chung, D. O. Martin, D. Sprecher, O. Wazni, A. Kanderian, C. A. Carnes, J. A. Bauer, P. J. Tchou, M. J. Niebauer, A. Natale, et al. C-Reactive Protein Elevation in Patients With Atrial Arrhythmias: Inflammatory Mechanisms and Persistence of Atrial Fibrillation Circulation, December 11, 2001; 104(24): 2886 - 2891. [Abstract] [Full Text] [PDF]
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