Characterization of the hyperpolarization-activated current, I(f), in ventricular myocytes from human failing heart

Circulation

Volumn 95, Issue 3, 1997, Pages 568-571

  Cerbai, Elisabetta ^a   Pino, Roberto ^a   Porciatti, Francesco ^a   Sani, Guido ^b   Toscano, Michele ^c   Maccherini, Massimo ^c   Giunti, Gabriele ^c   Mugelli, Alessandro ^a  

^a UNIVERSITY OF FLORENCE   (Italy)

^b UNIVERSITY OF CAGLIARI   (Italy)

^c UNIVERSITY OF SIENA   (Italy)

Author keywords

arrhythmia; electrophysiology; heart failure; hypertrophy; myocytes

Indexed keywords

ADULT; ARTICLE; CALCIUM TRANSPORT; CASE REPORT; HEART DILATATION; HEART ELECTROPHYSIOLOGY; HEART FAILURE; HEART VENTRICLE CONDUCTION; HEART VENTRICLE HYPERTROPHY; HUMAN; HUMAN TISSUE; HYPERPOLARIZATION; MALE; POTASSIUM CELL LEVEL; PRIORITY JOURNAL;

EID: 0031041032     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.CIR.95.3.568     Document Type: Article

References (17)

1. Kannel WB, Plehn JF, Cupples LA. Cardiac failure and sudden death in the Framingham study. Am Heart J. 1988;115:869-875.
2. Messerli FH, Ventura HO, Elilardi DJ, Dunn FG, Frohlich ED. Hypertension and sudden death: increased ventricular ectopic activity in left ventricular hypertrophy. Am J Med. 1984;77:18-22.
3. Levy D, Anderson K, Savage DD, Balkus SA, Kannel WB, Castelli WP. Risk of ventricular arrhythmias in left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol. 1987;60:560-565.
4. Pye MP, Cobbe SM. Mechanisms of ventricular arrhythmias in cardiac failure and hypertrophy. Cardiovasc Res. 1992;26:740-750.
5. Tomaselli GF, Beuckelmann DJ, Calkins HG, Berger RD, Kessler PD, Lawrence JH, Kass D, Feldman AM, Marban E. Sudden cardiac death in heart failure: the role of abnormal repolarization. Circulation. 1994;90:2534-2539.
6. + currents in isolated human ventricular myocytes from patients with terminal heart failure. Circ Res. 1993;73:379-385.
7. Cerbai E, Barbieri M, Li Q, Mugelli A. Ionic basis of action potential prolongation of hypertrophied myocytes isolated from the heart of hypertensive rats of different ages. Cardiovasc Res. 1994;28:1180-1187.
8. Bing OHL, Brooks WW, Robinson KG, Slawsky MT, Hayes JA, Litwin SE, Sen S, Conrad CH. The spontaneously hypertensive rat as a model of the transition from compensated left ventricular hypertrophy to failure. J Mol Cell Cardiol. 1995;27:383-396.
9. f, in ventricular myocytes isolated from hypertensive rats. J Physiol (Lond). 1994;481.3:585-591.
10. Di Francesco D. Pacemaker mechanisms in cardiac tissue. Annu Rev Physiol. 1993;55:455-472.
11. f, in ventricular myocytes from normotensive and hypertensive rats during aging. Circulation. 1996;94:1674-1681.
12. Cerbai E, Barbieri M, Porciatti F, Mugelli A. Ionic channels in hypertrophy and heart failure: relevance for arrhythmogenesis. New Trends Arrhythmia. 1995;9:135-139.
13. Veldkamp MW, van Ginneken ACG, Opthof T, Bouman LN. Delayed rectifier channels in human ventricular myocytes. Circulation. 1995;92:3497-3504.
14. Isenberg G, Klöckner U. Calcium tolerant ventricular myocytes prepared by preincubation in a 'KB' medium. Pflugers Arch. 1982;395:6-18.
15. DiFrancesco D. Characterization of the pacemaker current kinetics in calf Purkinje fibres. J Physiol (Lond). 1984;348:341-367.
16. Beuckelman DJ, Jansen E, Erdmann E. A pacemaker current is expressed in isolated ventricular myocytes from patients with heart failure. Circulation. 1995;92(suppl 1):I-505. Abstract.
17. Vermeulen JT, McGuire MA, Opthof T, Coronel R, de Bakker JMT, Klöpping C, Janse MJ. Triggered activity and automaticity in ventricular trabcculae of failing human and rabbit hearts. Cardiovasc Res. 1994;28:1547-1554.