Clinical recovery from end-stage heart failure using left-ventricular assist device and pharmacological therapy correlates with increased sarcoplasmic reticulum calcium content but not with regression of cellular hypertrophy

Circulation

Volumn 109, Issue 19, 2004, Pages 2263-2265

  Terracciano, Cesare M N ^a,b   Hardy, J ^a   Birks, E J ^a   Khaghani, A ^a   Banner, N R ^a   Yacoub, M H ^a  

^a IMPERIAL COLLEGE LONDON   (United Kingdom)

^b HAREFIELD HOSPITAL   (United Kingdom)

Author keywords

Electrophysiology; Heart failure; Mechanical devices; Myocytes; Sarcoplasmic reticulum

Indexed keywords

CALCIUM ION; CARDIOVASCULAR AGENT;

ARTICLE; CALCIUM CELL LEVEL; CELL HYPERPLASIA; CLINICAL ARTICLE; CONTROLLED STUDY; HEART ASSIST DEVICE; HEART FAILURE; HEART VENTRICLE WALL; HUMAN; HUMAN TISSUE; PRIORITY JOURNAL; REMISSION; SARCOPLASMIC RETICULUM;

CAFFEINE; CALCIUM; CALCIUM CHANNELS, L-TYPE; CALCIUM SIGNALING; CARDIOVASCULAR AGENTS; CELL SIZE; COMBINED MODALITY THERAPY; HEART FAILURE, CONGESTIVE; HEART TRANSPLANTATION; HEART VENTRICLES; HEART-ASSIST DEVICES; HUMANS; ION TRANSPORT; MYOCYTES, CARDIAC; REMISSION INDUCTION; SARCOPLASMIC RETICULUM; VENTRICULAR DYSFUNCTION, LEFT;

EID: 2442652789     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.CIR.0000129233.51320.92     Document Type: Article

References (15)

1. Rose EA, Gelijns AC, Moskowitz AJ, et al. Long-term mechanical left ventricular assistance for end-stage heart failure. N Engl J Med. 2001; 345:1435-1443.
2. Margulies KB. Reversal mechanisms of left ventricular remodeling: lessons from left ventricular assist device experiments. J Card Failure. 2002;8:S500-S505.
3. Yacoub MH. A novel strategy to maximize the efficacy of left ventricular assist devices as a bridge to recovery. Eur Heart J. 2001;22:534-540.
4. Hill JA, Karimi M, Kutschke W, et al. Cardiac hypertrophy is not a required compensatory response to short-term pressure overload. Circulation. 2000;101:2863-2869.
5. Botchway AN, Turner MA, Sheridan DJ, et al. Electrophysiological effects accompanying regression of left ventricular hypertrophy. Cardiovasc Res. 2003;60:510-517.
6. Terracciano CM, Harding SE, Adamson D, et al. Changes in sarcolemmal Ca entry and sarcoplasmic reticulum Ca content in ventricular myocytes from patients with end-stage heart failure following myocardial recovery after combined pharmacological and ventricular assist device therapy. Eur Heart J. 2003;24:1329-1339.
7. Frazier MD, Benedict MD, Radovancevic MD, et al. Improved left ventricular function after chronic left ventricular unloading. Ann Thorac Surg. 1996;62:675-682.
8. Harding SE, MacLeod KT, Jones SM, et al. Contractile responses of myocytes isolated from patients with cardiomyopathy. Eur Heart J. 1991;12(suppl D):44-48.
9. Varro A, Negretti N, Hester SB, et al. An estimate of the calcium content of the sarcoplasmic reticulum in rat ventricular myocytes. Pflugers Arch. 1993;423:158-160.
10. 2+ extrusion mechanisms to relaxation in guinea-pig ventricular myocytes. J Physiol. 1997;500:557-570.
11. Hobai IA, O'Rourke B. Decreased sarcoplasmic reticulum calcium content is responsible for defective excitation-contraction coupling in canine heart failure. Circulation. 2001;103:1577-1584.
12. 2+ current in cardiac cells. Am J Physiol. 1995;268:H916-H920.
13. Bers DM. Excitation-Contraction Coupling and Cardiac Contractile Force. Second ed. Dordrecht, The Netherlands: Kluwer Academic; 2001.
14. Tomaselli GF, Marban E. Electrophysiological remodeling in hypertrophy and heart failure. Cardiovasc Res. 1999;42:270-283.
15. Harding JD, Piacentino V III, Gaughan JP, et al. Electrophysiological alterations after mechanical circulatory support in patients with advanced cardiac failure. Circulation. 2001;104:1241-1247.