Chronic unloading by left ventricular assist device reverses contractile dysfunction and alters gene expression in end-stage heart failure

Circulation

Volumn 102, Issue 22, 2000, Pages 2713-2719

  Heerdt, P M ^a   Holmes, J W ^a   Cai, B ^a   Barbone, A ^a   Madigan, J D ^a   Reiken, S ^a   Lee, D L ^a   Oz, M C ^a   Marks, A R ^a   Burkhoff, D ^a  

^a NEW YORK PRESBYTERIAN HOSPITAL   (United States)

Author keywords

Calcium; Genes; Heart failure; Heart assist device; Sarcoplasmic reticulum

Indexed keywords

ADENOSINE TRIPHOSPHATASE (CALCIUM); RYANODINE RECEPTOR; SODIUM CALCIUM EXCHANGE PROTEIN;

ADULT; AGED; ARTICLE; CALCIUM TRANSPORT; CONTROLLED STUDY; FEMALE; GENE CONTROL; GENE EXPRESSION; HEART ASSIST DEVICE; HEART FAILURE; HEART LEFT VENTRICLE CONTRACTILITY; HEART MUSCLE CELL; HUMAN; HUMAN TISSUE; MALE; MUSCLE STRENGTH; PRIORITY JOURNAL; REGULATORY MECHANISM; SARCOPLASMIC RETICULUM;

EID: 0034727712     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.CIR.102.22.2713     Document Type: Article

References (28)

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7. Weaning from mechanical cardiac support in patients with idiopathic dilated cardiomyopathy
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15. FK506 binding protein associated with the calcium release channel (ryanodine receptor)
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20. Regression of cellular hypertrophy after left ventricular assist device support
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