title: Myocardial remodeling with aortic stenosis and after aortic valve replacement: mechanisms and future prognostic implications.
abstract: Aortic valve stenosis is a common cause of left ventricular pressure overload, a pathologic process that elicits myocyte hypertrophy and alterations in extracellular matrix composition, both of which contribute to increases in left ventricular stiffness. However, clinical and animal studies suggest that increased myocardial extracellular matrix fibrillar collagen content occurs later in the time course of left ventricular pressure overload at a time coincident with severe abnormalities in diastolic function followed by the development of symptomatic heart failure. Aortic valve replacement remains the most effective treatment for elimination of chronic pressure overload secondary to aortic stenosis but has traditionally been recommended only after the onset of clinical symptoms. Long-term follow-up of patients with symptomatic aortic stenosis after aortic valve replacement suggests that valve replacement may not result in complete reversal of the maladaptive changes that occur within the myocardial extracellular matrix secondary to the pressure overload state. To the contrary, residual left ventricular extracellular matrix abnormalities such as these are likely responsible for persistent abnormalities in diastolic function and increased morbidity and mortality after aortic valve replacement. Defining the mechanisms and pathways responsible for regulating the myocardial extracellular matrix during the natural history of aortic stenosis may provide a means by which to detect crucial structural milestones and thereby permit more precise identification of the development of maladaptive left ventricular remodeling.
authors.affiliation: Division of Cardiothoracic Surgery, Department of Medicine, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: William M
authors.initials: WM
authors.lastname: Yarbrough
authors.forename: Rupak
authors.initials: R
authors.lastname: Mukherjee
authors.forename: John S
authors.initials: JS
authors.lastname: Ikonomidis
authors.forename: Michael R
authors.initials: MR
authors.lastname: Zile
authors.forename: Francis G
authors.initials: FG
authors.lastname: Spinale
mesh_terms: D000818:Animals; D001024:Aortic Valve Stenosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D018450:Disease Progression; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D005355:Fibrosis; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D019918:Heart Valve Prosthesis Implantation / Q000009:adverse effects; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D018570:Risk Assessment; D012307:Risk Factors; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D016277:Ventricular Function, Left; D017725:Ventricular Pressure; D020257:Ventricular Remodeling
chemical_list: D016326:Extracellular Matrix Proteins