title: Hemodynamic performance and myosin light chain-1 expression of the hypertrophied left ventricle in aortic valve disease before and after valve replacement.
abstract: Previously, we have reported on the selective accumulation of an atrial-like myosin light chain-1 (ALC1) in different forms of human ventricular hypertrophy. The present study involves the determination of ALC1 content in a control group and in patients with aortic stenosis or insufficiency before and 56 +/- 23 months after valve replacement and compares the hemodynamic and angiographic parameters. ALC1 was quantified densitometrically after two-dimensional electrophoretic resolution of biopsy specimens from the left ventricle and was expressed in percent of total ventricular light chain-1. The mean ALC1 content was 11.2 +/- 9.2% in preoperative aortic stenosis and 4.5 +/- 1.4% in aortic insufficiency, both being significantly (p less than 0.001) higher than the control value of 0.3 +/- 0.3%. After valve replacement, mean ALC1 content was lower than before, 4.2 +/- 3.3% (p less than 0.05) in stenosis and 3.4 +/- 3.1% (p = NS) in insufficiency. Left ventricular systolic pressure yields a significant (p less than 0.01) linear correlation (r = 0.45) with the ALC1 content in all preoperative and postoperative patients. Patient group averages of ALC1 content correlate directly with left ventricular systolic and end-diastolic pressure and wall thickness (r = 0.94-0.98) and, in an exponential fashion, with peak systolic circumferential wall stress (r = 0.98) but not with muscle mass or any other parameter. The ventricular ALC1 binds to myosin in proportion to its occurrence in the myocardium. The content of the endogenous ventricular light chain-1 did not change under pathological hemodynamics. The response in expression of the ALC1 to pressure and volume overload suggests an adaptational process.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Division of Cardiology, University Hospital, Zurich, Switzerland.
authors.forename: G
authors.initials: G
authors.lastname: Sütsch
authors.forename: U T
authors.initials: UT
authors.lastname: Brunner
authors.forename: C
authors.initials: C
authors.lastname: von Schulthess
authors.forename: H O
authors.initials: HO
authors.lastname: Hirzel
authors.forename: O M
authors.initials: OM
authors.lastname: Hess
authors.forename: M
authors.initials: M
authors.lastname: Turina
authors.forename: H P
authors.initials: HP
authors.lastname: Krayenbuehl
authors.forename: M C
authors.initials: MC
authors.lastname: Schaub
mesh_terms: D000328:Adult; D000368:Aged; D000792:Angiography; D001022:Aortic Valve Insufficiency / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000601:surgery; D001024:Aortic Valve Stenosis / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000601:surgery; D006332:Cardiomegaly / Q000503:physiopathology*; D004586:Electrophoresis; D005260:Female; D005500:Follow-Up Studies; D006350:Heart Valve Prosthesis; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009218:Myosins / Q000032:analysis; D013997:Time Factors
chemical_list: D009218:Myosins