title: The effects of right ventricular hemodynamics on left ventricular configuration.
abstract: While abnormalities of right ventricular hemodynamics are known to affect interventricular septal position and shape, their effect on left ventricular shape and possibly function have been less well studied. Accordingly, the two-dimensional echocardiographic appearance of the left ventricle was studied in 11 patients with right ventricular volume overload, 16 with right ventricular pressure overload, nine with combined pressure and volume loads of the right heart and 17 normal control subjects. An index of left ventricular shape (SI) was calculated from end diastolic, mid systolic and end systolic left ventricular short axis area (A) and circumference (C) taken at the level of the tips of the mitral leaflets, using the formula SI = 4 pi A/C2. The left ventricles of normal subjects had relatively round configurations throughout the entire cardiac cycle (SI = 0.86 at end diastole, mid and end systole). Pure right ventricular volume overload produced left ventricular deformity at end diastole only (SI at end diastole = 0.78), with a return to normal configuration during systole. Pure right ventricular pressure load resulted in left ventricular deformation throughout the cardiac cycle, with shape indices ranging between 0.77 and 0.80. Combined pressure and volume overload produced left ventricular deformation during the entire cycle which was of an order of magnitude more severe than any other group (SI = 0.69, 0.70 and 0.65, at end diastole, mid and end systole, respectively). The shape index at end systole showed an inverse correlation with the relative right-to-left ventricular systolic pressure ratio (P = 0.001, r = 0.76). It is concluded that left ventricular configuration is affected by right ventricular hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Cardiac Ultrasound Laboratory Cardiac Unit, Massachusetts General Hospital, Boston.
authors.forename: K J
authors.initials: KJ
authors.lastname: Ascah
authors.forename: M E
authors.initials: ME
authors.lastname: King
authors.forename: L D
authors.initials: LD
authors.lastname: Gillam
authors.forename: A E
authors.initials: AE
authors.lastname: Weyman
mesh_terms: D000293:Adolescent; D000328:Adult; D006328:Cardiac Catheterization / Q000379:methods; D002302:Cardiac Output / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology*; D002648:Child; D002675:Child, Preschool; D003971:Diastole / Q000502:physiology; D004452:Echocardiography / Q000379:methods; D004694:Endocardial Cushion Defects / Q000503:physiopathology; D005260:Female; D006333:Heart Failure / Q000503:physiopathology*; D006344:Heart Septal Defects, Atrial / Q000503:physiopathology; D006345:Heart Septal Defects, Ventricular / Q000503:physiopathology; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D011666:Pulmonary Valve Stenosis / Q000503:physiopathology; D012189:Retrospective Studies; D013599:Systole / Q000502:physiology; D013771:Tetralogy of Fallot / Q000503:physiopathology; D014188:Transposition of Great Vessels / Q000503:physiopathology; D014262:Tricuspid Valve Insufficiency / Q000503:physiopathology