Author + information
- Received November 30, 1989
- Revision received February 28, 1990
- Accepted March 26, 1990
- Published online September 1, 1990.
- James D. Thomas, MD, FACC∗,
- Christopher Y.P. Choong, MB, BChir, PhD,
- Frank A. Flachskampf, MD1 and
- Arthur E. Weyman, MD, FACC
- ↵∗Address for reprints: James D. Thomas, MD, Noninvasive Cardiac Laboratory, Massachusetts General Hospital, Zero Emerson Place, Suite 2F, Boston, Massachusetts 02114.
Left ventricular filling (as assessed by Doppler echocardiography) has previously been shown to depend in a complex fashion on ventricular diastolic function (compliance and relaxation) as well as other variables, such as atrial pressure and compliance, ventricular systolic function and mitral valve impedance. To study the effect of isolated physiologic alterations on individual Doppler indexes, a mathematic model of mitral flow was analyzed.
By varying one physiologic variable at a time, it was shown that mitral velocity acceleration is affected directly by atrial pressure and inversely by the ventricular relaxation tune constant, with relatively little impact of chamber compliance. Deceleration rate was directly influenced by mitral valve area, atrial pressure and ventricular systolic dysfunction and inversely affected by atrial and ventricular compliance relations, with little impact of relaxation unless it was so delayed as to be incomplete during deceleration. Peak velocity was directly affected most strongly by initial left atrial pressure, and lowered somewhat by prolonged relaxation, low atrial and ventricular compliance and systolic dysfunction.
Strikingly different filling patterns emerged when the primary physiologic alterations were accompanied by simultaneous compensatory changes in atraal pressure designed to maintain stroke volume constant. Low ventricular compliance with preload compensation produced characteristic E waves with very short acceleration and deceleration times and high peak velocity. Thus, mathematic analysis of ventricular filling helps to explain the physical and physiologic basis for the transmitral velocity curve.
↵1 Dr. Flachskampf was supported by a grant from the Deutsche Forsch-ungsgemeinschaft, Bonn, Federal Republic of Germany.
☆ This study was supported by Grant 13-532-867 from the American Heart Association, Massachusetts Affiliate, Needham, Massachusetts. It was presented in part at the 62nd Annual Scientific Session, American Heart Association. November 1989.
- Received November 30, 1989.
- Revision received February 28, 1990.
- Accepted March 26, 1990.