Author + information
- Received February 2, 2000
- Revision received June 2, 2000
- Accepted July 14, 2000
- Published online December 1, 2000.
- Tohru Masuyama, MD, PhD, FACC∗,* (, )
- Kazuhiro Yamamoto, MD, PhD, FACC∗,
- Yasushi Sakata, MD∗,
- Reiko Doi, MD, PhD∗,
- Nagahiro Nishikawa, MD∗,
- Hiroya Kondo, MD, PhD∗,
- Keiko Ono, MD∗,
- Tsunehiko Kuzuya, MD, PhD∗,
- Motoaki Sugawara, PhD† and
- Masatsugu Hori, MD, PhD, FACC∗
- ↵*Reprint requests and correspondence: Dr. Tohru Masuyama, Department of Internal Medicine and Therapeutics (A8), Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871, Japan
The aim of our study was to explore evolving changes in a mitral flow velocity pattern (MFVP) and its hemodynamic and pathological correlates in hypertensive rats in an isolated diastolic heart failure model.
Development of left ventricular (LV) hypertrophy and concomitant diastolic dysfunction cause heart failure in hypertensive hearts even with normal systolic function; however, associated evolving change in MFVP is still unclear.
Mitral flow velocity pattern was recorded every 2 weeks from 7 to 19 weeks in six hypertensive rats. Hemodynamic and pathological correlates of Doppler mitral flow indexes were examined as an additional part of the study using the hypertensive rats at the age of 13 weeks (compensatory stage, n = 7) and at 19 weeks (heart failure stage, n = 8).
Initial development of pressure overload LV hypertrophy resulted in a decrease in early diastolic filling wave (E), a reciprocal increase in the filling wave due to atrial contraction (A) and prolongation of deceleration time of E wave (relaxation abnormality pattern). These changes were associated with an increase in tau, an index of LV relaxation, but without a change in LV end-diastolic pressure. Transition to congestive heart failure caused an increase in E, a decrease in A and shortening of deceleration time. These changes were not associated with further increase in tau but with elevation of LV end-diastolic pressure, reflecting marked LV hypertrophy and myocardial fibrosis.
Development of pressure overload LV hypertrophy is associated with evolving changes in MFVP from normal to relaxation abnormality pattern and, in turn, to pseudonormalized to restrictive pattern. Analysis of MFVP may be useful to follow not only functional but also constitutional changes of the myocardium in hypertensive hearts.
☆ Supported by the Ministry of Education and the Ministry of Health and Welfare of Japan.
- Received February 2, 2000.
- Revision received June 2, 2000.
- Accepted July 14, 2000.
- American College of Cardiology