Author + information
- Received December 12, 1994
- Revision received September 29, 1995
- Accepted October 11, 1995
- Published online March 1, 1996.
- Hidetsugu Asanoi, MD∗,†,
- Shinji Ishizaka, MD†,
- Shuji Joho, MD†,
- Tomoki Kameyama, MD†,
- Hiroshi Inoue, MD, FACC† and
- Shigetake Sasayama, MD, FACC∗
- ↵∗Address for correspondence: Dr. Hidetsugu Asanoi, The Secona Department of Internal Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitana, Toyama 930-01, Japan.
Objectives. The effects of increasing heart rate on left ventricular contraction and relaxation were examined in conscious dogs with tachycardia-induced heart failure under autonomically blocked conditions.
Background. Previous studies using isolated myocardium have shown attenuated positive inotropic responses to stimulation frequency in heart failure. However, these responses have not been well examined in intact preparations in the presence of heart failure with autonomic system blockade, where the intrinsic ventricular responses to increasing heart rate could be revealed.
Methods. Seven dogs were instrumented with a micromanometer and a conductance volume catheter. After autonomic blockade to eliminate neural reflexes, left ventricular contractile properties were quantified by the slope of the end-systolic pressure-volume relation (ventricular elastance), and left ventricular relaxation was assessed by the time constant of isovolumetric ventricular pressure decay.
Results. Increasing the heart rate by 60 beats/min enhanced ventricular elastance by 71 ± 18% (mean ± SD) and decreased end-systolic volume by 6 ± 5% in normal hearts. In failing hearts ventricular elastance increased by only 21 ± 20%, and end-systolic volume did not change appreciably. Although the reduction in left ventricular end-diastolic and minimal pressures by tachycardia was smaller in the failing heart, ventricular relaxation rate remained unaltered both in the normal heart and in the failing heart.
Conclusions. Under conscious but autonomically blocked conditions, effects of increasing heart rate on the failing left ventricle are characterized by a predominant attenuation of the inotropic response rather than of the lusitropic response.
☆ This study was supported by Grant-in-Aid for General Scientific Research 03454250 from the Ministry of Education, Science and Culture of Japan and by a research grant for Cardiovascular Diseases from the Ministry of Health and Welfare of Japan. This report was presented in part at the 64th Scientific Sessions of the American Heart Association, Anaheim, California, November 1991.
- Received December 12, 1994.
- Revision received September 29, 1995.
- Accepted October 11, 1995.