*Part of the data was presented at the 43rd Annual Meeting of the American College of Cardiology, New Orleans, USA, in March 1994.
AUGMENTED EXERCISE PLASMA NORADRENALINE WITH IMPAIRED CHRONOTROPIC RESPONSIVENESS IN PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY*
Article first published online: 28 JUN 2007
Clinical and Experimental Pharmacology and Physiology
Volume 25, Issue 12, pages 1018–1023, December 1998
How to Cite
Omodani, H., Kinugawa, T., Ogino, K., Furuse, Y., Yamaguchi, M., Mori, M., Endo, A., Kato, M., Kato, T., Osaki, S., Miyakoda, H., Igawa, O., Hisatome, I. and Shigemasa, C. (1998), AUGMENTED EXERCISE PLASMA NORADRENALINE WITH IMPAIRED CHRONOTROPIC RESPONSIVENESS IN PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY. Clinical and Experimental Pharmacology and Physiology, 25: 1018–1023. doi: 10.1111/j.1440-1681.1998.tb02177.x
- Issue published online: 28 JUN 2007
- Article first published online: 28 JUN 2007
- Received 5 February 1998; revision 25 June 1998; accepted 13 August 1998.
- chronotropic sympathetic responsiveness;
- exercise test;
- hypertrophic cardiomyopathy;
1. There is controversy regarding plasma catecholamine levels in patients with hypertrophic cardiomyopathy (HCM) and few data exist on serial plasma catecholamine measurements during exercise. The present study determined whether cardiovascular and plasma catecholamine responses to exercise were altered in patients with HCM.
2. Plasma noradrenaline (NA) and adrenaline were measured at rest, at the end of each stage during exercise and immediately and 5 min after submaximal treadmill exercise in 15 patients with non-obstructive HCM (13 males, two females; mean (±SEM) age 54 ± 3 years) and in 15 age- and sex-matched controls. The ratio of the increment in heart rate (HR) divided by the increment in plasma NA during exercise (ΔHR/ΔNA) was used as an index of chronotropic sympathetic responsiveness to exercise.
3. Exercise duration was shorter (11.2 ± 0.6 vs 8.7 ± 0.6 min for control vs HCM, respectively; P<0.01) and diastolic blood pressure was significantly higher at stages I and II of modified Bruce protocol HCM.
4. Resting plasma NA levels (149 ± 17 vs 167 ± 28 pg/mL for control vs HCM, respectively; NS) were not different, but plasma NA levels at stages I and H were significantly higher in HCM than in controls (243 ± 26 vs 399 ± 69pg/mL (P<0.05) and 308 ± 30 vs 548 ± 110pg/mL (P<0.05), respectively).
5. Peak plasma NA levels were not significantly higher in HCM than in controls (578 ± 59 vs 918 ± 184 pg/mL, respectively; NS).
6. The ratio AHR/ANA was significantly lower in HCM compared with control at stages I and II (0.49 ± 0.10 vs 0.21 ± 0.05 (P<0.05) and 0.38 ± 0.06 vs 0.20 ± 0.05 (P < 0.05), respectively). There were no differences in plasma adrenaline responses during exercise between the two groups.
7. Patients with HCM had augmented plasma NA levels during submaximal exercise with a higher diastolic blood pressure response. Chronotropic sympathetic responsiveness was impaired during the early stages of exercise in patients with HCM.