(Circulation. 1999;99:1822-1830.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Impaired Force-Frequency Relations in Patients With Hypertensive Left Ventricular Hypertrophy
A Possible Physiological Marker of the Transition From Physiological to Pathological Hypertrophy
From the Department of Clinical Laboratory Medicine (M.Y.) and the First Department of Internal Medicine (M. Inagaki, H.I., R.I., K.N., T.S.), Nagoya University School of Medicine, and Nagoya University School of Health Science (M. Iwase), Nagoya; and the Department of Geriatric Research (Y.Y.), National Institute for Longevity Science, and National Chubu Hospital (M.K.), Obu, Japan.
Correspondence to Mitsuhiro Yokota, MD, Cardiovascular Section, Department of Clinical Laboratory Medicine, Nagoya University Hospital, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8560, Japan. E-mail myokota{at}tsuru.med.nagoya-u.ac.jp
Background—The extent to which force-frequency and relaxation-frequency relations (FFR and RFR, respectively) and exercise-induced adrenergic stimulation affect myocardial inotropic and lusitropic reserves has not been established in patients with left ventricular (LV) hypertrophy (LVH).
Methods and Results—We calculated the maximum first derivative of LV pressure (LV dP/dtmax) and the LV pressure half-time (T1/2) during pacing, exercise, and isoproterenol infusion in 17 patients with hypertensive LVH and 9 control subjects to investigate the influence of increases in heart rate (HR) and adrenergic stimulation on inotropic and lusitropic reserves. Group A consisted of 10 LVH patients who showed a progressive increase in the HR-LV dP/dtmax relation. Group B consisted of 7 LVH patients in whom the HR-dP/dtmax relation at physiological pacing rates was biphasic. The LV mass index was larger and the LV ejection fraction was smaller in group B than in group A (244±72 g/m2 versus 172±22 g/m2 and 55±18% versus 72±6%, respectively; both P<0.05). The increase in LV dP/dtmax was greater during exercise than pacing alone for similar increases in HR in all groups (P<0.05) (group A, 111±22% versus 25±14%; group B, 105±35% versus 14±10%; control, 111±24% versus 25±12%). T1/2 was shorter (P<0.05) during exercise than with pacing alone in all groups (group A, 41±6% versus 11±3%; group B, 38±9% versus 14±4%; control, 44±6% versus 12±5%). Isoproterenol infusion caused similar increases in LV dP/dtmax and similar decreases in T1/2 in all groups.
Conclusions—The FFR was biphasic in patients with severe LVH irrespective of LV function but was preserved in patients with less severe LVH and control subjects. Importantly, the RFR and adrenergic control of both inotropic and lusitropic reserves were well preserved in all LVH patients. A biphasic FFR at physiological pacing rates may be one of the earliest markers of the transition from physiological adaptation to the pathological process in LVH patients.
Key Words: myocardial contraction • hypertrophy • hypertension
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