Circulation, Vol 62, 756-763, Copyright © 1980 by American Heart Association
Y Hirota
Left ventricular (LV) relaxation was studied in patients with hypertrophic
cardiomyopathy (HCM, n =18), congestive cardiomyopathy (CCM, n = 11),
hypertensive heart disease (HHD, n = 8), coronary artery disease (CAD)
without left ventricular (LV) asynergy (n = 9) and with LV asynergy (n
=17), mitral stenosis (MS, n = 16), and mitral regurgitation (MR, n = 8).
The time constant T and peak negative dP/dt were used as indexes of LV
relaxation, and 18 normal subjects served as controls. The time constant T
was higher in elderly patients among normal contros (r = 0.652, p <
0.01), which suggests that prolongation of relaxation is a phenomenon of
aging. The normal value of the time constant T was 33 +/- 8 msec (mean +/-
SD), and that of peak negative dp/dt was 1864 +/- 390 mm Hg/sec. The time
constant T was significantly higher in HCM (64 +/- 20 msec), CCM (56 +/- 14
msec), CAD without asynergy (53 +/- 16 msec), CAD with asynergy (57 +/- 13
msec) and MS (47 +/- 12 msec). Peak negative dP/dt was significantly lower
in HCM (998 +/- 303 mm Hg/sec), CCM (1060 +/- 334 mm Hg/sec), CAD with
asynergy (1370 +/- 299 mm Hg/sec), MS (1367 +/- 313 mm Hg/sec) and MR (1139
+/- 305 mm Hg/sec). Although the genesis of LV relaxation abnormality is
not clear from this investigation, it seems to have multiple causes.
Relaxation abnormality seems to be one of the earliest manifestations of
mechanical dysfunction of the human left ventricle.
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