Circulation, Vol 85, 2140-2148, Copyright © 1992 by American Heart Association
DM Gilligan, P Nihoyannopoulos, WL Chan and CM Oakley
BACKGROUND. Syncope and sudden death in hypertrophic cardiomyopathy may
have a hemodynamic basis. The presence of a small ventricular cavity with
high intracavity pressures may activate left ventricular baroreceptors and
cause reflex hypotension as described in other populations with syncope.
METHODS AND RESULTS. To investigate this potential mechanism of syncope in
hypertrophic cardiomyopathy, we studied 17 patients with a history of
syncope (syncopal), 19 without syncope (nonsyncopal), and nine normal
control subjects by using a head- up tilt test. Head-up tilt at 60 degrees
for 45 minutes was followed by 10-minute tilts during incremental doses of
isoprenaline. Heart rate, blood pressure, and two-dimensional and Doppler
echocardiography were monitored throughout. On tilting, hypertrophic
cardiomyopathy patients showed a decline in mean arterial pressure of -5
+/- 6 mm Hg (p less than 0.001) compared with no change in control subjects
(0.2 +/- 6 mm Hg, p = 0.9). Left ventricular outflow tract velocity
decreased on tilting in control subjects (-8 +/- 6 cm/sec, p = 0.004) but
increased in the syncopal and nonsyncopal patients (20 +/- 50 cm/sec, p =
0.05). Reflex hypotension with or without bradycardia, associated with
syncope or presyncope, was induced in seven syncopal patients, two
nonsyncopal patients, and two control subjects (p = 0.05). The early
response to tilt in these subjects was characterized by maintenance of
blood pressure but a greater increase in left ventricular fractional
shortening than in the other subjects (10 +/- 8% versus 1 +/- 1%, p =
0.002). The onset of hypotension was associated with a trend toward further
decreases in left ventricular diameters, outflow tract velocity, and
transmitral flow velocities. In the remaining patients who had a negative
test, transient hypotension (systolic pressure less than 100 mm Hg)
occurred in seven syncopal patients and three nonsyncopal patients compared
with none of the control subjects (p = 0.01). In total, hypotension was
demonstrated in 82% of syncopal patients compared with 26% of nonsyncopal
patients and 22% of control subjects (p = 0.001). CONCLUSIONS. Patients
with hypertrophic cardiomyopathy and a history of syncope frequently
display hypotension during head-up tilt. In some cases, sudden hypotension
occurs and is usually associated with bradycardia and a reduced cavity
size, findings compatible with activation of a ventricular baroreflex. In
other cases, transient hypotension occurs and could be explained by an
impairment of baroreceptor function. These mechanisms may contribute to the
occurrence of syncope in daily life.
ARTICLES
Investigation of a hemodynamic basis for syncope in hypertrophic cardiomyopathy. Use of a head-up tilt test
Department of Medicine (Clinical Cardiology), Royal Postgraduate Medical School, Hammersmith Hospital, London.
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