G. Grassi et al., SYMPATHETIC ACTIVATION AND LOSS OF REFLEX SYMPATHETIC CONTROL IN MILDCONGESTIVE-HEART-FAILURE, Circulation, 92(11), 1995, pp. 3206-3211
Background Baroreflex control of sympathetic activity is impaired in s
evere congestive heart failure (CHF), probably causing the marked symp
athetic activation typical of this condition. Little information exist
s, however, as to whether baroreflex impairment and related sympatheti
c activation also occur in mild CHF. Methods and Results We studied 19
patients (age, 57.5+/-2.2 years, mean+/-SEM) with CHF in New York Hea
rt Association (NYHA) class III or IV and with a marked reduction in l
eft ventricular ejection fraction (LVEF, 30.1+/-1.5% from echocardiogr
aphp) and 17 age-matched patients with CHF in NYHA class I or II and w
ith an only slightly reduced LVEF (44.9+/-3.3%) that never was <40%. S
eventeen age-matched healthy subjects served as control subjects. Prim
ary measurements included beat-to-beat arterial blood pressure (with t
he Finapres technique), heart rate (from EGG), and postganglionic musc
le sympathetic nerve activity (MSNA, from microneurography at the pero
neal nerve). Measurements were performed at baseline and during barore
ceptor stimulation (intravenous phenylephrine infusion), baroreceptor
deactivation (intravenous nitroprusside infusion), and cold-presser te
st. Baseline blood pressure was similar in the three groups, whereas h
eart rate was progressively greater from control subjects to patients
with mild and severe CHF. MSNA (bursts per 100 heart beats) increased
significantly and markedly from control subjects to patients with mild
and severe CHF (47.1+/-2.9 versus 64.4+/-6.2 and 82.1+/-3.4, P<.05 an
d P<.01, respectively). Heart rate and MSNA were progressively reduced
by phenylephrine infusion and progressively increased by nitroprussid
e infusion. Compared with control subjects, the responses were strikin
gly impaired in severe CHF patients, but a marked impairment also was
seen in mild CHF patients. On average, baroreflex sensitivity in mild
CHF patients was reduced by 59.1+/-5.5% (MSNA) and 64.8+/-4.8% (heart
rate). In contrast, reflex responses to the cold-presser rest were sim
ilar in the three groups. Conclusions These results demonstrate chat i
n mild CHF patients the baroreceptor inhibitory influence on heart rat
e and MSNA is already markedly impaired. This impairment may be respon
sible for the early sympathetic activation that occurs in the course o
f CHF.