Manolis AJ, Olympios C, Sifaki M, Handanis S, Bresnahan M,
Gavras I, Gavras H
Suppressing sympathetic activation in congestive heart
failure
Hypertension
(Nov) 26:719-724 1995
It is well known that clonidine, which lowers blood pressure by
acting as an alpha-2 agonist on inhibitory symnpathetic neurons
in the CNS, lowers sympathetic outflow. It is also well known
that patients with CHF have heightened sympathetic tone, as well
as increased plasma levels of NEPI, AVP, PRA, and other
vasoactive hormones. This group treated 20 patients with Class
IV NYHA heart failure with clonidine (0.15 mg BID) and compared
hemodynamic measurements (obtained by right heart
catheterization) before therapy as well as 2-3 hours and 7 days
later. They found that clonidine not only lowered MAP, but also
right atrial, mean pulmonary artery, and wedge pressures.
Cardiac output was unchanged, but stroke volume index increased
substantially, suggesting a possible improvement in LV
compliance. The changes at 2-3 hours appeared to be sustained
over 7 days. Plasma NEPI levels were markedly reduced (by 62%
after 1 week), but plasma AVP levels increased. On the basis of
these findings the authors propose adding clonidine to current
vasodilator regimens for CHF, or even trying clonidine per se.
Comment: Sounds good, but this therapy cannot be
firmly recommended until trials show it to be beneficial in
actual practice.
(Daugirdas)
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H: Drug therapy :
Sympatholytics
H: Pathophysiology :
Heart in hypertension