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