Circulation, Vol 73, 409-417, Copyright © 1986 by American Heart Association
GG Neri Serneri, GF Gensini, G Masotti, R Abbate, L Poggesi, R Laureano, D Prisco, PG Rogasi and S Castellani
Peripheral vascular resistance (PVR) and thromboxane A2(TxA2) synthesis
after the cold pressor test were investigated in different subsets of
patients with angina (10 with stable effort angina, 36 with resting angina
[24 in an active phase and 12 in an inactive phase], and five with
Prinzmetal's variant angina) and in 41 control subjects of equivalent age
and risk factors. Left ventricular end-diastolic pressure, ejection
fraction, extent of coronary angiographic lesions, and baseline PVR were
not significantly different among the various patient groups. In all
patient groups, except those with variant angina, the cold pressor test
resulted in a higher increase in PVR than in the control subjects (p less
than .001 for all groups). In patients with variant angina the
vasoconstrictor response was increased only in proximity (about 1 hr) to
ischemic attacks. In patients with active resting angina the
vasoconstrictor response was on the average four times longer than that in
patients with effort angina and with inactive resting angina (p less than
.001). This exaggerated vasoconstrictor response was associated with
elevated TxA2 resting levels in plasma and with increased TxA2 synthesis
after the cold pressor test. A linear relationship was found between the
area of the vascular response and the area of TxA2 production after the
cold pressor test in patients with active resting angina (r = .87, p less
than .001). The increased TxA2 synthesis and the inappropriate increase of
peripheral vascular response to sympathetic stimulation revert back to
normal in the inactive phase.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Enhanced peripheral vasoconstrictor response and increased thromboxane A2 synthesis after the cold pressor test in patients with angina at rest
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