Circulation, Vol 90, 895-907, Copyright © 1994 by American Heart Association
L Gregorini, J Fajadet, G Robert, B Cassagneau, M Bernis and J Marco
BACKGROUND: Vasoconstriction occurs after percutaneous transluminal
coronary angioplasty (PTCA) along the dilated vessel. The vasomotor
changes, initiated by the mechanical stretch of the stenotic region, are
thought to be due to various mechanisms but whether the sympathetic nervous
system plays a role in this phenomenon remains unknown. METHODS AND
RESULTS: Quantitative angiography (ARTREK) was performed in 45 patients
undergoing an epicardial vessel PTCA for a stenosis of 76 +/- 1% (1) in
basal conditions, (2) after PTCA, and (3) 30 minutes after PTCA
(vasoconstriction). In 14 control patients, the same measurements were
obtained up to 60 minutes after PTCA. Coronary diameters were measured
along the PTCA vessel at the narrowest stenosis level and at a level
peripheral to stenosis. In 36 patients two diameters were also measured at
a proximal segment and at a distal segment along a nonmanipulated vessel.
Thirty minutes after PTCA the dilated segment underwent a -31 +/- 2% (mean
+/- SEM, ANOVA, P < .05) reduction in diameter when compared with PTCA
values, and the segment peripheral to stenosis showed a reduction of -17
+/- 2% (P < .05). In all patients a significant vasoconstriction also
was observed along the control vessel (proximal segment, -14 +/- 3%; P <
.05 versus basal; and distal segment, -17 +/- 2%). At the time of maximal
vasoconstriction (30 minutes after PTCA), the patients (treatment groups)
received (1) 18 micrograms/kg IC phentolamine (Phe, n = 7), (2) 14
micrograms/kg IC yohimbine (YO, n = 7), (3) 16 micrograms/kg IC propranolol
(Pro) followed by 18 micrograms/kg IC phentolamine (Pro+Phe, n = 7), and
(4) 0.2 mg/kg IC bretylium (Bre, n = 10). In 14 patients (control groups)
an intracoronary injection of warm saline was given. After drug injections,
angiograms were repeated at 5-minute intervals for 20 minutes and ended
after a 300-micrograms intracoronary trinitroglycerin injection. At
stenosis level, Phe and Bre counteracted vasoconstriction, inducing a
dilatation of +19 +/- 3% and +22 +/- 6%, respectively, while Pro+Phe caused
a dilatation of +16 +/- 9% above the PTCA values (P < .05 versus PTCA).
YO only partially reversed vasoconstriction (from -33 +/- 4% to -12 +/- 4%,
P = NS versus PTCA). At peripheral-to-stenosis level, vasoconstriction was
abolished by Phe (+26 +/- 7%, P < .05 versus basal), while it was still
present after Pro+Phe (-23 +/- 2%) and Bre (-18 +/- 4%). In addition, Phe
and Bre dilated the control vessel at the proximal segment (+17 +/- 6% and
+8 +/- 4%, respectively, P < .05 versus basal), while YO and Pro+Phe
only counteracted vasoconstriction (from -15 +/- 3% to +7.6 +/- 1% and from
- 16 +/- 3% to +4 +/- 5%, respectively, P = NS versus basal). At the distal
segment only Phe produced a vasodilatation of +23 +/- 1%; YO counteracted
constriction (from -16 +/- 2% to +9 +/- 6%, P < .05 versus basal),
whereas after Pro+Phe and Bre, the vasoconstriction persisted. CONCLUSIONS:
The mechanical stretch and ischemia caused by balloon inflation induced
vasoconstriction mediated by alpha-adrenergic receptors (mainly alpha 1),
overcoming a beta-mediated dilatation. The use of different antiadrenergic
drugs showed that Phe counteracts post- PTCA vasoconstriction, and the
simultaneous use of alpha- and beta- receptor blocking agents (Pro+Phe and
Bre) reveals the presence of a peripheral, predominant beta-mediated
dilatation. The presence of vasoconstriction also along the control vessels
not branching from the stretched ramus provides evidence for the existence
of neural sympathetic vasoconstrictor reflexes.
ARTICLES
Coronary vasoconstriction after percutaneous transluminal coronary angioplasty is attenuated by antiadrenergic agents
Clinica Medica Generale, Universita di Milano, Italy.
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