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Coronary vasoconstriction after percutaneous transluminal coronary angioplasty is attenuated by antiadrenergic agents
L Gregorini1, J Fajadet, G Robert
1Clinica Medica Generale, Università di Milano, Italy.
Insights
Percutaneous transluminal coronary angioplasty (PTCA) causes vasoconstriction mediated by alpha-adrenergic receptors. Alpha-adrenergic blockers like phentolamine effectively counteract this post-PTCA vasoconstriction, indicating sympathetic nervous system involvement.
Area of Science:
- Cardiovascular Medicine
- Interventional Cardiology
- Autonomic Nervous System Research
Background:
- Vasoconstriction is a known complication following percutaneous transluminal coronary angioplasty (PTCA).
- The underlying mechanisms of this post-PTCA vasomotor change are not fully understood, particularly the role of the sympathetic nervous system.
Purpose of the Study:
- To investigate the role of the sympathetic nervous system in mediating vasoconstriction after PTCA.
- To determine the specific adrenergic receptor subtypes involved in post-PTCA vasomotor responses.
Main Methods:
- Quantitative angiography (ARTREK) was used to measure coronary artery diameters in 45 patients before, immediately after, and 30 minutes post-PTCA.
- Intracoronary administration of adrenergic blocking agents (phentolamine, yohimbine, propranolol, bretylium) was performed to assess their effects on vasoconstriction.
- Control vessels and segments peripheral to the stenosis were also analyzed to differentiate local from reflex effects.
Main Results:
- Significant vasoconstriction occurred in both the dilated segment (-31%) and the peripheral segment (-17%) 30 minutes after PTCA.
- Vasoconstriction was also observed in control, non-manipulated vessels, suggesting a neural reflex.
- Phentolamine and bretylium effectively counteracted vasoconstriction at the stenosis level, while yohimbine had a partial effect. Propranolol followed by phentolamine indicated a peripheral beta-mediated dilatation.
Conclusions:
- Post-PTCA vasoconstriction is primarily mediated by alpha-adrenergic receptors, predominantly alpha-1.
- The sympathetic nervous system plays a significant role, evidenced by vasoconstriction in control vessels.
- Pharmacological blockade with alpha-adrenergic agents can reverse post-PTCA vasoconstriction.
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.