Distal myocardial protection with intracoronary beta blocker when added to a Gp IIb/IIIa platelet receptor blocker during percutaneous coronary intervention improves clinical outcome.
OBJECTIVE
The present study tested the hypothesis that intracoronary (IC) propranolol improves clinical outcomes with percutaneous coronary intervention (PCI) when used with background Gp IIb/IIIa receptor blockade.


BACKGROUND
We have previously shown that administration of a relatively large weight-based IC dose of the beta blocker propranolol before PCI decreases the incidence of post-PCI myocardial infarction (MI) and improves short- and long-term outcome. It has previously been shown that administration of a Gp IIb/IIIa receptor blocker decreases post-PCI MI and improves short- and long-term clinical outcome.


METHODS
Patients undergoing PCI (n = 400) were randomized in a prospective double-blind fashion to IC propranolol (n = 200) or placebo (n = 200) with eptifibatide administered to all the patients. Myocardial isoform of creatine kinase was measured during the first 24 hr and clinical outcomes at 30 days and 1 year.


RESULTS
MI after PCI was seen in 21.5% of placebo and 12.5% of propranolol patients (relative risk reduction 0.42; 95%CI 0.09, 0.63; P = 0.016). At 30 days, the composite end point of death, post-procedural MI, urgent target lesion revascularization, or MI after index hospitalization occurred in 22.5% of placebo vs. 13.5% of propranolol patients (risk reduction 0.43; 95%CI 0.08, 0.65; P = 0.018). Similar results were observed at 1 year with adverse outcomes in 21.5% of propranolol and 32.5% of placebo patients (P = 0.01).


CONCLUSIONS
IC propranolol administration with the background Gp IIb/IIIa receptor blockade significantly reduces the incidence of post-PCI MI and improves the short- and long-term clinical outcome when compared with a Gp IIb/IIIa blocker alone.
Uretsky
Barry F
BF
Division of Cardiology, University of Texas Medical Branch at Galveston, Texas, USA. buretsky@sparks.org
Birnbaum
Yochai
Y
Osman
Abdulfatah
A
Gupta
Rajiv
R
Paniagua
Oscar
O
Chamoun
Antonio
A
Pohwani
Amir
A
Lui
Charles
C
Lev
Eli
E
McGehee
Todd
T
Kumar
Darren
D
Akhtar
Asif
A
Anzuini
Angelo
A
Schwarz
Ernst R
ER
Wang
Fen Wei
FW
D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage*; D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D003324:Coronary Artery Disease / Q000401:mortality / Q000628:therapy*; D052279:Creatine Kinase, MB Form / Q000097:blood; D004311:Double-Blind Method; D004333:Drug Administration Routes; D004359:Drug Therapy, Combination; D000077542:Eptifibatide; D005260:Female; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000201:enzymology / Q000209:etiology / Q000401:mortality / Q000517:prevention & control*; D010455:Peptides / Q000008:administration & dosage*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D011433:Propranolol / Q000008:administration & dosage*; D011446:Prospective Studies; D013997:Time Factors; D016896:Treatment Outcome
D000319:Adrenergic beta-Antagonists; D015415:Biomarkers; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D011433:Propranolol; D052279:Creatine Kinase, MB Form; D000077542:Eptifibatide