Nicardipine and adenosine "flush cocktail" to prevent no-reflow during rotational atherectomy

Rotational atherectomy (RA) has a unique mechanism of action-it utilizes plaque abrasion with microparticle embolization in order to achieve luminal enlargement. This microscopic atheroembolic debris can lead to platelet activation, with vasoconstriction and/or mechanical obstruction of distal coronary resistance vessels, leading to no-reflow and myocardial necrosis.

We developed a prospective registry to evaluate the efficacy of the prophylactic administration of intracoronary nicardipine and adenosine within the RA "flush cocktail" as a method of preventing no-reflow and non-Q-wave myocardial infarction (MI) in patients treated with RA in their native coronary arteries.

One hundred seventy-six consecutive patients (204 lesions; mean age, 66+/-12 years) were treated with a flush cocktail containing nicardipine (10 microg/ml), adenosine (5 microg/ml), nitroglycerin (10 microg/ml), and unfractionated heparin (1 IU/ml) during RA. The primary study end points were postprocedural Thrombolysis in Myocardial Infarction (TIMI) flow score and non-Q-wave MI, as determined by creatine phosphokinase (CPK) and creatine phosphokinase-MB (CPK-MB) levels. Secondary end points included baseline and acute final minimum lumen diameters, and percent diameter stenosis.

TIMI flow scores were analyzable in 155 of 176 patients (88%), and in 181 of 204 treated vessels/lesions (88.7%). As compared to baseline, the final TIMI score worsened in 4 patients (2%), was unchanged in 121 patients (78%), and improved in 30 patients (19%). One hundred fifty of 155 patients (96.7%), and 175 of 181 treated vessels (96.6%) had TIMI 3 flow at the completion of the procedure. Excluding those patients with elevated baseline CPK values of >190 IU/l (n=7), only 5 of 176 (2.8%) patients had CPK-MB values more than three times the upper limit of normal at 12-18 h postprocedure. There were no in-hospital Q-wave MIs or deaths.

An intracoronary flush cocktail containing a combination of two potent arteriolar vasodilators, nicardipine and adenosine, appears to be a safe and effective regimen for minimizing no-reflow events and periprocedural myonecrosis during RA.