Intracoronary Adenosine Administered During Rotational Atherectomy of Complex Lesions in Native Coronary Arteries Reduces the Incidence of No-Reflow Phenomenon George P. Hanna, MD, Peter Yhip, MD, Ken Fujise, MD, George W. Schroth, MD, Oscar R. Rosales, MD, H. Vernon Anderson, MD, and Richard W. Smalling,* MD, PhD Rotational atherectomy (RA) of complex, calcified lesions has been associated with a high incidence of no reflow ranging from 6%–15% and concomitant myocardial necrosis with adverse prognostic implications. There are no uniform strategies for preventing this complication. The role of intracoronary adenosine for the prevention of this phenomenon during RA has not been fully evaluated. We studied the procedural outcome of 122 patients who underwent RA of complex native coronary artery lesions. Fifty-two patients received no adenosine but a variety of other agents. Seventy patients received intracoro- nary adenosine boluses (24 to 48 g prior to and after each RA run). There was no difference in the type of lesion studied, run time, or Burr to artery ratio (0.6–0.7) between the two groups. Six patients without adenosine experienced no reflow (11.6%), with resultant infarction in the target artery territory, while only 1 of 70 patients (1.4%, P 0.023) in the adenosine group experienced no reflow. No untoward complications were observed during adenosine infusion. Intracoronary adenosine bolus administered during rotational atherectomy is easy, safe, and may significantly reduce the incidence of no reflow, which may improve the 30-day outcome of this procedure. Cathet. Cardiovasc. Intervent. 48:275–278, 1999. 1999 Wiley-Liss, Inc. Key words: rotational atherectomy; no reflow; adenosine INTRODUCTION Since the initial observations made in experimental animal models of acute myocardial infarction in the early seventies [1,2], the concept of no flow/slow flow remains a mystery that haunts clinical cardiologists in general and interventional cardiologists, in particular with its adverse prognostic implications. No-reflow has been shown to complicate management of patients presenting with acute myocardial infarction who receive thrombolytic therapy or undergo percutaneous revascularization [3–5]. This phenomenon manifests as reduced coronary flow (TIMI 1) as detected by angiography without concomi- tant target artery dissection, spasm, thrombus formation, or severe residual stenosis obstructing coronary flow. Many theories have been proposed to delineate the underly- ing pathophysiology culminating in this phenomenon; how- ever, these theories remain speculative and the culprit mecha- nisms obscure. Nonetheless, potential etiologies may include vasospasm, free-radical–induced endothelial dysfunction, macro- and microdebris/thrombus distal embolization, capil- lary plugging by erythrocytes and neutrophils, and cellu- lar edema with intramural hemorrhage [1,2]. Rotational atherectomy is a safe and effective percuta- neous technique utilized in the treatment of calcified and fibrotic lesions either for debulking or as a primary therapy. Quantitative angiographic analysis demonstrated that RA achieved lumen diameter that was 90% of the selected burr size [6]. Some have suggested that lumen diameter may even increase further in the following 24 hr, likely due to release of vasospam or elastic recoil [7]. Although safe and efficacious, RA has been associated with higher rates of no flow/slow flow than other coronary revascularization devices. Safian et al. [6] reported no-reflow rate of 6.1% while Ellis et al. [8] reported slow flow rate of 9.1%. The clinical sequelae of this event may encompass a wide spectrum of ischemic complications from conduction disturbances, hypoten- sion, myocardial infarction, cardiogenic shock, and death Department of Medicine, Division of Cardiology, University of Texas Medical School and Hermann Hospital, Houston, Texas *Correspondence to: Dr. Richard W. Smalling, 6431 Fannin, MSB 1.246, Houston, TX 77030. Received 10 June 1998; Revision accepted 27 April 1999 Catheterization and Cardiovascular Interventions 48:275–278 (1999) 1999 Wiley-Liss, Inc.