Editorial Comment

No-Reflow? No Way!

Joel K. Kahn, MD

William Beaumont Hospital,Royal Oak, Michigan

There are few things in the catheterization laboratoryas enjoyable to an interventional cardiologist as watchingthe effects of initial balloon inflations on an acutelyoccluded coronary vessel in the setting of a myocardialinfarction. The restoration of blood flow where previ-ously there had been none, the lessening and resolutionof ischemic pain, and the normalization of elevated STsegments provide a satisfaction that makes the late-nightdrive to the hospital and the disturbed sleep worthwhile.The opportunity to restudy a patient with a previouslyakinetic myocardial region during acute infarction andview the return of regional function to nearly normal isanother pleasing moment. Harmony has returned to asystem temporarily out of balance.

Alas, not every story has a happy ending and not everyinfarct intervention follows the script outlined above. Thedevelopment of the no-reflow phenomenon in a substantialnumber of infarct procedures has challenged our focus onepicardial revascularization as the sole endpoint of infarctwork. The endpoint is shifting to strategies that return thecoronary microcirculation to normal and provide maximumsalvage of ischemic myocardium. Whether no-reflow is dueto microparticulate debris, vasoconstriction, endothelialdamage, myocardial edema, or combinations of these pro-posed pathways, it throws a monkey wrench in the efforts ofthe coronary interventionalist and exposes the patient to ahigher risk of complications.

Over the years, a number of measures have been tried totreat or prevent no-reflow in the setting of acute infarctintervention. Nitroglycerin and more recently verapamil-administered intracoronary have been associated with im-proved blood flow in a number of patients but not all.Intra-aortic balloon counterpulsation has been used to im-prove coronary flow and resolve no-reflow. None of thesestrategies is highly effective and none has been shown toprevent the development of a no-reflow situation consis-tently. Therefore, the report of Assali et al. on the use inintracoronary adenosine during acute infarct revasculariza-tion to prevent the no-reflow phenomenon is welcome.Recognizing the obvious limitations of a retrospective da-tabase analysis, the group in Houston reports that adenosine

administered before and after balloon inflations reduced thedevelopment of no-reflow from 29% to 6% and was asso-ciated with fewer complications. Adenosine was given as aslow infusion through either the guide catheter or the bal-loon lumen with the guidewire removed.

There were some differences between the group thatreceived adenosine compared with the no-adenosine group.There were a higher percentage of shock patients, lowejection fractions, and anterior infarctions in the group notreceiving adenosine. The authors did not comment on thepossible reasons for these differences. I wonder if thesepotentially sicker patients had adenosine withheld for fearof hypotension or transient heart block. The authors did notmention any complications from adenosine, nor did theyprovide any guidelines for which patients might be betterserved by avoiding adenosine administration. It was notstated whether temporary pacemakers were in place andused in any cases. These questions will need to be answeredbefore broader application of adenosine during acute myo-cardial infarction can be endorsed.

Assali et al. further report that the ejection fraction in thegroup treated with adenosine was higher than that of theno-adenosine group. We do not know if the ejection fractiondata were available for all patients or not. We do not knowif the ejection fractions were evaluated before or after cor-onary revascularization and whether they were assessed inthe catheterization laboratory or later in the hospital stay.These issues aside, it is exciting to wonder if the goal ofpreserving greater amounts of jeopardized myocardium inacute infarction is obtainable with adenosine.

A final consideration is whether adenosine is an effec-tive therapy once the no-reflow phenomenon has devel-oped. Assali et al. administered adenosine before ballooninflations. More data will be needed know whether it isnecessary to administer adenosine as a prevention for allpatients or whether it can be reserved for those in whomthe no-reflow phenomenon develops.

Much work needs to be done before adenosine can beconsidered ready for routine use in infarct angioplastyprocedures. An ongoing randomized double-blind trial ofintravenous adenosine as an adjunct for acute infarctartery revascularization is underway in many centers. Fornow, we have an additional tool in our therapeutic arma-mentarium to consider when we observe no-reflow.Hopefully in a short while we can say, “No-reflow, noway!” and make greater strides toward uniform and op-timal normalization of myocardial blood flow and tissuesalvage in infarct angioplasty patients.

Catheterization and Cardiovascular Interventions 51:32 (2000)

© 2000 Wiley-Liss, Inc.