JACC Vol . IN. Nn . JSeptember 1991 :6716

Editorial Comment

Prognostic Implications of LesionIrregularitf - onCoronary Angiography*JOHN A. AMBROSE, MD, FACCNew York, New York

The complex coronary plaque . Qualitative analysis oflesion morphology on angiography has generated consider-able interest over the past few years (1-3) . Significant lesions(<100% occlusion) with irregular borders, overhangingedges or intraluminal filling defects are strongly associatedwith the presence of the acute coronary syndrome of eitherunstable angina or acute myocardial infarction. Such "cul-prit" lesions are found in approximately 70% of patients witheither diagnosis, but they are seen infrequently (10% to 20%)in patients with stable angina and no prior history of an acutecoronary syndrome .

Although these complex plaques are associated with anacute syndrome, is there any prognostic information that canbe derived from their presence? Limited information isavailable suggesting that lesion irregularity or the presenceof filling defects is associated with persistence of symptomsor an adverse in-hospital clinical outcome in unstable angina(4-6) . However, because it is customary in unstable anginato intervene with coronary angioplasty or bypass surgerywhen significant disease is demonstrated, the natural historyof these lesions is largely undetermined . An increased inci-dence of myocardial infarction has also been found onfollow-up in patients with irregular lesions independent ofthe initial clinical presentation (7) .

The present study. In this issue of the Journal, Davies etat . (8) report on the effect of lesion irregularity on prognosisin another subset of patients with an acute coronary syn-drome. Seventy-two patients undergoing thrombolysis withstreptokinase for evolving acute myocardial infarction un-derwent elective cardiac catheterization I to 8 days later .Lesion irregularity as quantified by a plaque ulceration indexwas related to the subsequent in-hospital clinical course. Inthe 10 days after angiography, 15 patients with clinicalinstability had a plaque ulceration index of 6 .7 (medianvalue) compared with an index of 3 .3 in those with a stablecourse (p < 0.001). Although these data are of potentially

'Editorialspublished in tuurnnt ftirAmerkueCulleyeofCardin(oyredect the views of the authors and do not neces,arily represent the views of1ACC or the American College of Cardiology .

From the Department of Medicine, Division of Cardiology. Mount SinaiMedical Center. New York . New Fur k .

Address for reprints: John A . Ambro,e . MD. Box 1030. Mount SinaiMedical Center, One Gustave L . Levy Place . New York. New York 10029 .

1,1991 by the American College of Cariiulupy

great importance, several questions are not answered in theMethods and Results . This missing information . in myopinion • clouds interpretation of their conciasions.

1 . Patient selection. Patients underwent crtheterizationI w 8 days after receiving intravenous streptokinase . All

patients received intravenous heparin for 4 to I I days afterthrombolysis . This period may have allowed time for remod-eling of lesions in those patients undergoing angiography lateafter i nfarction. as these same authors (9) reported in a priorstudy of the same patients . The amount of acute intracoro-nary thrombus formation is presumably larger in patientswith acute myocardial infarction titan in meat paticr •. :, withunstable angina (10). Therefore, the remodeling process inpatients w+ ;i complex lesions is likely to be more extensiveafter infarction than in unstable angina . It would have beenpreferable to study all patients early and at a set intervalafter myocardial infarction to study the relation betweenlesion irregularity and clinical instability . Additionally, weare not told what medical therapy patients received (otherthan heparin) after thrombolysis . The absence of aspirin inmost patients may also have affected the incidence of clinicalinstability caused by reocclusion as reported in ISIS 11 (I1) .

2 . Time coarse of elittical instability. Davies et al . (81 dor. it tell us when instability occurred after thrombolysis orwhether patients with clinical instability underwent angiog-raphy earlier after thrombolysis than did patients with aclinically stable course . Furthermore, although we are toldthat all patients underwent catheterization electively, it isunknown whether any had recurrent pain after thrombolysisbut before angiography and whether the 24% of patients withan occluded infarct-related artery on angiography were inarv way clinically different from patients without totalocclusion . Sixty percent of patients in the clinically stablegroup required angioplasty or coronary bypass surgery atfollow-up . As the timing and indications for revasculariza-

tion were not given for patients in the stable group it isunknown whether these factors might have changed therelation between lesion irregularity and in-hospital clinicalinstability . For example, if a large group of patients whowere clinically stable were readmitted soon after hospitaldischarge with recurrent unstable angina or disabling pain,the relation between lesion irregularity and in-hospital insta-bility might be of only marginal clinical significance .

3 . Percent diameter stenosis u-us greater in patients oititclinical instability than in patients whose corlditioo remainedstable. This finding approached significance (p = 0 .05) and

may have been responsible, at least in part, for the pourerin-hospital course of these patients . Because lesions areoften translucent after thrombolysis, a more quantitativeapproach . utilizing videodensitometry, for example- mayhave been more appropriate than the method used by Davieset al . (8) . Flow characteristics distal to the stenosis were alsonot reported . Thrombolysis in Mv:reardial Infarction (TIMI)flow class after thrombolysis '-as been shown to correlatewith subsequent in-hospital survival after myocardial infarc-

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lion. Patients with a TIMI flow class of 3 90 min afterthrombolysis had a better survival rate than did patients withlower TIMI flow classes (12,13) .

Clinical relevance. These objections represent specula-tion on my part and should not overshadow the fact thatDavies et al . (8) found a strong relation between qualitativemorphology and subsequent in-hospital outcome in thisgroup of patients. For those who insist on a quantitativemeasure of irregularity, this index, as modified by theauthors from Wilson et al. (14), can be easily applied andmay distinguish patient groups better than subjective in-dexes of lesion irregularity. Because many lesions classifiedas complex do not necessarily contain an ulceration, lesionswith a high plaque ulceration index require further study toassess their potential for causing continued clinical instabil-ity . It has been our experience that these ulcerated lesionsare found more commonly after myocardial infarction thanafter unstable angina. Perhaps these lesions represent trueulceration or fissuring of plaques rather than residual throm-bus, Additional studies should be performed with appropri-ate methodology to assess this finding . If further data cor-roborate the conclusions of the present study, it wouldsupport the use of angiography routinely in the assessmentof patients after thrombolysis for acute myocardial infarc-tion .

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2. Cowley MJ . DiSciascio G, Rehr RB, Vetrovee GW. Angiographic obser-

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