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Circulation. 1998;98:1824-1827

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(Circulation. 1998;98:1824-1827.)
© 1998 American Heart Association, Inc.


Correspondence

Natural History of Infarct-Related Lesions

Fernando Alfonso, MD, PhD, FESC

Cardiopulmonary Department Hospital Universitario, San Carlos, Madrid, Spain

To the Editor:

We read with great interest the elegant study of Van Belle et al1 describing the natural history of the infarct-related lesion using coronary angioscopy. They found that most patients had yellow plaques (79%) and thrombus (77%) without appreciable changes in these features according to the elapsed time from the infarction. They concluded that infarct-related lesions require more than a month to heal, or in other words, that during this time most patients still have unstable plaques. They further suggested that these findings could explain the unique, untoward behavior of recently infarcted lesions either spontaneously or after percutaneous treatment. We wish to draw attention to some methodological aspects of their report. First, the true "natural history" of the pathological substrate of the infarct-related lesion would require serial angioscopic examinations (with each patient being his/her own control), with the obvious ethical implications. Alternatively, a much larger cohort of patients would have been required to derive definitive insights about the potential influence of the elapsed time from the infarction on the angioscopic data. Second, only 7% of the patients had postinfarction angina, and no information was provided concerning other clues for ischemia. Therefore, most patients underwent the procedure on anatomic grounds alone. In this context, the reasons to perform cardiac catheterization early or late (24 hours to 4 weeks) after infarction could imply a selection bias that may have influenced the results. Finally, any explanation for the "unique adverse behavior" of the infarct-related lesions will necessarily require that the angioscopic features of these patients are different from those of other patients with unstable angina and a more benign course. Furthermore, a control group seems especially necessary when the reported incidence of yellow plaque and thrombus was rather similar to that found in other patients with unstable angina.2 3

In a previous study,4 we analyzed the angioscopic characteristics of patients with recurrent ischemia (24 hours to 4 weeks) after infarction. Compared with other patients with unstable angina (but without previous infarction), patients with postinfarction ischemia had similar plaque characteristics (yellow plaque 80% versus 84%) but a higher incidence of associated thrombi (95% versus 68%), mainly at the expense of protruding occlusive thrombi. Although the simplified angioscopic classification used in the 2 studies was slightly different, it is of interest that the results of Van Belle et al1 fall in the middle of our 2 groups of patients.4 This further corroborates the suggestion4 that the presence of a red thrombus (mainly if occlusive) plays a significant pathogenic role in the recurrence of ischemia after myocardial infarction.

References

  1. Van Belle E, Lablanche J-M, Bauters C, Renaud N, McFadden EP, Bertrand ME. Coronary angioscopic findings in the infarct-related vessel within 1 month of acute myocardial infarction: natural history and the effect of thrombolysis. Circulation. 1998;97:26–33.
  2. Alfonso F, Goicolea J, Hernandez R, Goncalves M, Segovia J, Bañuelos C, Zarco P, Macaya C. Angioscopic findings of coronary angioplasty of coronary occlusions. J Am Coll Cardiol. 1995;26:135–141.
  3. deFeyter PJ, Ozaki P, Baptista J, Escaned J, Dimario C, deJaegere PPT, Serruys PW, Roelandt JR. Ischemia-related lesion characteristics in patients with stable and unstable angina: a study with intracoronary angioscopy and ultrasound. Circulation. 1995;92:1408–1413.
  4. Alfonso F, Segovia J, Goicolea J, Hernandez R, Fernandez-Ortiz A, Bañuelos C, Macaya C. Angioscopic characteristics of coronary narrowing in patients with recurrent myocardial ischemia after myocardial infarction. Am J Cardiol. 1997;79:1394–1396.

Response

Eric Van Belle, MD, PhD; Jean-Marc Lablanche, MD; Christophe Bauters, MD; Nathalie Renaud, MD; Eugène P. McFadden, MRCPI; ; Michel E. Bertrand, MD

Service de Cardiologie B et Hémodynamique, Hôpital Cardiologique, Lille, France

We welcome the opportunity to respond to the letter of Dr Alfonso regarding our recent article, in which we showed that the majority of infarct-related lesions had angioscopic evidence of instability even when studied 1 month after myocardial infarction.1

We agree with Dr Alfonso that the ideal approach to determine the "natural history" of the infarct-related lesion would be to perform serial angioscopic studies in a cohort of patients. However, as he points out, this would be difficult to justify on ethical grounds.

Second, as we stated in our article, our institutional policy during the period of the study was to perform diagnostic catheterization after myocardial infarction and to perform ad hoc angioplasty in those patients with suitable anatomy. The findings of our study in such unselected patients cannot therefore be extrapolated to a population in whom the indications for angiography are more restrictive. However, we do not believe that the timing of angiography had a significant influence on our findings, because the major message of the article was that even when angioscopy was performed 1 month after infarction, there was a high incidence of angioscopic "instability."

Finally, we agree that the presence of protruding red thrombi seems to be an important indicator of plaque instability, as suggested by the study performed by Dr Alfonso et al.2 In fact, in a previous study,3 we showed that the presence of protruding thrombi was a powerful predictor of late vessel occlusion after balloon angioplasty. The results of our study, which demonstrates a high prevalence of thrombus even in asymptomatic patients after myocardial infarction, extends the work of Dr Alfonso by demonstrating that clinical stability in the postinfarction patient does not necessarily imply plaque stability.

The results of Dr Alfonso's study in conjunction with our article emphasize the need for further research into the factors that influence plaque instability, both in patients with unstable angina and in those who have suffered a myocardial infarction.

References

  1. Van Belle E, Lablanche JM, Bauters C, Renaud N, McFadden EP, Bertrand ME. Coronary angioscopic findings in the infarct-related vessel within 1 month of acute myocardial infarction: natural history and the effect of thrombolysis. Circulation. 1998;97:26–33.
  2. Alfonso F, Segovia J, Goicolea J, Hernandez R, Fernandez-Ortiz A, Banuelos C, Macaya C. Angioscopic characteristics of coronary narrowing in patients with recurrent myocardial ischemia after myocardial infarction. Am J Cardiol. 1997;79:1394–1396.
  3. Bauters C, Lablanche JM, McFadden EP, Hamon M, Bertrand ME. Relation of coronary angioscopic findings at coronary angioplasty to angiographic restenosis. Circulation. 1995;92:2473–2479.




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