Editorial Comment

How Did We Get Here FromThere?

David R. Holmes, Jr., MD

Adult Cardiac Catheterization Laboratory,Mayo Clinic,Rochester, Minnesota

Occlusive coronary lesions remain a multifacetedproblem for interventional cardiology with implicationsfor both etiologic mechanisms as well as treatment strat-egies. Interventional cardiology has learned a great dealabout specific types of occlusions, including acute coro-nary occlusions in the setting of ST segment elevationmyocardial infarction, chronic total occlusions, and de-layed subacute closure. In acute coronary syndromes,there is typically a significant thrombotic burden with aruptured or eroded plaque. In this setting, the underlyingcoronary stenosis may not be severe. These lesions aretypically soft, have the potential to embolize, but can bewell treated with percutaneous techniques. Chronic totalocclusions, on the other hand, present very differentproblems. Typically, they are hard and fibrotic with littlefresh or organized thrombus. We know from multipleseries that the success rates in these chronic total lesionsare limited, mainly due to failure to cross with a guide-wire even using advanced interventional techniques. Inaddition, in this group, unless a stent can be placed,restenosis rates are very high. A final group of occlusionsare those that are delayed subacute closure either early orlate after stent implantation. Patients with this syndrometend to present acutely ill and have a high incidence ofthe combined endpoint of death and myocardial infarc-tion. These lesions typically are soft and thrombotic.

There is a fourth group of occlusions about which weknow relatively little and these form the basis of thiscurrent study by Shah et al., namely, the phenomenon oflate total occlusion following coronary stent implanta-tion. The etiology of this finding could be delayed sub-acute closure, a progressive neointimal hyperplasia lead-ing to the obliteration of the lumen, or a combinationwith some in-stent restenosis and then a small amount ofthrombotic occlusion after collaterals have had a chanceto develop. Sorting out which specific mechanism isinvolved may be difficult, but it has important implica-tions. During the FDA review of vascular brachytherapy,a number of late occlusions were noted during follow-up

angiography. Depending on how they were adjudicated,the incidence of the discrete endpoint varied, and theinterpretation of the effects of the index treatment pro-cedure also could have varied. For example, if all latetotal occlusions were secondary to neointimal hyperpla-sia, then changes in adjunctive antithrombotic therapymay not help. Alternatively, if all late total occlusionswere secondary to a thrombotic event, then intensiveefforts should be made to prevent that.

What have we learned from the preceding article [1]?One, the incidence of late total occlusion is low; in this

series, 1.6%. Admittedly, the angiographic follow-uprate was only 71%, so this figure may be an underesti-mate.

Two, there is still confusion about terms and etiology.For example, the authors used the phrase “angiogramsobtained between 15 days and 6 months postprocedurethat showed restenosis.” An angiogram at 15 days withsignificant narrowing or occlusion would typically have adifferent etiology than one at 6 months and is more likelyrelated to occlusive thrombotic thrombus formationrather than neointimal hyperplasia.

Three, these patients do not present like those withdelayed subacute closure, in which the majority of pa-tients develop death or myocardial infarction. In contrast,in this series, 40% of patients were asymptomatic, 46%had recent exertional symptoms only, and only 13.3%presented with unstable angina but no ST segment myo-cardial infarction. This observation lends credence to thehypothesis that the process includes progressive neointi-mal hyperplasia alone or with a smaller amount of throm-bus formation but not sudden thrombotic occlusion.

Four, although a variety of models were tested in thisstudy, there were only 15 patients to begin with; accord-ingly, the ability to construct relevant accurate modelswith such a small number should be and is limited.Despite this limitation, it makes some intuitive sense thathigher plaque burden, smaller vessels, prior neointimalhyperplasia, and longer stents would be associated with amore progressive subsequent course.

How then did we get here, to the finding of late totalocclusion, from there, where we started with a superb

Recieved 00 Month 2003; Revision accepted 00 Month 2003

DOI 10.1002/ccd.10672Published online in Wiley InterScience (www.interscience.wiley.com).

Catheterization and Cardiovascular Interventions 60:352–353 (2003)

© 2003 Wiley-Liss, Inc.

initial result? It seems most likely that a larger amount ofthis journey is related to progressive neointimal hyper-plasia with some smaller contribution of thrombus. For-tunately, it remains uncommon.

REFERENCE

1. Shah P, Cutlip D, Popma J, Kuntz R, Ho K. Incidence and predic-tors of late total occlusion following coronary stenting. CatheterCardiovasc Interv 2003;60:344–351.

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