Recurrence after coronary angioplasty

Abstract

Recurrence (restenosis) after coronary angioplasty has undermined the initial success of the procedure and has compromised, to some extent, the attractiveness of the technique in the treatment of ischemic heart disease. Assessment of recurrence predictors has been problematic due to lack of coordination of angioplasty recurrence research and includes: incomplete angiographic documentation, variations in definitions of restenosis anatomically and the results of restenosis physiologically (ie, myocardial ischemia), the dirth of morphologic specifications of subsets under investigation and late outcome pathology, limitations in statistical analyses used, and minimal efforts to classify the available data on recurrence. A review of the literature suggests that all findings regarding recurrence after angioplasty can be organized in four categories: (1) clinical, (2) morphologic, (3) technical (or procedural), and (4) pharmacologic. The reported findings with high concordance as risk factors for recurrence after angioplasty include the clinical factors of diabetes mellitus, hyperlipidemia, and angina of short duration or unstable presentation. Morphologic factors which have been corroborated vis‐à‐vis recurrence include stenoses with diameter reduction of greater than 90% before and greater than 30% after angioplasty, residual trans‐stenotic pressure gradients of greater than 20 mmHg after angioplasty, and lesions that are diffuse, long, eccentric, or calcified. Technical factors associated with recurrence include lower balloon/vessel (or graft) ratios and the absence of (uncomplicated) “intimal dissection.” The category most deficient in research regarding recurrence after angioplasty is pharmacologic. Since there are statistically documented and reproducible factors predictive of restenosis, to ignore or minimize these findings or resist further evaluation (because of the ease and safety of performing repeat angioplasty) is to deny the opportunity to understand the mechanisms and favorably affect the incidence of recurrence. This review concludes with two major implications of the restenosis research: (1) certain clinical, technical, and pharmacologic factors, if addressed, may predictably decrease the rate of restenosis and (2) certain clinical and morphologic factors may increase the risk of restenosis; these factors may be less readily modified (eg, diabetes, lesion calcification) and thus must be considered in the decision for angioplasty. Finally, this review recommends that there be more effective coordination of angioplasty recurrence research with agreement on a single anatomic definition of restenosis with consistent physiologic correlatives, more lucid statistical presentation and improved efforts to clarify and organize the information so that meaningful conclusions regarding the causes (and therefore the prevention) of recurrence may be achieved.