Restenosis after percutaneous transluminal coronary angioplasty

Percutaneous transluminal coronary angioplasty (PTCA) is now practised worldwide and ottered to patients as a viable alternative to coronary artery bypass graft surgery or pharmacological therapy. However, despite its undoubted popularity, there is still a substantial amount of mystery surrounding this treatment modality. Firstly, we really don't know how it 'works' or, why it 'works' in some patients and not in others; secondly, we're not quite certain how to describe the impact ot treatment with PTCA on the beneficiary insert; by the effect on the lesion itself as measured by coronary angiography, or by the effect on coronary blood flow, which is also measurable by various techniques, or by the effect on myocardial perfusion which can also be 'objectively assessed', or indeed, by its impact on the well-being of the patient, which cannot actually be measured, but is the primary aim of the treatment as offered to the patient - since there is no evidence supporting a beneficial effect for PTCA on longevity (unlike CABG in certain patient subgroups). Thirdly, similar difficulties exist regarding the assessment of the long-term benefit of PTCA, which are further compounded by the variable response, over time, of the vessel wall to balloon dilatation, a process known as 'restenosis', or the 'Achilles heel'. The main difficulties in this area are that: a) the pathology of the process is poorly understood, and much mystery and doubt still lingers, b) there is no universal agreement on how to define 'restenosis', c) although angiography appears to be the best widely available descriptive technique, many investigators continue to use antiquated analysis methodology, the inaccuracy of which has been frequently and conclusively demonstrated. Fourthly, the introduction of new devices, instead of bringing answers or solutions, has further compounded the problem, by thus far failing to reduce restenosis, while increasing the armimentarium, and therefore, 'the doctor's dilemma'. In this treatise we present the pathological theory of restenosis and its clinical correlations, we identify the difficulties in its assessment, and propose our solution to this significant aspect of the problem. We provide an extensive summary of pharmacological attempts to prevent restenosis, a description of the new devices and their potential role, as well as a thought for the future.