Abstract
The major limitation of the long term success of percutaneous transluminal coronary angioplasty (PTCA) is still restenosis and is a complex process that is only partially understood [1, 2]. Histologic studies of coronary arteries after dilation, obtained by either autopsy or atherectomy, have provided evidence that strongly supports the concept of intimal hyperplasia or proliferation of smooth muscle cells, with abundant matrix production, of medial or intimai origin as the underlying cause of luminal narrowing after angioplasty [3–5]. Pharmacological agents aimed at reducing the absolute amount of intimai hyperplasia are currently being investigated in many clinical trials. In these trials it is presumed that the clinical outcome is related to an anatomical substrate, i.e. the prevention or reduction of reactive intimai hyperplasia after angioplasty. If restenosis is viewed as an intraluminal growth process after a successful angioplasty, risk factors for restenosis should be risk factors for this growth process. The angiographically determined change in lumen diameter at follow-up is currently the only reliable indicator of the amount of reactive hyperplasia applicable to large study populations. Quantitative coronary analysis is the most reliable available method of assessing coronary arterial luminal changes over time and has demonstrated that the change in minimal luminal diameter between post-PTCA and follow-up angiography is the most non-ambiguous measurement to describe the continuous process of restenosis at present time [6–9].
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Hermans, W.R.M., Rensing, B.J., Serruys, P.W. (1994). Quantitative coronary angiography in the assessment of risk factors for luminal renarrowing. In: Serruys, P.W., Foley, D.P., De Feyter, P.J. (eds) Quantitative Coronary Angiography in Clinical Practice. Developments in Cardiovascular Medicine, vol 145. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-8358-9_27
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DOI: https://doi.org/10.1007/978-94-015-8358-9_27
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