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  • Review Article
  • Published:

Restenosis after PCI. Part 1: pathophysiology and risk factors

Abstract

Restenosis is a complex disease for which the pathophysiological mechanisms have not yet been fully elucidated, but are thought to include inflammation, proliferation, and matrix remodeling. Over the years, many predictive clinical, biological, (epi)genetic, lesion-related, and procedural risk factors for restenosis have been identified. These factors are not only useful in risk stratification of patients, they also contribute to our understanding of this condition. Furthermore, these factors provide evidence on which to base treatment tailored to the individual and aid in the development of novel therapeutic modalities. In this Review, we will evaluate the available evidence on the pathophysiological mechanisms of restenosis and provide an overview of the various risk factors, together with the possible clinical application of this knowledge.

Key Points

  • Restenosis is a complex disease for which the causative mechanisms have not yet been fully identified

  • Diabetes mellitus is the most consistently reported clinical parameter increasing the risk of restenosis

  • The inflammatory response evoked by vascular damage during angioplasty is thought to be the main contributor to the development of restenosis

  • Some patients seem to have an inherent predisposition toward developing restenosis, which can be partly explained by their specific genetic background

  • Risk models including clinical, procedural, and biological factors are likely to be the best method of implementing available evidence for risk prediction and patient stratification

  • An improved understanding of the mechanisms of restenosis is important for risk stratification of patients and for identifying new and optimal targets for therapy

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Figure 1: Factors involved in the development of restenosis.
Figure 2: Mechanisms of restenosis.

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Acknowledgements

J. W. Jukema has received funding from the European Union Seventh Framework Program (FP7/2007-2013) under grant agreement number HEALTH-F2-2009-223,004 and he is supported by grants from the Interuniversity Cardiology Institute of the Netherlands (ICIN) and the Durrer Center for Cardiogenetic Research both Institutes of the Netherlands Royal Academy of Arts and Sciences (KNAW), the Netherlands Heart Foundation, the Center for Medical Systems Biology (CMSB), a center of excellence approved by the Netherlands Genomics Initiative/Netherlands Organization for Scientific Research (NWO), the Netherlands Consortium for Healthy Ageing (NCHA). T. A. N. Ahmed would like to thank the Egyptian Ministry of Higher Education and Asyut University for financially supporting him during his research and clinical fellowship in the Netherlands. P. H. A. Quax is an established investigator of the Netherlands Heart Foundation (M93-001). The funders had no role in the preparation of, or decision to publish, the manuscript.

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J. W. Jukema, T. A. N. Ahmed and J. J. W. Verschuren researched data for and wrote the article. All authors contributed to the discussion of content. J. W. Jukema, J. J. W. Verschuren and P. H. A. Quax reviewed/edited the article before submission. J. W. Jukema and J. J. W. Verschuren contributed equally to this paper.

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Correspondence to J. Wouter Jukema.

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Jukema, J., Verschuren, J., Ahmed, T. et al. Restenosis after PCI. Part 1: pathophysiology and risk factors. Nat Rev Cardiol 9, 53–62 (2012). https://doi.org/10.1038/nrcardio.2011.132

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