Article

Development of a Science-based Drug-eluting Balloon

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Abstract

The continuous development of medical devices, more specifically devices for interventional cardiology, ensures constant improvement in the treatment of patients with coronary artery diseases (CAD), satisfying the increasing needs and demands of patients and cardiologists. These increased demands combined with expanding regulations have created the necessity to transform standard product development into science-based, evidence-guided projects. Two newly approved drug-eluting balloon (DEB) products, Protégé and Pioneer, developed by Blue Medical, are based on such scientific evidence gathered using new, innovative methods and combining independent science data during all development phases, leading to scientifically supported improved patient care.

Disclosure:The author is an employee of Blue Medical Devices.

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Support:The publication of this article was funded by Blue Medical Devices.

Correspondence Details:Ferry van der Linde, Blue Medical Devices, Steenovenweg 19, NL-5708 HN Helmond, The Netherlands. E: ferry.vanderlinde@bluemedical.com

Copyright Statement:

The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content.

Recently, a novel type of interventional device has become available on the market: the drug-eluting balloon (DEB). The established performance of the percutaneous transluminal coronary angioplasty (PTCA) balloon catheter has been combined with the proven efficacy of antiproliferative drugs.

The usefulness of DEBs has been established,1–6 especially for treating in-stent restenosis (ISR), when compared with drug-eluting stents (DES).7 This device has the potential to be the next step in interventional cardiology and can offer better care for patients with coronary artery disease (CAD). The DEB developed by Blue Medical, Protégé, is intended for all CAD indications. The Protégé is based on evidence that also supports the idea that a DEB can be the next step in interventional cardiology, especially with the co-development of its sibling, Pioneer, a DEB with a pre-mounted bare metal cobalt chromium (CoCr) stent. The Pioneer not only enhances the potential of the DEB by combining it with a bare-metal stent (BMS) but could serve patients not suitable for DES or long-term antiplatelet therapy.

The basics required for a DEB to be effective are to deliver a reliable, reproducible and sufficient concentration of drug, in this case paclitaxel, to the arterial wall during a reasonable balloon inflation time. Short-term exposure of smooth muscle cells (SMC) to paclitaxel is effective in the inhibition of SMC proliferation.8 Axel et al. found that short exposure to paclitaxel was effective with a minimum concentration of 0.1μM.8,9

Ex Vivo Testing – Prove the Basics

Pioneer and Protégé have been tested on dose dependency, release as a function of inflation time and multiple inflations, by HemoLab at the University of Technology, Eindhoven; every group tested consisted of n=6. Tests were performed in an ex vivo set-up to simulate percutaneous coronary intervention (PCI) under normal physiological haemodynamic conditions. Arteries were obtained at a slaughterhouse from pigs that were slaughtered for consumption. Arterial segments of an approximate length of 40mm were placed in the set-up with a reservoir connected to it, with heparinised blood at 38ºC. The DEB catheter was introduced via a guiding catheter that was connected to the set-up with a connection port. Standard protocol was to soak the catheter for two minutes in the set-up before inflation of 30 seconds.

The results on the Protégé as well as Pioneer describe a dose- and time-dependent release. A nominal load (3μg/mm2 loaded balloon surface) led to average concentrations of 17.7±8.3μM and 24.7±12.7μM for the Protégé and Pioneer, respectively, for the dose-dependency study. The average load at 30 seconds inflation time for Pioneer and Protégé are 16.8±6.9μM and 26.2±12.1μM, respectively, for the time-dependency study. The concentrations found in the dose and inflation time dependency study correspond identically. In addition, results described a repeatable vessel wall dose and limited drug loss in the bloodstream.

In Vivo Porcine Model

The same ex vivo dosages were investigated in a dose-dependency study with balloon overstretch injury in a porcine model with four weeks of angiographic and histological follow-up for both Protégé and Pioneer. In addition, Pioneer was tested against the BMS Track. Track is the same stent that is crimped on the Pioneer. The Protégé and Pioneer used a balloon to artery overstretch of 1.3:1 and 1.15:1, respectively.

In Tables 1 and 2 the values are expressed in means ± standard deviation. Statistical analysis was performed with analysis of variance (ANOVA) and supplemented with t-test, where a value of p≤0.05 was considered statistically different. The dose response of Protege shows an optimum with respect to late lumen loss (LLL), per cent area stenosis and maximal neointima thickness for the nominal dose. The latter two are significantly different.

The LLL, per cent area stenosis and maximal neointima thickness of the Pioneer are significantly smaller than the BMS Track.

The re-endothelialisation was 77.8%, 88.9% and 59.3% complete for the Protege half nominal dose, nominal dose and triple nominal dose, respectively. In the case of the Pioneer the endothelialisation was 99.3%, and 99.3% for the BMS Track. The results in the porcine model indicate an optimum effect for the nominal dose with respect to LLL, neointima thickness and per cent area stenosis. In addition, the re-endothelialisation of the Pioneer was not significantly different from the BMS, suggesting fast healing of the arterial segment. In vivo results confirmed the ex vivo findings and in addition suggested a significant reduction of LLL for Pioneer compared with BMS without a difference in re-endothelialisation.

In Vivo Re-endothelialisation

From studies conducted by Joner et al. and Finn et al. it was defined that 28 days of follow-up to analyse re-endothelialisation usually shows complete re-endothelialisation.10,11 At this time-point it is thus not possible to properly discriminate between different devices. A more proper time-point would be 14 days.10,11

Furthermore, a rabbit model was chosen to better visualise the differences between the devices, since re-endothelialisation in porcine models goes faster than in a rabbit model.10 The Pioneer was tested against the BMS Track (same stent) and against Taxus Liberte and Xience V in a rabbit model (performed by CVPath Institute, Inc., Gaithersburg). The test method used was the same as described in the article by Joner et al. on re-endothelialisation of DES.10

Table 3 shows the results after 14 days of follow-up by scanning electron microscopy (SEM). The Pioneer and BMS differ significantly on re-endothelialisation compared with Xience V and Taxus Liberte, both between as well as above struts. The Pioneer and BMS do not differ significantly.

Conclusion

The Pioneer, tested in the studies described above, shows that fast re-endothelialisation is possible when drugs are used to inhibit cell proliferation. The short time that paclitaxel is present in the artery12,13 and the fact that endothelial cells start migrating from adjacent, untreated areas after a few days14,15 ensure that the treated arterial segment will be lined with endothelial cells as if it was a BMS. These findings could impact current antiplatelet therapy requirements.

In the porcine model, it is shown that Pioneer is able to significantly reduce LLL, percent area stenosis and neointima thickness compared with a BMS without negatively influencing re-endothelialisation, which is important for the healing process of the artery and reducing the risks of late thrombus.11,16 The concentrations detected in the ex vivo studies are within the therapeutic window determined by Axel et al.8 and the data generated in the porcine and rabbit models support that these concentrations are effective at reducing restenosis without limiting the re-growth of endothelial cells.

Combing science-based, independent evidence in innovative development settings will ensure tiled science support, confirming the prior development step while adding additional scientific evidence and understanding. Pioneer and Protégé are currently in human trials confirming angiographic reduced LLL at six months and early re-endothelialisation through optical coherence tomography (OCT), rounding the scientific evidence to actual patient benefit.

References

  1. Tepe G, Zeller T, Albrecht T, et al., Local delivery of paclitaxel to inhibit restenosis during angioplasty of the leg, N Engl J Med, 2008;358:689–99.
    Crossref | PubMed
  2. Unverdoben M, Vallbracht C, Cremers B, et al., Paclitaxelcoated balloon catheter versus paclitaxel-coated stent for the treatment of coronary in-stent restenosis, Circulation, 2009;119:2986–94.
    Crossref | PubMed
  3. Scheller B, PEPCAD I and PEPCAD II, Presented at: EuroPCR Barcelona, 2008.
  4. Scheller B, State of the Art Drug Coated Ballon, Presented at: Lugano MTE, Lugano, 2010.
  5. Scheller B, Hehrlein C, Bocksch W, et al., Treatment of coronary in-stent restenosis with a paclitaxel-coated balloon catheter, N Engl J Med, 2006;355:2113–24.
    Crossref | PubMed
  6. Scheller B, Speck U, Romeike B, et al., Contrast media as carriers for local drug delivery, Eur Soc Cardiol, 2002;24:1462–7.
    Crossref | PubMed
  7. Scheller B, Hehrlein C, Bocksch W, et al., Two year follow-up after treatment of coronary in-stent restenosis with a paclitaxel-coated balloon catheter, Clin Res Cardiol, 2008;97:773–81.
    Crossref | PubMed
  8. Axel DI, Kunert W, Goggelmann C, et al., Paclitaxel inhibits arterial smooth muscle cell proliferation and migration in vitro and in vivo using local drug delivery, Circulation, 1997;96(2):636–45.
    Crossref | PubMed
  9. Wiskirchen J, Schober W, Schart N, et al., The effects of paclitaxel on the three phases of restenosis: smooth muscle cell proliferation, migration, and matrix formation: an in vitro study, Invest Radiol, 2004;39(9):565–71.
    Crossref | PubMed
  10. Joner M, Nakazawa G, Finn AV, et al., Endothelial cell recovery between comparator polymer-based drug-eluting stents, J Am Coll Cardiol, 2008;52(5):333–42.
    Crossref | PubMed
  11. Finn AV, Nakazawa G, Joner M, et al., Vascular responses to drug eluting stents – importance of delayed healing, Aterioscler Thromb Vasc Biol, 2007;27:1500–10.
    Crossref | PubMed
  12. Spratlin J, Sawyer MB, Pharmacogenetics of paclitaxel metabolism, Crit Rev Oncol Hematol, 2007;61(3):222–9.
    Crossref | PubMed
  13. Farb A, Heller PF, Shroff S, et al., Pathological analysis of local delivery of paclitaxel via a polymer-coated stent, Circulation, 2001;104(4):473–9.
    Crossref | PubMed
  14. Ferns GAA, Avades TY, The mechanisms of coronary restenosis: insights from experimental models, Int J Exp Path, 2000;81:63–88.
    Crossref | PubMed
  15. Schwartz RS, Chronos NA, Virmani R, Preclinical restenosis models and drug-eluting stents: still important, still much to learn, J Am Coll Cardiol, 2004;44(7):1373–85.
    Crossref | PubMed
  16. Joner M, Finn AV, Farb A, et al., Pathology of drug-eluting stents in humans: delayed healing and late thrombotic risk, J Am Coll Cardiol, 2006;48(1):193–202.
    Crossref | PubMed