Abstract
Cardiovascular disease is a major cause of morbidity and mortality, especially in developed countries. Most academic research efforts in cardiovascular disease management focus on pharmacological interventions, or are concerned with discovering new disease markers for diagnosis and monitoring. Nonpharmacological interventions with therapeutic devices, conversely, are driven largely by novel materials and device design. Examples of such devices include coronary stents, heart valves, ventricular assist devices, and occluders for septal defects. Until recently, development of such devices remained largely with medical device companies. We trace the materials evolution story in two of these devices (stents and occluders), while also highlighting academic contributions, including our own, to the evolution story. Specifically, it addresses not only our successes, but also the challenges facing the translatability of concepts generated via academic research.
Highlights
Advances in nonpharmacological management of cardiovascular disease are largely driven by clever use of established biomaterials, or the development of new ones
While the bare metal stent was being deployed more and more widely, it was noted that restenosis rates were still around 20–30%; this restenosis was triggered largely by uninhibited growth of smooth muscle cells (SMCs) in response to the trauma caused by the stenting procedure
It is recognized that opening and closing of selected body vessels or defects is preferably done with a temporary scaffold rather than a biostable one, whose permanence may lead to serious side effects
Summary
Advances in nonpharmacological management of cardiovascular disease are largely driven by clever use of established biomaterials, or the development of new ones. The bare metal stent has undergone significant design and material changes to the present-day Co-Cr stent, which has a strut thickness of about 90 microns.[4] Ironically, while the bare metal stent was being deployed more and more widely, it was noted that restenosis rates were still around 20–30%; this restenosis was triggered largely by uninhibited growth of smooth muscle cells (SMCs) in response to the trauma caused by the stenting procedure This led to the invention of a drug-eluting stent (DES), a combination of pharmaceutical/device action, first developed by Johnson & Johnson and approved in 2003.5 For a while, DES enjoyed the lion’s share of the stent market until late-stage thrombotic events began to be noticed in long-term studies following deployment.
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